Honorary Faculty Emeritus, Epidemiology and Population Health
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Scientific interests: 1) cancer etiology (diet and familial), 2) cancer surveillance, and 3) cancer outcomes. Director of the Northern California Cancer Center (NCCC) from 1992-2002, currently Chief Scientific Officer. Professor of Epidemiology and Associate Director of Population Sciences at the Stanford Comprehensive Cancer Center, since 2005.
In the 1970’s authored papers of diet and colon, stomach, and oral cancers in New York. In Utah, Principal Investigator (PI) for a Program Grant of diet and colon cancer. Created a nutrient database, including home preserved foods and examined diet by site in the colon - fat was related to cancer in the ascending colon and protein in the descending colon (West, et al. Am J. Epid. 130:883-894, 1989). Reported effects of iron, energy, physical activity, tobacco, alcohol, coffee, and caffeine. Pl of a study of diet and prostate cancer, publishing the effects body mass, tobacco, alcohol, coffee, tea, theobromine, cadmium, occupation, and dietary nutrients. Significant associations for older men with aggressive tumors - total energy and dietary fat had significant associations, while none were found for body mass, physical activity, zinc, cadmium, selenium, vitamin C, or Beta-carotene (West, et al. Cancer Causes and Control, 2:85-94, 1991). Published on genetic and non-genetic factors in androgen production and clearance, familial factors and plasma and sex-steroid levels, and nutrition on sex-steroid levels in male twins (Bishop, et al. Genetic Epidemiology, 5:43-59,1988).
In California, investigator in collaborative study of prostate cancer, finding dietary fat associated with prostate cancer but not inter-ethnic differences (Whittemore, et al. J Natl Cancer Inst, 87:652-61, 1995). Published papers on diet and thyroid cancer and diet and cancer in a cohort of California teachers (Horn-Ross, et al. Cancer Causes Control 13:407-415,2002).
In the 1980’s, published regarding cancer in Mormons and non-Mormons (West et al. J Natl Cancer Inst. 65:1083-1095, 1980). As PI of the Greater Bay Area Cancer Registry, developed a surveillance research team that published on cancer incidence and survival trends, especially Asians (e.g. O’Malley et al. Cancer, 97:5:1303-1311, 2003; Phren, et al. Cancer Incidence in Chinese, Japanese, and Filipinos in the US and Asia, 1988-1992. Union City, CA: NCCC, 1999.) Identified the extent and characteristics of misclassified Hispanic (Stewart et al. Am J Epidemiol,149:1063-71, 1999) and Asian (Swallen et al Ethnic Dis., 8:218-227, 1998) patients.
Recent focus on cancer treatment and outcomes - finding use of adjuvant chemotherapy for stage III colon or stage II or III rectal cancer varied from 88%-11% in young and old patients and by hospital (51%-79%) (Ayanian, et al. J Clin Oncol. 21:7:1293-1300, 2003). Co-Investigator of the Cancer Care Outcomes Research Study (CanCORS) for colorectal and lung cancer that recruited over 5,000 colorectal and 5,000 lung cancer patients from which interview and medical record information regarding quality of life, treatment, health communications, and outcomes is being collected. (Ayanian J, et al. J Clin Oncology, 22 (15), 2992-2996, 2004). Contributed to collaborative studies such as the National Bladder Cancer Study (Hartge et al. J Natl Cancer Inst. 70:1021-1026, 1983), the cancer and steroid hormones (CASH) study, and a study of young Asian women and breast cancer (Ziegler et al. J Natl Cancer Inst, 85:1819-1827,1993). Co-Investigator of the Northern California component of the Collaborative Family Registry (CFR) for breast cancer. Group has recruited over 11,000 families for which epidemiologic, family history, and biospecimen data are available (John, et al. Breast Cancer Research, 6,:R375-R389, 2004. Helped create the California Teachers Study (cohort of 133,000 California teachers) who are followed for cancer and other outcomes. (Bernstein, et al. Causes Control, 13:625-635, 2002).
To compare breast cancer prognosis in BRCA1 and BRCA2 mutation carriers with that in patients with sporadic disease.An international population-based cohort study was conducted in Canada, the United States, and Australia of 3,220 women with incident breast cancer diagnosed between 1995 and 2000 and observed prospectively. Ninety-three had BRCA1 mutations; 71, BRCA2 mutations; one, both mutations; 1,550, sporadic breast cancer; and 1,505, familial breast cancer (without known BRCA1 or BRCA2 mutation). Distant recurrence and death were analyzed.Mean age at diagnosis was 45.3 years; mean follow-up was 7.9 years. Risks of distant recurrence and death did not differ significantly between BRCA1 mutation carriers and those with sporadic disease in univariable and multivariable analyses. Risk of distant recurrence was higher for BRCA2 mutation carriers compared with those with sporadic disease in univariable analysis (hazard ratio [HR], 1.63; 95% CI, 1.02 to 2.60; P = .04). Risk of death was also higher in BRCA2 carriers in univariable analysis (HR, 1.81; 95% CI, 1.15 to 2.86; P = .01). After adjustment for age, tumor stage and grade, nodal status, hormone receptors, and year of diagnosis, no differences were observed for distant recurrence (HR, 1.00; 95% CI, 0.62 to 1.61; P = 1.00) or death (HR, 1.12; 95% CI, 0.70 to 1.79; P = .64).Outcomes of BRCA1 mutation carriers were similar to those of patients with sporadic breast cancer. Worse outcomes in BRCA2 mutation carriers in univariable analysis seem to reflect the presence of more adverse tumor characteristics in these carriers. Similar outcomes were identified in BRCA2 carriers and those with sporadic disease in multivariable analyses.
View details for DOI 10.1200/JCO.2010.33.0068
View details for Web of Science ID 000302617900009
View details for PubMedID 22147742
Women with germline BRCA1 and BRCA2 mutations have five- to 20-fold increased risks of developing breast and ovarian cancer. A recent study claimed that women testing negative for their family-specific BRCA1 or BRCA2 mutation (noncarriers) have a five-fold increased risk of breast cancer. We estimated breast cancer risks for noncarriers by using a population-based sample of patients with breast cancer and their female first-degree relatives (FDRs).Patients were women with breast cancer and their FDRs enrolled in the population-based component of the Breast Cancer Family Registry; patients with breast cancer were tested for BRCA1 and BRCA2 mutations, as were FDRs of identified mutation carriers. We used segregation analysis to fit a model that accommodates familial correlation in breast cancer risk due to unobserved shared risk factors.We studied 3,047 families; 160 had BRCA1 and 132 had BRCA2 mutations. There was no evidence of increased breast cancer risk for noncarriers of identified mutations compared with FDRs from families without BRCA1 or BRCA2 mutations: relative risk was 0.39 (95% CI, 0.04 to 3.81). Residual breast cancer correlation within families was strong, suggesting substantial risk heterogeneity in women without BRCA1 or BRCA2 mutations, with some 3.4% of them accounting for roughly one third of breast cancer cases.These results support the practice of advising noncarriers that they do not have any increase in breast cancer risk attributable to the family-specific BRCA1 or BRCA2 mutation.
View details for DOI 10.1200/JCO.2010.34.4440
View details for PubMedID 22042950
View details for PubMedCentralID PMC3236651
Although underweight and obesity have been associated with increased risk of mortality, it remains unclear whether the associations differ by hormone therapy (HT) use and smoking. The authors examined the relationship between body mass index (BMI) and mortality within the California Teachers Study (CTS), specifically considering the impact of HT and smoking. The authors examined the associations of underweight and obesity with risks of all-cause and cause-specific mortality, among 115,433 women participating in the CTS, and specifically examined whether HT use or smoking modifies the effects of obesity. Multivariable Cox proportional hazards regression provided estimates of relative risks (RRs) and 95% confidence intervals (CIs). During follow up, 10,574 deaths occurred. All-cause mortality was increased for underweight (BMI <18.5; adjusted RR = 1.33, 95% CI = 1.20-1.47) and obese participants (BMI ? 30: RR = 1.27, 95% CI = 1.19-1.37) relative to BMI of 18.5-24.9). Respiratory disease mortality was increased for underweight and obese participants. Death from any cancer, and breast cancer specifically, and cardiovascular disease was observed only for obese participants. The obesity and mortality association remained after stratification on HT and smoking. Obese participants remained at greater risk for mortality after stratification on menopausal HT and smoking. Obesity was associated with increased all-cause mortality, as well as death from any cancer (including breast), and cardiovascular and respiratory diseases. These findings help to identify groups at risk for BMI-related poor health outcomes.
View details for DOI 10.1002/ijc.25905
View details for Web of Science ID 000295231000021
View details for PubMedID 21207419
A previous Australian population-based breast cancer case-control study found indirect evidence that control participation, although high, was not random. We hypothesized that unaffected sisters may provide a more appropriate comparison group than unrelated population controls.Three population-based case-control-family studies of breast cancer in women of white European origin were carried out by the Australian, Ontario and Northern California sites of the Breast Cancer Family Registry. We compared risk factors between 3643 cases, 2444 of their unaffected sisters and 2877 population controls and conducted separate case-control analyses based on population and sister controls using unconditional multivariable logistic regression.Compared with sister controls, population controls were more highly educated, had an earlier age at menarche, fewer births, their first birth at a later age and their last birth more recently. The established breast cancer associations detected using sister controls, but not detected using population controls, were decreasing risk with each of later age at menarche, more births, younger age at first birth and greater time since last birth.Since participation of population controls might be unintentionally related to some risk factors, we hypothesize that sister controls could provide more valid relative risk estimates and be recruited at lower cost. Given declining study participation by population controls, this contention is highly relevant to epidemiologic research.
View details for DOI 10.1093/ije/dyr110
View details for Web of Science ID 000296634900025
View details for PubMedID 21771852
View details for PubMedCentralID PMC3204209
We describe early dissemination patterns for first-line bevacizumab given for metastatic colorectal cancer treatment.We analyzed patient surveys and medical records for a population-based cohort with metastatic colorectal cancer treated in multiple regions and health systems in the United States (US). Eligible patients were diagnosed with metastatic colorectal cancer and initiated first-line chemotherapy after US Food & Drug Administration (FDA) bevacizumab approval in February 2004. First-line bevacizumab therapy was defined as receiving bevacizumab within 8 weeks of starting chemotherapy for metastatic colorectal cancer. We evaluated factors associated with first-line bevacizumab treatment using logistic regression.Among 355 patients, 31% received first-line bevacizumab in the two years after FDA approval, including 26% of men, 41% of women, and 16% of those ? 75 years. Use rose sharply within 6 months after FDA approval, then plateaued. 20% of patients received bevacizumab in combination with irinotecan; 53% received it with oxaliplatin. Men were less likely than women to receive bevacizumab (adjusted OR 0.55; 95% CI 0.32-0.93; p = 0.026). Patients ? 75 years were less likely to receive bevacizumab than patients < 55 years (adjusted OR 0.13; 95% CI 0.04-0.46; p = 0.001).One-third of eligible metastatic colorectal cancer patients received first-line bevacizumab shortly after FDA approval. Most patients did not receive bevacizumab as part of the regimen used in the pivotal study leading to FDA approval.
View details for DOI 10.1186/1471-2407-11-354
View details for Web of Science ID 000294950400001
View details for PubMedID 21846341
Individuals diagnosed and treated for cancer often report high levels of distress, continuing even after successful treatment. Spiritual well-being (SpWB) has been identified as an important factor associated with positive health outcomes. This study had two aims: (1) examine the associations between SpWB (faith and meaning/peace) and health-related quality of life (HRQL) outcomes and (2) examine competing hypotheses of whether the relationship among distress, SpWB, and HRQL is better explained by a stress-buffering (i.e., interaction) or a direct (main effects) model.Study 1 consisted of 258 colorectal cancer survivors (57% men) recruited from comprehensive cancer centers in metropolitan areas (age, M=61; months post-diagnosis, M=17). Study 2 consisted of 568 colorectal cancer survivors (49% men) recruited from a regional cancer registry (age, M=67; months post-diagnosis, M=19). Participants completed measures of SpWB (functional assessment of chronic illness therapy-spiritual well-being (FACIT-Sp)) and HRQL (functional assessment of cancer therapy-colorectal) in both studies. Measures of general distress (profile of mood states-short form) and cancer-specific distress were also completed in study 1 and study 2, respectively.After controlling for demographic and clinical variables, faith and meaning/peace were positively associated with HRQL. However, meaning/peace emerged as a more robust predictor of HRQL outcomes than faith. Planned analyses supported a direct rather than stress-buffering effect of meaning/peace.This study provides further evidence of the importance of SpWB, particularly meaning/peace, to HRQL for people with colorectal cancer. Future studies of SpWB and cancer should examine domains of the FACIT-Sp separately and explore the viability of meaning-based interventions for cancer survivors.
View details for DOI 10.1007/s00520-010-0871-4
View details for Web of Science ID 000290029700005
View details for PubMedID 20405147
Urinary bladder cancer is two to four times more common among men than among women, a difference in risk not fully explained by established risk factors. Our objective was to determine whether hormonal and reproductive factors are involved in female bladder cancer.We analyzed data from two population-based studies: the Los Angeles-Shanghai Bladder Cancer Study, with 349 female case-control pairs enrolled in Los Angeles and 131 female cases and 138 frequency-matched controls enrolled in Shanghai, and the California Teachers Study (CTS), a cohort of 120,857 women with 196 incident cases of bladder urothelial carcinoma diagnosed between 1995 and 2005. We also conducted a meta-analysis summarizing associations from our primary analyses together with published results.In primary data analyses, parous women experienced at least 30% reduced risk of developing bladder cancer compared with nulliparous women (Shanghai: OR = 0.38, 95% CI: 0.13-1.10; CTS: RR = 0.69, 95% CI: 0.50-0.95) consistent with results of a meta-analysis of nine studies (summary RR = 0.73, 95% CI: 0.63-0.85). The CTS, which queried formulation of menopausal hormone therapy (HT), revealed a protective effect for use of combined estrogen and progestin compared with no HT (RR = 0.60, 95% CI: 0.37-0.98). Meta-analysis of three studies provided a similar effect estimate (summary RR = 0.65, 95% CI: 0.48-0.88).A consistent pattern of reduced bladder cancer risk was found among parous women and those who used estrogen and progestin for HT.These results suggest that more research is warranted to investigate hormonal and reproductive factors as possible contributors to bladder cancer risk.
View details for DOI 10.1158/1055-9965.EPI-11-0017
View details for Web of Science ID 000291308600013
View details for PubMedID 21493870
Germline mutations in the two breast cancer susceptibility genes, BRCA1 and BRCA2 account for a significant portion of hereditary breast/ovarian cancer. De novo mutations such as multiple exon deletion are rarely occurred in BRCA1 and BRCA2. During our mutation screening for BRCA1/2 genes to Chinese women with risk factors for hereditary breast/ovarian cancer, we identified a novel germline mutation, consisting of a deletion from exons 1 to 12 in BRCA1 gene, in a patient diagnosed with early onset triple negative breast cancer with no family history of cancer. None of her parents carried the mutation and molecular analysis showed that this novel de novo germline mutation resulted in down-regulation of BRCA1 gene expression.
View details for DOI 10.1007/s10689-011-9429-y
View details for Web of Science ID 000290937500008
View details for PubMedID 21404118
View details for PubMedCentralID PMC3100488
Results from studies examining the association between hormone therapy (HT) and lung cancer risk disagree.We examined the associations between HT use and lung cancer risk among 60,592 postmenopausal women enrolled in the prospective California Teachers Study cohort. Between 1995 and 2007, a total of 727 women had a diagnosis of lung cancer. Multivariable Cox proportional hazards regression models were fit using age as the time metric.No measure of HT use was associated with lung cancer risk (all P(trend) values ?0.4). In addition, no variations in risk by smoking status (never, ever, former, current), type of HT [estrogen (E)-alone, E + progestin (P) use], type of menopause, or lung cancer histology were observed.Our findings do not support an association between HT and lung cancer.This large-scale, prospective study, which capitalizes on the detailed hormone use, smoking history, and type of menopause information available within this unique cohort, was unable to find any association between intake of HT and lung cancer risk.
View details for DOI 10.1158/1055-9965.EPI-10-1182
View details for Web of Science ID 000288067200019
View details for PubMedID 21266521
We examined whether dietary intake of isoflavones, lignans, isothiocyanates, antioxidants, or specific foods rich in these compounds is associated with reduced risk of B-cell non-Hodgkin lymphoma (NHL), multiple myeloma (MM), or Hodgkin lymphoma (HL) in a large, prospective cohort of women.Between 1995-1996 and 31 December 2007, among 110,215 eligible members of the California Teachers Study cohort, 536 women developed incident B-cell NHL, 104 developed MM, and 34 developed HL. Cox proportional hazards regression, with age as the time scale, was used to estimate adjusted rate ratios (RRs) with 95% confidence intervals (CIs) for risk of lymphoid malignancies.Weak inverse associations with risk of diffuse large B-cell lymphoma were observed for isothiocyanates (RR for ?12.1 vs. <2.7 mcM/day = 0.67, 95% CI: 0.43-1.05) and an antioxidant index measuring hydroxyl radical absorbance capacity (RR for ?2.2 vs. <0.9 ?M Trolox equiv/g/day = 0.68, 95% CI: 0.42-1.10; p (trend) = 0.08). Risk of other NHL subtypes, overall B-cell NHL, MM, or HL was not generally associated with dietary intake of isoflavones, lignans, isothiocyanates, antioxidants, or major food sources of these compounds.Isoflavones, lignans, isothiocyanates, and antioxidant compounds are not associated with risk of most B-cell malignancies, but some phytocompounds may decrease the risk of selected subtypes.
View details for DOI 10.1007/s10552-010-9692-5
View details for Web of Science ID 000286465000009
View details for PubMedID 21107674
View details for PubMedCentralID PMC3074494
Patients with early-onset breast and/or ovarian cancer frequently wish to know if they inherited a mutation in one of the cancer susceptibility genes, BRCA1 or BRCA2. Accurate carrier prediction models are needed to target costly testing. Two widely used models, BRCAPRO and BOADICEA, were developed using data from non-Hispanic Whites (NHW), but their accuracies have not been evaluated in other racial/ethnic populations.We evaluated the BRCAPRO and BOADICEA models in a population-based series of African American, Hispanic, and NHW breast cancer patients tested for BRCA1 and BRCA2 mutations. We assessed model calibration by evaluating observed versus predicted mutations and attribute diagrams, and model discrimination using areas under the receiver operating characteristic curves.Both models were well-calibrated within each racial/ethnic group, with some exceptions. BOADICEA overpredicted mutations in African Americans and older NHWs, and BRCAPRO underpredicted in Hispanics. In all racial/ethnic groups, the models overpredicted in cases whose personal and family histories indicated >80% probability of carriage. The two models showed similar discrimination in each racial/ethnic group, discriminating least well in Hispanics. For example, BRCAPRO's areas under the receiver operating characteristic curves were 83% (95% confidence interval, 63-93%) for NHWs, compared with 74% (59-85%) for African Americans and 58% (45-70%) for Hispanics.The poor performance of the model for Hispanics may be due to model misspecification in this racial/ethnic group. However, it may also reflect racial/ethnic differences in the distributions of personal and family histories among breast cancer cases in the Northern California population.
View details for DOI 10.1158/1055-9965.EPI-08-1090
View details for PubMedID 19336551
There are established differences in breast cancer epidemiology between Asian and white individuals, but little is known about hereditary breast cancer in Asian populations. Although increasing numbers of Asian individuals are clinically tested for BRCA1/2 mutations, it is not known whether computer models that predict mutations work accurately in Asian individuals. We compared the performance in Asian and white individuals of two widely used BRCA1/2 mutation prediction models, BRCAPRO and Myriad II.We evaluated BRCAPRO and Myriad II in 200 Asian individuals and a matched control group of 200 white individuals who were tested for BRCA1/2 mutations at four cancer genetics clinics, by comparing numbers of observed versus predicted mutation carriers and by evaluating area under the receiver operating characteristic curve (AUC) for each model.BRCAPRO and Myriad II accurately predicted the number of white BRCA1/2 mutation carriers (25 observed v 24 predicted by BRCAPRO; 25 predicted by Myriad II, P > or = .69), but underpredicted Asian carriers by two-fold (49 observed v 25 predicted by BRCAPRO; 26 predicted by Myriad II; P < or = 3 x 10(-7)). For BRCAPRO, this racial difference reflects substantial underprediction of Asian BRCA2 mutation carriers (26 observed v 4 predicted; P = 1 x 10(-30)); for Myriad II, separate mutation predictions were not available. For both models, AUCs were nonsignificantly lower in Asian than white individuals, suggesting less accurate discrimination between Asian carriers and noncarriers.Both BRCAPRO and Myriad II underestimated the proportion of BRCA1/2 mutation carriers, and discriminated carriers from noncarriers less well, in Asian compared with white individuals.
View details for DOI 10.1200/JCO.2008.16.8310
View details for PubMedID 18779604
Lung cancer is a leading cause of cancer death worldwide. Although smoking remains the predominant cause of lung cancer, lung cancer in never smokers is an increasingly prominent public health issue. However, data on this topic, particularly lung cancer incidence rates in never smokers, are limited.We reviewed the existing literature on lung cancer incidence and mortality rates among never smokers and present new data regarding rates in never smokers from the following large, prospective cohorts: Nurses' Health Study; Health Professionals Follow-Up Study; California Teachers Study; Multiethnic Cohort Study; Swedish Lung Cancer Register in the Uppsala/Orebro region; and First National Health and Nutrition Examination Survey Epidemiologic Follow-Up Study.Truncated age-adjusted incidence rates of lung cancer among never smokers age 40 to 79 years in these six cohorts ranged from 14.4 to 20.8 per 100,000 person-years in women and 4.8 to 13.7 per 100,000 person-years in men, supporting earlier observations that women are more likely than men to have non-smoking-associated lung cancer. The distinct biology of lung cancer in never smokers is apparent in differential responses to epidermal growth factor receptor inhibitors and an increased prevalence of adenocarcinoma histology in never smokers.Lung cancer in never smokers is an important public health issue, and further exploration of its incidence patterns, etiology, and biology is needed.
View details for DOI 10.1200/JCO.2006.07.2983
View details for PubMedID 17290054
A distinct morphologic and molecular phenotype has been reported for BRCA1-associated breast cancers; however, the phenotype of BRCA2-associated breast cancers is less certain. To comprehensively characterize BRCA2-associated breast cancers we performed a retrospective case control study using tumors accrued through the Breast Cancer Family Registry. We examined the tumor morphology and hormone receptor status in 157 hereditary breast cancers with germline mutations in BRCA2 and 314 control tumors negative for BRCA1 and BRCA2 mutations that were matched for age and ethnicity. Tissue microarrays were constructed from 64 BRCA2-associated and 185 control tumors. Tissue microarray sections were examined for HER2/neu protein overexpression, p53 status and the expression of basal markers, luminal markers, cyclin D1, bcl2, and MIB1 by immunohistochemistry. The majority of BRCA2-associated tumors and control tumors were invasive ductal, no special-type tumors. In contrast to control tumors, BRCA2-associated cancers were more likely to be high grade (P<0.0001) and to have pushing tumor margins (P=0.0005). Adjusting for grade, BRCA2-associated tumors were more often estrogen receptor positive (P=0.008) and exhibited a luminal phenotype (P=0.003). They were less likely than controls to express the basal cytokeratin CK5 (P=0.03) or to overexpress HER2/neu protein (P=0.06). There was no difference in p53, bcl2, MIB1, or cyclin D1 expression between BRCA2-associated and control tumors. We have demonstrated, in the largest series of BRCA2-associated breast cancers studied to date, that these tumors are predominantly high-grade invasive ductal carcinomas of no special type and they demonstrate a luminal phenotype despite their high histologic grade.
View details for Web of Science ID 000243236000015
View details for PubMedID 17197928
First-degree relatives of patients with breast or ovarian cancer have increased risks for these cancers. Little is known about how their risks vary with the patient's cancer site, carrier status for predisposing genetic mutations, or age at cancer diagnosis.We evaluated breast and ovarian cancer incidence in 2,935 female first-degree relatives of non-Hispanic White female patients with incident invasive cancers of the breast (n = 669) or ovary (n = 339) who were recruited from a population-based cancer registry in northern California. Breast cancer patients were tested for BRCA1 and BRCA2 mutations. Ovarian cancer patients were tested for BRCA1 mutations. We estimated standardized incidence ratios (SIR) and 95% confidence intervals (95% CI) for breast and ovarian cancer among the relatives according to the patient's mutation status, cancer site, and age at cancer diagnosis.In families of patients who were negative or untested for BRCA1 or BRCA2 mutations, risks were elevated only for the patient's cancer site. The breast cancer SIR was 1.5 (95% CI, 1.2-1.8) for relatives of breast cancer patients, compared with 1.1 (95% CI, 0.8-1.6) for relatives of ovarian cancer patients (P = 0.12 for difference by patient's cancer site). The ovarian cancer SIR was 0.9 (95% CI, 0.5-1.4) for relatives of breast cancer patients, compared with 1.9 (95% CI, 1.0-4.0) for relatives of ovarian cancer patients (P = 0.04 for difference by site). In families of BRCA1-positive patients, relatives' risks also correlated with the patient's cancer site. The breast cancer SIR was 10.6 (95% CI, 5.2-21.6) for relatives of breast cancer patients, compared with 3.3 (95% CI, 1.4-7.3) for relatives of ovarian cancer patients (two-sided P = 0.02 for difference by site). The ovarian cancer SIR was 7.9 (95% CI, 1.2-53.0) for relatives of breast cancer patients, compared with 11.3 (3.6-35.9) for relatives of ovarian cancer patients (two-sided P = 0.37 for difference by site). Relatives' risks were independent of patients' ages at diagnosis, with one exception: In families ascertained through a breast cancer patient without BRCA mutations, breast cancer risks were higher if the patient had been diagnosed before age 40 years.In families of patients with and without BRCA1 mutations, breast and ovarian cancer risks correlate with the patient's cancer site. Moreover, in families of breast cancer patients without BRCA mutations, breast cancer risk depends on the patient's age at diagnosis. These patterns support the presence of genes that modify risk specific to cancer site, in both carriers and noncarriers of BRCA1 and BRCA2 mutations.
View details for DOI 10.1158/1055-9965.EPI-05-0687
View details for PubMedID 16492929
To estimate minimally important differences (MIDs) on the Functional Assessment of Cancer Therapy-Colorectal (FACT-C) instrument using anchor- and distribution-based methods.Preliminary MIDs were generated for FACT-C scores based on published results for two samples (n = 60 and n = 63) from the FACT-C validation study. Preliminary MIDs were confirmed using data from a Phase II randomized controlled clinical trial (n = 104) and a population-based observational study (n = 568). MIDs were estimated for the colorectal cancer subscale (CCS); the FACT-C Trial Outcome Index (TOI-C), which is the sum of the CCS, physical well-being, and functional well-being subscales; and the FACT-C total score. Both cross-sectional and longitudinal analyses were used.MIDs were stable across the different patient samples. The recommended MIDs ranged from 2 to 3 points for the CCS, 4 to 6 points for the TOI-C, and 5 to 8 points for the FACT-C total score.MIDs can enhance the interpretability of FACT-C scores, and they can be used to provide a basis for sample size estimation and to determine clinical benefit in combination with other measures of efficacy. General guidelines for estimating MIDs for other FACT instruments are suggested.
View details for DOI 10.1016/j.jclinepi.2005.07.008
View details for Web of Science ID 000233767900005
View details for PubMedID 16291468
Public health surveillance systems relevant to cancer, centered around population-based cancer registration, have produced extensive, high-quality data for evaluating the cancer burden. However, these resources are underutilized by the epidemiology community due, we postulate, to under-appreciation of their scope and of the methods and software for using them. To remedy these misperceptions, this paper defines cancer surveillance research, reviews selected prior contributions, describes current resources, and presents challenges to and recommendations for advancing the field. Cancer surveillance research, in which systematically collected patient and population data are analyzed to examine and test hypotheses about cancer predictors, incidence, and outcomes in geographically defined populations over time, has produced not only cancer statistics and etiologic hypotheses but also information for public health education and for cancer prevention and control. Data on cancer patients are now available for all US states and, within SEER, since 1973, and have been enhanced by linkage to other population-based resources. Appropriate statistical methods and sophisticated interactive analytic software are readily available. Yet, publication of papers, funding opportunities, and professional training for cancer surveillance research remain inadequate. Improvement is necessary in these realms to permit cancer surveillance research to realize its potential in resolving the growing cancer burden.
View details for DOI 10.1007/s10552-005-4501-2
View details for Web of Science ID 000232139900002
View details for PubMedID 16184466
To identify opportunities for improving care, we evaluated patients' perceptions of the quality of their cancer care by race, ethnicity, and language.We surveyed a population-based cohort of 1,067 patients with colorectal cancer in northern California approximately 9 months after diagnosis. Adjusting for clinical and demographic factors, mean problem scores were analyzed on a 100-point scale for six domains of care.Mean problem scores were highest for health information (47.8), followed by treatment information (32.3), psychosocial care (31.7), coordination of care (21.3), confidence in providers (13.1), and access to cancer care (12.7). In adjusted comparisons with white patients, African American patients reported more problems with coordination of care (difference, 9.8; P < .001), psychosocial care (difference, 7.2; P = .03), access to care (difference, 6.6; P = .03), and health information (difference, 12.5; P < .001). Asian/Pacific Islander patients reported more problems than did white patients with coordination of care (difference, 13.2; P < .001), access to care (difference, 15.5; P < .001), and health information (difference, 12.6; P = .004). Hispanic patients tended to report more problems with coordination of care (difference, 4.4; P = .06), access to care (difference, 5.8; P = .08), and treatment information (difference, 7.0; P = .06). Non-English-speaking white patients reported more problems than other white patients with coordination of care (difference, 21.9; P < .001), psychosocial care (difference, 16.1; P = .009), access to care (difference, 19.8; P = .003), and treatment information (difference, 17.8; P = .002). Non-English-speaking Hispanic patients reported more problems than other Hispanic patients with confidence in providers (difference, 16.9; P = .01).Efforts to improve patients' experiences with cancer care should address disparities by race, ethnicity, and language, particularly in coordination of care, access to care, and the provision of relevant information.
View details for DOI 10.1200/JCO.2005.06.102
View details for Web of Science ID 000232233100021
View details for PubMedID 16116149
Recent oral contraceptive use has been associated with a small increase in breast cancer risk and a substantial decrease in ovarian cancer risk. The effects on risks for women with germ line mutations in BRCA1 or BRCA2 are unclear.Subjects were population-based samples of Caucasian women that comprised 1,156 incident cases of invasive breast cancer diagnosed before age 40 (including 47 BRCA1 and 36 BRCA2 mutation carriers) and 815 controls from the San Francisco Bay area, California, Ontario, Canada, and Melbourne and Sydney, Australia. Relative risks by carrier status were estimated using unconditional logistic regression, comparing oral contraceptive use in case groups defined by mutation status with that in controls.After adjustment for potential confounders, oral contraceptive use for at least 12 months was associated with decreased breast cancer risk for BRCA1 mutation carriers [odds ratio (OR), 0.22; 95% confidence interval (CI), 0.10-0.49; P < 0.001], but not for BRCA2 mutation carriers (OR, 1.02; 95% CI, 0.34-3.09) or noncarriers (OR, 0.93; 95% CI, 0.69-1.24). First use during or before 1975 was associated with increased risk for noncarriers (OR, 1.52 per year of use before 1976; 95% CI, 1.22-1.91; P < 0.001).There was no evidence that use of current low-dose oral contraceptive formulations increases risk of early-onset breast cancer for mutation carriers, and there may be a reduced risk for BRCA1 mutation carriers. Because current formulations of oral contraceptives may reduce, or at least not exacerbate, ovarian cancer risk for mutation carriers, they should not be contraindicated for a woman with a germ line mutation in BRCA1 or BRCA2.
View details for Web of Science ID 000227113800010
View details for PubMedID 15734957
Few studies have examined the effect of breast implants after mastectomy on long-term survival in breast cancer patients, despite growing public health concern over potential long-term adverse health effects.We analyzed data from the Surveillance, Epidemiology and End Results Breast Implant Surveillance Study conducted in San Francisco-Oakland, in Seattle-Puget Sound, and in Iowa. This population-based, retrospective cohort included women younger than 65 years when diagnosed with early or unstaged first primary breast cancer between 1983 and 1989, treated with mastectomy. The women were followed for a median of 12.4 years (n = 4968). Breast implant usage was validated by medical record review. Cox proportional hazards models were used to estimate hazard rate ratios for survival time until death due to breast cancer or other causes for women with and without breast implants, adjusted for relevant patient and tumor characteristics.Twenty percent of cases received postmastectomy breast implants, with silicone gel-filled implants comprising the most common type. Patients with implants were younger and more likely to have in situ disease than patients not receiving implants. Risks of breast cancer mortality (hazard ratio, 0.54; 95% confidence interval, 0.43-0.67) and nonbreast cancer mortality (hazard ratio, 0.59; 95% confidence interval, 0.41-0.85) were lower in patients with implants than in those patients without implants, following adjustment for age and year of diagnosis, race/ethnicity, stage, tumor grade, histology, and radiation therapy. Implant type did not appear to influence long-term survival.In a large, population-representative sample, breast implants following mastectomy do not appear to confer any survival disadvantage following early-stage breast cancer in women younger than 65 years old.
View details for DOI 10.1186/bcr974
View details for Web of Science ID 000227583300010
View details for PubMedID 15743498
Data from several countries indicate that 1% to 2% of Ashkenazi Jews carry a pathogenic ancestral mutation of the tumor suppressor gene BRCA1. However, the prevalence of BRCA1 mutations among non-Ashkenazi Whites is uncertain. We estimated mutation carrier prevalence in U.S. non-Hispanic Whites, specific for Ashkenazi status, using data from two population-based series of San Francisco Bay Area patients with invasive cancers of the breast or ovary, and data on breast and ovarian cancer risks in Ashkenazi and non-Ashkenazi carriers. Assuming that 90% of the BRCA1 mutations were detected, we estimate a carrier prevalence of 0.24% (95% confidence interval, 0.15-0.39%) in non-Ashkenazi Whites, and 1.2% (95% confidence interval, 0.5-2.6%) in Ashkenazim. When combined with U.S. White census counts, these prevalence estimates suggest that approximately 550,513 U.S. Whites (506,206 non-Ashkenazim and 44,307 Ashkenazim) carry germ line BRCA1 mutations. These estimates may be useful in guiding resource allocation for genetic testing and genetic counseling and in planning preventive interventions.
View details for PubMedID 15598764
In the general population, ovarian cancer risk is inversely associated with oral contraceptive use, tubal ligation, and childbearing. Among carriers of BRCA1 gene mutations, the data are conflicting. The authors identified women diagnosed with incident invasive epithelial ovarian cancer in the San Francisco Bay Area of California from March 1997 through July 2001. They compared the contraceptive and reproductive histories of 36 carrier cases and 381 noncarrier cases with those of 568 controls identified by random digit dialing who were frequency matched to cases on age and race/ethnicity. In both carriers and noncarriers, reduced risk was associated with ever use of oral contraceptives (odds ratio = 0.54 (95% confidence interval (CI): 0.26, 1.13) for carriers and 0.55 (95% CI: 0.41, 0.73) for noncarriers), duration of oral contraceptive use (risk reduction per year = 13% (p = 0.01) for carriers and 6% (p < 0.001) for noncarriers), history of tubal ligation (odds ratio = 0.68 (95% CI: 0.25, 1.90) for carriers and 0.65 (95% CI: 0.45, 0.95) for noncarriers), and increasing parity (risk reduction per childbirth = 16% (p = 0.26) for carriers and 24% (p < 0.001) for noncarriers). These data suggest that BRCA1 mutation carriers and noncarriers have similar risk reductions associated with oral contraceptive use, tubal ligation, and parity.
View details for PubMedID 15383404
Vitamin D inhibits prostate cancer cell growth, angiogenesis, and metastasis. These actions are mediated by the vitamin D receptor. We examined associations between prostate cancer risk and five polymorphisms in the VDR gene: four single nucleotide polymorphisms (FokI, BsmI, ApaI, and TaqI restriction sites) and the polyadenylic acid microsatellite. Specifically, we genotyped population-based samples of young African Americans (113 cases and 121 controls) and Whites (232 cases and 171 controls) and members of 98 predominantly White families with multiple cases of prostate cancer. Among Whites, there was no evidence for association between prostate cancer risk and alleles at any of the five polymorphic sites regardless of how the men were ascertained. Moreover, estimated five-locus haplotype frequencies were similar in White cases and controls. Among African Americans, prostate cancer risk was associated with homozygosity for the F allele at the FokI site (odds ratio 1.9, 95% confidence interval 1.0-3.3). In addition, estimated haplotype frequencies differed significantly (P < 0.01) between African American cases and controls. These findings need replication in other studies of African Americans. Homozygosity for the F allele at the FokI site is more prevalent in the African American population than in U.S. Whites. If the FokI association noted here were causal, this difference could account for some of the disease burden among African Americans and some of the excess risk in African Americans compared with Whites.
View details for Web of Science ID 000223155500010
View details for PubMedID 15298953
Alcohol consumption of approximately two drinks or more per day has been associated with elevated breast cancer risk in the California Teachers Study cohort as well as in many other populations. The objective of this analysis is to examine effects of age at drinking and drinking patterns and to identify effect modifiers. Of the 103,460 at-risk cohort members, age <85, who resided in California and completed the baseline alcohol assessment, 1,742 were diagnosed with invasive breast cancer after joining the cohort and before January 2001. Incident breast cancers were identified through the California Cancer Registry and follow-up for death and confirmation of continued California residence used various sources. Multivariate Cox proportional hazards regression models were used to estimate relative risks (RRs). Elevated breast cancer risk was most evident for recent drinking [RR = 1.28, 95% confidence interval (CI): 1.06-1.54 for >/=20 g/day versus nondrinkers], with no clear pattern for consumption during earlier periods of life. This elevation in risk was 32% among postmenopausal women (95% CI: 1.06-1.63) and 21% among pre/perimenopausal women (95% CI: 0.76-1.92). Highest risks associated with heavy alcohol consumption were observed among postmenopausal women with a history of biopsy-diagnosed benign breast disease (RR = 1.97, 95% CI: 1.39-2.79 compared to nondrinkers without benign breast disease) or who had used combination hormone replacement therapy (HRT) (RR = 2.24, 95% CI: 1.59-3.14 compared to nondrinkers who never used HRT). Recent alcohol consumption equivalent to two or more drinks per day increases the risk of invasive breast cancer, with the greatest RRs observed among heavy drinkers who are also postmenopausal and have a history of benign breast disease or who use HRT.
View details for Web of Science ID 000220081000012
View details for PubMedID 15006916
The etiology of familial breast cancer is complex and involves genetic and environmental factors such as hormonal and lifestyle factors. Understanding familial aggregation is a key to understanding the causes of breast cancer and to facilitating the development of effective prevention and therapy. To address urgent research questions and to expedite the translation of research results to the clinical setting, the National Cancer Institute (USA) supported in 1995 the establishment of a novel research infrastructure, the Breast Cancer Family Registry, a collaboration of six academic and research institutions and their medical affiliates in the USA, Canada, and Australia.The sites have developed core family history and epidemiology questionnaires, data dictionaries, and common protocols for biospecimen collection and processing and pathology review. An Informatics Center has been established to collate, manage, and distribute core data.As of September 2003, 9116 population-based and 2834 clinic-based families have been enrolled, including 2346 families from minority populations. Epidemiology questionnaire data are available for 6779 affected probands (with a personal history of breast cancer), 4116 unaffected probands, and 16,526 relatives with or without a personal history of breast or ovarian cancer. The biospecimen repository contains blood or mouthwash samples for 6316 affected probands, 2966 unaffected probands, and 10,763 relatives, and tumor tissue samples for 4293 individuals.This resource is available to internal and external researchers for collaborative, interdisciplinary, and translational studies of the genetic epidemiology of breast cancer. Detailed information can be found at the URL http://www.cfr.epi.uci.edu/.
View details for DOI 10.1186/bcr801
View details for Web of Science ID 000222828200022
View details for PubMedID 15217505
View details for PubMedCentralID PMC468645
A comprehensive framework for cancer surveillance should span the entire lifespan and be capable of providing information on risk, burden, disparity, cost, cancer care, survival, and death. Cancer incidence, the point in the continuum when an individual is diagnosed with cancer, has a strong, well-developed system to produce information about newly diagnosed cancer cases. However, in the future, this system must be enhanced and integrated with other cancer surveillance networks and other systems to provide timely information on the burden of newly diagnosed patients with respect to various cross-cutting population characteristics (e.g., social, economic, race/ethnic, urbanicity, or access to care) to define, monitor, and reduce incidence and various disparities noted among population groups. Collaboration in data collection, standard setting, surveillance activities, research, education and training, data use, and advocacy among all registries and national programs will be important to the continued success of the cancer incidence surveillance system. The cancer registry is an integral part of the infrastructure to reduce the burden of cancer, including the numbers of newly diagnosed cases.
View details for Web of Science ID 000185261300008
View details for PubMedID 14575364
Population-based cancer registries represent a potentially valuable tool to evaluate treatment; however, information on the completeness of registry treatment data is sparse.To evaluate the completeness of registry treatment data for patients with colorectal cancer and to identify predictors of complete reporting.We surveyed physicians or reviewed office records of 1956 northern California patients diagnosed with colorectal cancer during 1996 to 1997 to assess the completeness of registry data regarding use of adjuvant chemotherapy and radiation therapy.For patients with a record of receipt of chemotherapy in either the registry or physician survey, information was in the original registry records for 82.0%. In the multivariate analysis, completeness of chemotherapy reporting was lower for patients aged 65 to 74, those with colon cancer, [corrected] and higher for patients treated in hospitals that are part of a large health maintenance organization (HMO). For patients with a record of receipt of radiation therapy, information was in the original registry records for 90.2%. In the multivariate analysis, completeness of radiation therapy reporting was higher for patients aged 18 to 54 and those treated in HMO hospitals.Because the completeness of the registry treatment data varied by patient and hospital characteristics, use of registry data without supplementation could bias estimates of the proportion of patients treated, and of the patient and provider characteristics associated with treatment. Enhanced cancer registry data could be a valuable component of population-based cancer data systems for assessing quality of cancer care.
View details for Web of Science ID 000185014700002
View details for PubMedID 12972840
Randomized trials have demonstrated that adjuvant chemotherapy improves survival for patients with stage III colon cancer and that chemotherapy combined with radiation therapy improves survival for patients with stage II or III rectal cancer. This population-based study was designed to assess use of these treatments in clinical practice.From the California Cancer Registry, we identified all patients diagnosed during 1996 to 1997 with stage III colon cancer (n = 1,422) and stage II or III rectal cancer (n = 534) in 22 northern California counties. To supplement registry data on adjuvant therapies and ascertain reasons they were not used, we surveyed physicians or reviewed office records for 1,449 patients (74%).Chemotherapy rates varied widely by age from 88% (age < 55 years) to 11% (age >or= 85 years), and radiation therapy varied similarly. Adjusting for demographic, clinical, and hospital characteristics, chemotherapy was used less often among older and unmarried patients, and radiation therapy was used less often among older patients, black patients, and those initially treated in low-volume hospitals. Adjusted rates of chemotherapy varied significantly (P <.01) among individual hospitals: 79% and 51%, respectively, at one SD above and below average (67%). Physicians' reasons for not providing adjuvant therapy included patient refusal (30% for chemotherapy, 22% for radiation therapy), comorbid illness (22% and 14%, respectively), or lack of clinical indication (22% and 45%, respectively).Use of adjuvant therapy for colorectal cancer varies substantially by age, race, marital status, hospital volume, and individual hospital, indicating opportunities to improve care. With enhanced data on adjuvant therapies, population-based registries could become a valuable resource for monitoring the quality of cancer care.
View details for Web of Science ID 000181973400014
View details for PubMedID 12663717
In the US, Koreans are a rapidly growing group and comprised 10.5% of the total Asian population as of 2000. However, little has been published regarding cancer patterns in this subpopulation.Using data from the Surveillance, Epidemiology, and End Results program, the California Cancer Registry, and the International Association for Research on Cancer, we compared age-adjusted and age-specific incidence rates for cancers of the prostate, breast, cervix, lung, colon, rectum, stomach, liver, and esophagus in US Koreans with rates of these cancers in residents of Kangwha, South Korea, and in US whites as a reference.While the most frequently diagnosed cancer was lung among US Korean males and breast among US Korean females, it was stomach cancer for both sexes in Kangwha. Rates of prostate, breast, and colon cancer were considerably higher for Koreans in the US than in Kangwha, but were not as high as in whites. Cervical and stomach cancers showed the opposite racial/ethnic pattern, with rates highest in Kangwha, intermediate among US Koreans, and lowest among whites. Rates of rectal cancer in females and esophageal cancer in males were two-times higher in Kangwha than in US Koreans but esophageal cancer rates were similar between US Koreans and whites. Liver cancer rates were similar between Kangwha residents and US Koreans, but nearly 10-times lower among whites.Although these comparisons may have methodologic limitations, including data quality and racial/ethnic misclassification, the differences seen in migrant and native Koreans for some cancers warrant further investigation in this growing subpopulation.
View details for Web of Science ID 000182447400008
View details for PubMedID 12749722
Although overall survival for invasive breast carcinoma remains high, black women experience poorer survival than whites. Less is known about the survival of Hispanics and Asians, who may share clinical and socioeconomic risk factors similar to blacks. To better understand racial/ethnic survival patterns, we investigated the effect of socioeconomic status (SES) and disease stage on racial/ethnic differences in breast carcinoma survival in a large population-based cohort.Using data from the Surveillance, Epidemiology, and End Results program (SEER), we identified 10,414 white, 940 black, 1100 Hispanic, and 1180 Asian females diagnosed with breast carcinoma in the Greater San Francisco Bay Area between 1988 and 1992. We used the Kaplan-Meier method to generate survival rates and Cox proportional hazards regression to estimate the risk of death by race/ethnicity, after adjustment for clinical, demographic, and census-derived SES variables.The 10-year unadjusted survival rates were 81% for whites, 69% for blacks, 75% for Hispanics, and 79% for Asians. Adjusting for stage decreased the relative risk of mortality for blacks from 1.81 to 1.29; the stage-adjusted relative risk for Hispanics (1.11) and Asians (1.02) did not differ significantly from whites. Additional adjustment for age, tumor characteristics, and treatment factors did little to alter the relative risk in blacks; adding blue-collar status to the model further decreased the relative risks for blacks to 1.22. Residing in a blue-collar neighborhood was independently associated with a 1.16 increase in risk of death.After adjustment for multiple factors, blacks continue to have slight but significantly poorer survival after breast carcinoma compared with whites, whereas the survival of Hispanics and Asians did not differ from whites.
View details for Web of Science ID 000181190000022
View details for PubMedID 12599239
Much of what is known about breast cancer in African-American (AA) women is based on existing cancer surveillance data. Thus, it is important to consider the accuracy of these resources in describing the impact of breast cancer in AA populations.National cancer surveillance data bases are described, their most recent findings are presented, their limitations are outlined, and recommendations are made for improving their utility.Breast cancer characteristics have been studied well in urban (but not in rural) and Southern AA populations. The recent Surveillance, Epidemiology, and End Results (SEER) Program expansion and the continued improvement of state cancer registry operations will provide opportunities to study larger and more diverse AA subpopulations. Recommendations for improving the utility of surveillance data bases include adding new items to better describe correlates of advanced stage at diagnosis and reduced survival of AA women with breast cancer by linking surveillance data bases with other large data bases to provide area-level socioeconomic status, health insurance status, and retrieving new information about patient comorbidities and biomarkers from medical records; improving the completeness and accuracy of treatment and survival information already collected for all patients; working to improve the dissemination of appropriate cancer data to nonresearch consumer communities, including clinicians, patients, advocates, politicians, and health officials; and the development of new training programs for cancer registrars and researchers.The continued improvement of cancer surveillance systems should be considered important activities in this research agenda, because these data will play a far-reaching role in the prevention and control of breast cancer in AA women.
View details for PubMedID 12491484
Many studies have examined racial/ethnic differences in treatment for localized breast carcinoma, but to the authors' knowledge few have included Asian/Pacific Islander (API) women.The population-based study included API and non-Hispanic white women diagnosed with localized invasive breast carcinoma in the Greater San Francisco Bay Area during 1994 (n = 1772). Multiple logistic regression was used to assess the association between race/ethnicity and type of surgery, radiation therapy following breast-conserving surgery (BCS), and hormone therapy for estrogen receptor-positive tumors while adjusting for demographic, medical, and census block-group socioeconomic characteristics.API women were significantly more likely to undergo mastectomies than white women (58% vs. 42%). This difference remained for Chinese and Filipino women after multivariate adjustment (odds ratio vs. whites [OR] = 2.4, 95% confidence interval [95% CI] = 1.4-4.2; OR [95%CI] = 1.8[1.0-3.1], respectively). Chinese women were also more likely than white women to not receive adjuvant therapy, be it radiation after BCS or hormone therapy for estrogen receptor-positive disease. Other API women did not differ from white women in adjuvant therapy use.This population-based study identified differences in treatment for localized breast carcinoma by race/ethnicity that were not explained by differences in demographic, medical, or socioeconomic characteristics. These results underscore the importance of looking at treatment patterns separately for API subgroups and support the need for research into cultural differences that may influence breast carcinoma treatment choices.
View details for DOI 10.1002/cncr.10965
View details for Web of Science ID 000179371400003
View details for PubMedID 12436431
Nearly 600,000 persons have immigrated to the United States from Vietnam since the end of the Vietnam War. Despite the rapid growth of the U.S. Vietnamese population, little is known about cancer incidence in this migrant group. Using population-based data from the Surveillance, Epidemiology and End Results program, California Cancer Registry and International Agency for Research on Cancer, we compared cancer incidence rates for Vietnamese in the United States (1988-1992) to rates for residents of Ha Noi, Vietnam (1991-1993); non-Hispanic whites were included to serve as the U.S. reference rates. Lung and breast cancers were the most common among Vietnamese males and females, respectively, regardless of geographic region. Rates of cancers more common to U.S. whites, such as breast, prostate and colon cancers, were elevated for U.S. Vietnamese compared to residents in Ha Noi but still lower than rates for U.S. whites. Rates of cancers more common to Asian countries, such as stomach, liver, lung and cervical cancers, were likewise elevated for U.S. Vietnamese compared to residents of Ha Noi and exceeded corresponding rates for whites. Incidence patterns for stomach, liver, lung and cervical cancers may reflect increased risk of exposures in this migrant population and should be further explored to uncover the relative contributions of environmental and genetic factors to cancer etiology.
View details for DOI 10.1002/ijc.10725
View details for Web of Science ID 000179013100015
View details for PubMedID 12402312
To describe factors associated with vitamin supplement use in a large cohort of adult women.California teachers and administrators (n = 133,479) completed a questionnaire on lifestyle factors and medical history. Specific supplement users regularly used at least one specific vitamin supplement in the past year; multivitamin users regularly used a multivitamin; and multivitamin and specific supplement users took a multivitamin and one or more specific supplements. Associations between supplement use and other variables were quantified using means, cross-tabulations, and age-adjusted prevalence odds ratios.Multivitamin and specific supplement users tended to be older and Caucasian. Compared to non-users, they were also leaner (odds ratio [OR] for BMI > or = 30 kg/m2 = 0.6 for specific supplement users with or without multivitamins, and OR = 0.7 for multivitamin only users), and were less likely to be current smokers (OR for current smoking = 0.8 for multivitamin plus specific supplement users, OR = 0.9 for specific supplement only users, and OR = 0.7 for multivitamin only users). Specific supplement users (with or without multivitamins) were more likely to use cancer screening tests, eat fruits and vegetables, and exercise than were multivitamin only users or non-users.A variety of demographic, dietary, and health-related factors were associated with different categories of supplement use.
View details for Web of Science ID 000178063700006
View details for PubMedID 12420952
In 1983-87, we conducted a population-based case-control study of breast cancer in Asian women living in California and Hawaii, in which migration history (a composite of the subject's place of birth, usual residence in Asia (urban/rural), length of time living in the West, and grandparents' place of birth) was associated with a six-fold risk gradient that paralleled the historical differences in incidence rates between the US and Asian countries. This provided the opportunity to determine whether endogenous hormones vary with migration history in Asian-American women. Plasma obtained from 316 premenopausal and 177 naturally premenopausal study controls was measured for levels of estrone (E1), estradiol (E2), estrone sulphate (E1S), androstenedione (A), testosterone (T), dehydroepiandrosterone (DHEA), dehydroepiandrosterone sulphate (DHEAS), progesterone (PROG) and sex hormone-binding globulin (SHBG). Levels of the oestrogens and sex hormone-binding globulin did not differ significantly between Asian- and Western-born women, although among premenopausal women, those least westernised had the lowest levels of E1, E2, and E1S. Androgen levels, particularly DHEA, were lower in women born in the West. Among premenopausal women, age-adjusted geometric mean levels of DHEA were 16.5 and 13.8 nmol l(-1) in Asian- and Western-born women respectively; in postmenopausal women these values were 11.8 and 9.2 nmol l(-1), (P<0.001) respectively. Among postmenopausal women, androgens tended to be highest among the least westernised women and declined as the degree of westernisation increased. Our findings suggest that aspects of hormone metabolism play a role in population differences in breast cancer incidence.
View details for DOI 10.1038/sj.bjc.6600339
View details for Web of Science ID 000176878400010
View details for PubMedID 12085256
The impact, if any, on breast cancer risk of modifying adult dietary intake is an area of much interest. We take the opportunity to address the relationship between recent adult diet and breast cancer risk during the first two years of follow-up of the large California Teachers Study cohort.Of the 111.526 at-risk cohort members who resided in California and completed a baseline dietary assessment, 711 were diagnosed with invasive breast cancer after joining the cohort and before January 1998. Average daily nutrient intake was computed based on a food-frequency questionnaire assessing usual dietary intake and portion size during the year prior to joining the cohort. Incident breast cancers were identified through the California Cancer Registry and follow-up for death and confirmation of continued California residence utilized a variety of data sources. Cox proportional hazards models were used to calculate relative hazards.The following components of recent dietary intake were not associated with breast cancer risk: energy, fat, fiber, antioxidant vitamins, and phytoestrogens. Only recent average alcohol consumption of 20 or more grams per day (approximately two or more glasses of wine) was associated with increased risk (RR= 1.5, 95% CI: 1.2-2.0 compared to non-drinkers; P(trend) = 0.01 across quintiles).With the exception of alcohol consumption, this study provides no evidence that recent macro- or micronutrient composition of adult diet is likely to have a direct effect on breast cancer risk. Some reduction of alcohol consumption among those consuming more than one drink per day may be beneficial.
View details for Web of Science ID 000175947900003
View details for PubMedID 12146845
Some data suggest that brothers of prostate cancer patients have higher disease risk than their fathers, supporting an X-linked or recessive mode of inheritance. However, higher observed frequencies in brothers than fathers may merely reflect the strong temporal changes in US incidence rates.(a) to evaluate the fit of X-linked, recessive, and dominant modes of inheritance to prostate cancer incidence, specific for calendar year, age, and race, in population-based samples of US and Canadian families; and (b) to evaluate a simple multifactorial model for familial aggregation of prostate cancer due to shared low-penetrance variants of many genes or shared lifestyle factors.The data consist of reported prostate cancer incidence in first-degree relatives of 1,719 white, African-American, and Asian-American men with and without prostate cancer at ages <70 years. Model parameters were estimated by maximizing a pseudo-likelihood function of the data, and goodness of model fit was assessed by evaluating discrepancies between observed and expected numbers of pairs of relatives with prostate cancer.After adjusting for temporal trends in prostate cancer incidence rates we found that the X-linked model fit poorly. underpredicting the observed number of affected father-son pairs. This also was true of the recessive model, although the evidence for poor fit did not achieve statistical significance. In contrast, the dominant model provided adequate fit to the data. In this model the race-specific penetrance estimates for carriers of deleterious genotypes were similar among African-Americans and whites, but lower among Asian-Americans: risk by age 80 years for carriers born in 1900 was estimated as 75.3% for African-Americans and whites, and 44.4% for Asian-Americans. None of the Mendelian models fit the data better than did the simple multifactorial model.The good fit of the multifactorial model suggests that multiple genes, each having low penetrance, may be responsible for most inherited prostate cancer susceptibility, and that the contribution of rare highly penetrant mutations is small.
View details for PubMedID 12146852
Information is limited for Asian subgroups regarding survival after diagnosis of the common cancers amenable to routine screening. The authors examined survival after carcinomas of the prostate, colon/rectum, breast, and cervix separately for Chinese, Japanese, Filipinos, and non-Hispanic whites in the United States.Using data from the Surveillance, Epidemiology, and End Results program, the authors compared the distributions of stage at diagnosis and computed 5-year cause specific survival probabilities, overall and by stage of disease, for cancer patients whose diagnosis was in 1988-1994 and who were observed through 1997.Among males, Filipinos were more likely to be diagnosed with advanced stage colorectal and prostate carcinomas than other Asians and non-Hispanic whites; they also experienced worse survival after these cancers. This survival deficit occurred across all stages of colorectal carcinoma and remained apparent within distant stage prostate carcinoma. Among females, Chinese were less likely to receive diagnoses of early stage colorectal carcinoma than Japanese and Filipinas. In addition, their survival was consistently lower across more advanced stages of disease. Chinese also experienced somewhat worse survival after diagnosis of early stage cervical carcinoma. Japanese were more likely to be diagnosed with early stage carcinomas but also tended to experience better survival after prostate, colorectal, and breast carcinomas regardless of stage.Chinese, Japanese, and Filipinos experienced unequal survival after these screenable carcinomas, indicating that certain groups may benefit from more aggressive screening efforts. The heterogeneity of cancer outcomes observed within the community classified as Asian reinforces the need for cancer statistics to be reported for disaggregated subgroups.
View details for DOI 10.1002/cncr.10319
View details for Web of Science ID 000173907600037
View details for PubMedID 11920489
Elevated rates of breast cancer in affluent Marin County, California, were first reported in the early 1990s. These rates have since been related to higher regional prevalence of known breast cancer risk factors, including low parity, education, and income. Close surveillance of Marin County breast cancer trends has nevertheless continued, in part because distinctive breast cancer patterns in well-defined populations may inform understanding of breast cancer etiology.Using the most recent incidence and mortality data available from the California Cancer Registry, we examined rates and trends for 1990-1999 for invasive breast cancer among non-Hispanic, white women in Marin County, in other San Francisco Bay Area counties, and in other urban California counties. Rates were age adjusted to the 2000 US standard, and temporal changes were evaluated with weighted linear regression.Marin County breast cancer incidence rates between 1990 and 1999 increased 3.6% per year (95% confidence interval, 1.8-5.5), six times more rapidly than in comparison areas. The increase was limited to women aged 45-64 years, in whom rates increased at 6.7% per year (95% confidence interval, 3.8-9.6). Mortality rates did not change significantly in Marin County despite 3-5% yearly declines elsewhere.Patterns of breast cancer incidence and mortality in Marin County are unlike those in other California counties, and they are probably explained by Marin County's unique sociodemographic characteristics. Similar trends may have occurred in other affluent populations for which available data do not permit annual monitoring of cancer occurrence.
View details for Web of Science ID 000178822900002
View details for PubMedID 12473174
Research on the relationship between iodine exposure and thyroid cancer risk is limited, and the findings are inconclusive. In most studies, fish/shellfish consumption has been used as a proxy measure of iodine exposure. The present study extends this research by quantifying dietary iodine exposure as well as incorporating a biomarker of long-term (1 year) exposure, i.e., from toenail clippings. This study is conducted in a multiethnic population with a wide variation in thyroid cancer incidence rates and substantial diversity in exposure. Women, ages 20-74, residing in the San Francisco Bay Area and diagnosed with thyroid cancer between 1995 and 1998 (1992-1998 for Asian women) were compared with women selected from the general population via random digit dialing. Interviews were conducted in six languages with 608 cases and 558 controls. The established risk factors for thyroid cancer were found to increase risk in this population: radiation to the head/neck [odds ratio (OR), 2.3; 95% confidence interval (CI), 0.97-5.5]; history of goiter/nodules (OR, 3.7; 95% CI, 2.5-5.6); and a family history of proliferative thyroid disease (OR, 2.5; 95% CI, 1.6-3.8). Contrary to our hypothesis, increased dietary iodine, most likely related to the use of multivitamin pills, was associated with a reduced risk of papillary thyroid cancer. This risk reduction was observed in "low-risk" women (i.e., women without any of the three established risk factors noted above; OR, 0.53; 95% CI, 0.33-0.85) but not in "high-risk" women, among whom a slight elevation in risk was seen (OR, 1.4; 95% CI, 0.56-3.4). However, no association with risk was observed in either group when the biomarker of exposure was evaluated. In addition, no ethnic differences in risk were observed. The authors conclude that iodine exposure appears to have, at most, a weak effect on the risk of papillary thyroid cancer.
View details for Web of Science ID 000170899000011
View details for PubMedID 11535551
We conducted a genomewide screen for prostate cancer-susceptibility genes on the basis of data from 98 families from the United States and Canada that had three or more verified diagnoses of prostate cancer among first- and second-degree relatives. We found a statistically significant excess of markers for which affected relatives exhibited modest amounts of excess allele-sharing; however, no single chromosomal region contained markers with excess allele-sharing of sufficient magnitude to indicate unequivocal evidence of linkage. Positive linkage signals of nominal statistical significance were found in two regions (5p-q and 12p) that have been identified as weakly positive in other data sets and in region 19p, which has not been identified previously. All these signals were considerably stronger for analyses restricted to families with mean age at onset below the median than for analyses of families with mean age at onset above the median. The data provided little support for any of the putative prostate cancer-susceptibility genes identified in other linkage studies.
View details for Web of Science ID 000170108100015
View details for PubMedID 11404817
View details for PubMedCentralID PMC1226029
Men with higher endogenous 5alpha-reductase activity may have higher prostate cancer risk. This hypothesis raises two questions: (a) Could racial differences in 5alpha-reductase activity explain the observed racial differences in prostate cancer risk? and (b) Could a man reduce his activity level by modifying his lifestyle? To address these questions, we measured two hormonal indices of 5alpha-reductase activity [serum levels of androstane-3alpha-17beta-diol glucuronide (3alpha-diol G) and androsterone glucuronide (AG)] in healthy, older African-American, white, and Asian-American men, who are at high, intermediate, and low prostate cancer risk, respectively. We also examined associations between these metabolite levels and such lifestyle characteristics as body size and physical activity as well as select aspects of medical history and family history of prostate cancer. Men included in this cross-sectional analysis (n = 1054) had served as control subjects in a population-based case-control study of prostate cancer we conducted in California, Hawaii, and Vancouver, Canada and provided information on certain personal attributes and donated blood between March 1990 and March 1992. In this study, concentrations of 3alpha-diol G declined significantly with age and increased significantly with body mass index. Mean levels of 3alpha-diol G, adjusted for age and body mass index, were 6.1 ng/ml in African-Americans, 6.9 ng/ml in whites and 4.8 ng/ml in Asian-Americans. These differences were statistically significant (African-Americans versus whites: P < 0.01; whites versus Asian-Americans: P < 0.001). Concentrations of AG decreased significantly with age, but only in whites, and were unrelated to any of the reported personal attributes. Mean levels of AG, adjusted for age, were 44.1 ng/ml in African-Americans, 44.9 ng/ml in whites, and 37.5 ng/ml in Asian-Americans (Asian-Americans versus whites, P < 0.001). In conclusion, older African-American and white men have similar levels of these two indices of 5alpha-reductase activity, and these levels are higher than those of older Asian-American men. This difference may be related to the lower prostate cancer risk in Asian-Americans.
View details for Web of Science ID 000168737800016
View details for PubMedID 11352865
The evidence for a protective effect of vegetables, fruits, and legumes against prostate cancer is weak and inconsistent. We examined the relationship of these food groups and their constituent foods to prostate cancer risk in a multicenter case-control study of African-American, white, Japanese, and Chinese men. Cases (n = 1619) with histologically confirmed prostate cancer were identified through the population-based tumor registries of Hawaii, San Francisco, and Los Angeles in the United States and British Columbia and Ontario in Canada. Controls (n = 1618) were frequency-matched to cases on ethnicity, age, and region of residence of the case, in a ratio of approximately 1:1. Dietary and other information was collected by in-person home interview; a blood sample was obtained from control subjects for prostate-specific antigen determination. Odds ratios (OR) were estimated using logistic regression, adjusting for age, geographic location, education, calories, and when indicated, ethnicity. Intake of legumes (whether total legumes, soyfoods specifically, or other legumes) was inversely related to prostate cancer (OR for highest relative to lowest quintile for total legumes = 0.62; P for trend = 0.0002); results were similar when restricted to prostate-specific antigen-normal controls or to advanced cases. Intakes of yellow-orange and cruciferous vegetables were also inversely related to prostate cancer, especially for advanced cases, among whom the highest quintile OR for yellow-orange vegetables = 0.67 (P for trend = 0.01) and the highest quintile OR for cruciferous vegetables = 0.61 (P for trend = 0.006). Intake of tomatoes and of fruits was not related to risk. Findings were generally consistent across ethnic groups. These results suggest that legumes (not limited to soy products) and certain categories of vegetables may protect against prostate cancer.
View details for Web of Science ID 000088719500005
View details for PubMedID 10952096
Breast cancer incidence has historically been 4-7 times higher in the United States than in Asia. A previous study by the authors in Asian-American women demonstrated a substantial increase in breast cancer risk in women who migrated from Asia to the United States, with the risk almost doubling during the first decade after migration. Increased use of oral contraceptives soon after migration to the United States could possibly explain this rapid rise in risk. In a population-based case-control study of Chinese, Filipino, and Japanese-American women, aged 20-55 years, who lived in San Francisco-Oakland, California; Los Angeles, California; and Oahu, Hawaii during 1983-1987, 597 cases (70% of those eligible) and 966 controls (75%) were interviewed. Controls were matched to cases on age, ethnicity, and area of residence. Oral contraceptive (OC) use increased with time since migration; 15.0% of Asian-born women who had been in the West <8 years, 33.4% of Asian-born women who had been in the West > or =8 years, and 49.6% of Asian women born in the West had ever used OCs. However, duration of OC use (adjusted for age, ethnicity, study area, years since migration, education, family history of breast cancer and age at first full-term birth) was not associated with increased risk of breast cancer. Moreover, neither OC use before age 25 years nor before first full-term birth was associated with increased risk. Results were unchanged when restricted to women under age 45 years or under age 40 years. After adjustment for duration of OC use, women who had been in the United States > or =8 years were still at almost twice the risk of breast cancer compared with women who had been in the United States 2-7 years. This study suggests that OC use cannot explain the elevated risk observed in Asian women who migrated to the United States > or =7 years ago.
View details for Web of Science ID 000082602300003
View details for PubMedID 10489994
The accuracy of ethnic classification can substantially affect ethnic-specific cancer statistics. In the Greater Bay Area Cancer Registry, which is part of the Surveillance, Epidemiology, and End Results (SEER) Program and of the statewide California Cancer Registry, Hispanic ethnicity is determined by medical record review and by matching to surname lists. This study compared these classification methods with self-report. Ethnic self-identification was obtained by surveying 1,154 area residents aged 20-89 years who were diagnosed with cancer in 1990 and were reported to the registry as being Hispanic or White non-Hispanic. Predictive value positive, sensitivity, and relative bias were used to assess the accuracy of Hispanic classification by medical record and surname. Among those persons classified as Hispanic by either or both of these sources, only two-thirds agreed (predictive value positive = 66%), and many self-identified Hispanics were classified incorrectly (sensitivity = 68%). Classification based on either medical record or surname alone had a lower sensitivity (59% and 61%, respectively) but a higher predictive value positive (77% and 70%, respectively). Ethnic classification by medical record alone resulted in an underestimate of Hispanic cancer cases and incidence rates. Bias was reduced when medical records and surnames were used together to classify cancer cases as Hispanic.
View details for Web of Science ID 000080524100012
View details for PubMedID 10355383
The purpose of this paper was to investigate the relationship between food and beverage consumption and the development of breast cancer in men.Possible relationships of dietary factors to risk of breast cancer in men were assessed in a case-control study conducted between 1983 and 1986. Cases (N = 220) were ascertained from ten population-based cancer registries. Controls (N = 291) were selected by random-digit dialing (< age 65) and from Health Care Financing Administration Medicare beneficiary lists (> or = age 65).No trends in risk were observed with increasing intakes of specific foods, except for an increase in risk with citrus fruits. No increase in risk with increasing amounts of specific fats, vitamins, or minerals or with amounts of protein, fiber, carbohydrate, starches, nitrites, or alcohol consumed was observed, except for an increase in risk with dietary vitamin C consumption. A decreasing trend in risk with dietary niacin and with coffee and an increasing trend in risk with tea consumption were observed. No associations were found with use of any dietary supplements, including vitamin C.The observed associations are not consistent with findings from studies of breast cancer in women and probably do not represent causal relationships. Dietary factors are unlikely to be strong determinants of breast cancer in men.
View details for Web of Science ID 000079944600002
View details for PubMedID 10231158
Evidence from case-control studies suggests, although not entirely consistently, that soy intake may protect against breast cancer. The designs and findings of studies conducted in Asian women living in Japan, Singapore, China, and the United States are reviewed. Because of the considerably higher intake of soy by native Asians than by Asian Americans living in California and Hawaii, these studies investigated different segments of the dose-response relation between soy intake and breast cancer risk. Data are not sufficient to determine the amount or frequency of soy intake effective in protecting against breast cancer. Of concern is that soy intake may be homogeneously high in Asia, making it difficult to identify differences in breast cancer risk between high and moderate daily consumers. In studies conducted in Asian Americans, it is difficult to be certain that soy intake is not a marker of other factors related to Western lifestyle that are causally associated with risk of breast cancer. Additional studies assessing the role of soy and breast cancer are needed. These studies should assess intake of all food sources of soy, considering portion size as well as other dietary and nondietary factors that may confound the soy-breast cancer association. A better understanding of the mechanisms whereby soy intake may influence the risk of breast cancer is also needed. Dietary intervention studies with soy will provide information on the acute effects of soy on endogenous hormone concentrations. Cross-sectional and longitudinal studies are necessary to investigate the longer-term relations between hormone concentrations and soy intake in women.
View details for Web of Science ID 000077392300020
View details for PubMedID 9848513
We used readily accessible, existing data to assess whether or not geographic variation in breast cancer incidence rates in the San Francisco Bay Area was related to the unequal distribution of known breast cancer risk factors.Cancer registry and 1990 census block-group data were used to look at the associations between breast cancer incidence and known risk factors (including parity, urban/rural status, and socioeconomic indicators) in 25 California counties. Average annual age-adjusted invasive breast cancer incidence rates were calculated for the period 1988-1992, and adjusted morbidity ratios were computed.While breast cancer incidence in Marin County was 9 percent higher than that of the other 24 counties combined (relative risk = 1.09, 95 percent confidence interval = 1.01-1.18), this increase appeared to be due to the unequal distribution of known risk factors. Block-groups that had a high level of any risk factor had higher incidence rates, regardless of geographic location. After multivariate adjustment, breast cancer incidence no longer differed between Marin and the other counties (adjusted morbidity ratio = 1.02).The results suggest that the unequal distribution of known risk factors was responsible for Marin County's high breast cancer incidence rate.
View details for Web of Science ID 000078379700004
View details for PubMedID 9934716
Although ethnic population counts measured by the United States Census are based on self-identification, the same is not necessarily true of cases reported to cancer registries. The use of different ethnic classification methods for numerators and denominators may therefore lead to biased estimates of cancer incidence rates. The extent of such misclassification may be assessed by conducting an ethnicity survey of cancer patients and estimating the proportion misclassified using double sampling models that account for sample stratification. For two ethnic categories, logistic regression may be used to model self-identified ethnicity as a function of demographic variables and the fallible classification method. Incidence rates then may be adjusted for misclassification using regression results to estimate the number of cancer cases of a given age, sex, and site in each self-identified ethnic group. An example is given using this method to estimate ethnic misclassification of San Francisco Bay area Hispanic cancer patients diagnosed in 1990. Results suggest that the number of cancer cases reported as Hispanic is an underestimate of the number of cases self-identified as Hispanic, resulting in an underestimate of Hispanic cancer rates.
View details for Web of Science ID 000074161600033
View details for PubMedID 9629656
Racial classification of Asian subgroups is increasingly important for health statistics, given the growing Asian-American populations. This study reports the reliability of racial classification of Vietnamese in population-based cancer registry data from northern California. From the Greater Bay Area Cancer Registry, we selected 2240 persons diagnosed with cancer in 1989-1992 and whom the registry considered Vietnamese by birthplace and/or registry race and/or surname, or who were Southeast Asian or Chinese by race. One thousand ninety persons (49%) were interviewed. Sensitivity and predictive value positive, and cancer incidence rates, were calculated using different combinations of the classification factors (birthplace, registry race, and name). By registry-reported race alone, 74% of those the registry classified as Vietnamese agreed with this classification on interview, while 90% of those identifying themselves as Vietnamese were so classified. With classification based on 2 of 3 factors, 78% of those classified as Vietnamese agreed, and 91% of self-reported Vietnamese were correctly classified. Misclassification was associated with age, sex, year of immigration, education, and language use. Registry-based annual age-adjusted all-site cancer incidence rates per 100,000 for Vietnamese were 287.7 for males and 221.3 for females. Rates adjusted for self-reported ethnicity were 242.8 (male) and 213.7 (female). Registry classification of Vietnamese is currently problematic. Approximately 20% of cancer cases classified as Vietnamese are probably not Vietnamese. The higher incidence rates for Vietnamese in the United States than in Vietnam partly may reflect such classification error.
View details for PubMedID 9681287
Hispanic ethnicity is often used as a category for calculating population-based rates or assessing risk of epidemiologic studies. However, ethnic misclassification can lead to false conclusions unless the extent of misclassification and the characteristics of those misclassified are understood.This study explored determinants of ethnic misclassification in a sample of 1154 cancer cases in the San Francisco-Oakland cancer registry, where ethnic classification is based on surname or medical record report. We compared the following: correctly classified Hispanics, persons classified as Hispanic who self-identified as non-Hispanic, and persons classified as non-Hispanic who self-identified as Hispanic.Among men classified as Hispanic, those most likely to self-identify as non-Hispanic did not speak Spanish, had non-Spanish surnames, and were recent immigrants. Women misclassified as Hispanic did not speak Spanish or have Spanish maiden names, nor did they have mothers with Spanish maiden names. Persons who called themselves Hispanic, but were misclassified by the registry, were likely to be non-Spanish speaking college-education males.Researchers using ethnicity should be aware of how ethnicity was determined and how this classification may bias or confound their results.
View details for Web of Science ID A1997WX57800007
View details for PubMedID 9141643
Breast cancer rates among Asian-Americans are lower than those of US whites but considerably higher than rates prevailing in Asia. It is suspected that migration to the US brings about a change in endocrine function among Asian women, although reasons for this change remain obscure. The high intake of soy in Asia and its reduced intake among Asian-Americans has been suggested to partly explain the increase of breast cancer rates in Asian-Americans. We conducted a population-based case-control study of breast cancer among Chinese-, Japanese-, and Filipino-American women in Los Angeles County MSA, San Francisco Oakland MSA, and Oahu, Hawaii. Using a common questionnaire which assessed frequency of intake of some 90 food items, 597 Asian-American women (70% of those eligible) diagnosed with incident, primary breast cancer during 1983-1987 and 966 population-based controls (75% of those eligible) were interviewed. Controls were matched to cases on age, ethnicity, and area of residence. This analysis compares usual adult intake of soy (estimated primarily from tofu intake) among breast cancer cases and control women. After adjustment for age, ethnicity and study area, intake of tofu was more than twice as high among Asian-American women born in Asia (62 times per year) compared to those born in the US (30 times per year). Among migrants, intake of tofu decreased with years of residence in the US. Risk of breast cancer decreased with increasing frequency of intake of tofu after adjustment for age, study area, ethnicity, and migration history; the adjusted OR associated with each additional serving per week was 0.85 (95% CI = 0.74-0.99). The protective effect of high tofu intake was observed in pre- and postmenopausal women. This association remained after adjustment for selected dietary factors and menstrual and reproductive factors. However, this study was not designed specifically to investigate the role of soy intake and our assessment of soy intake may be incomplete. We cannot discount the possibility that soy intake is a marker of other protective aspects of Asian diet and/or Asian lifestyle.
View details for Web of Science ID A1996VR59600008
View details for PubMedID 8922298
The presence of concurrent health conditions (comorbidity) at the time of breast cancer diagnosis has an adverse effect on survival. It is unclear, however, whether the strength of the association between comorbidity and survival varies in different populations of breast cancer patients. It is necessary, therefore, to establish (1) whether a comorbidity index derived from a general population of patients (mostly white) would predict survival in a black population, and (2) whether comorbidity would have the same degree of relationship to mortality in black as in white populations. We studied 1196 breast cancer patients who were members of the Kaiser Permanente Medical Care Program and were diagnosed with local (n = 708), regional (n = 446), or remote (n = 49) stage breast cancer from 1973 to 1986. Mortality follow-up was completed to December 1994. Ten-year survival was studied in relation to the Charlson comorbidity index for black women and for white women, and for both groups of women combined. Compared to women with a Charlson comorbidity score of 0 (no comorbidity), patients with scores of 1, 2, and 3+ had risk ratios for ten-year mortality of 1.23 (P = 0.10), 2.58 (P < 0.001), and 3.44 (P < 0.001), respectively. This pattern of risk associated with comorbidity was similar to that found in the original Charlson study. The pattern of risk ratios for different levels of comorbidity was very similar for black and white patients. The results confirm previous studies indicating that comorbidity (in particular, the Charlson Comorbidity Index) predicts the survival of women with breast cancer, independently of other factors, such as stage of breast cancer at diagnosis. The Charlson index has prognostic significance for both black and white populations. Research is needed to determine whether the Charlson index can be improved by including health conditions that are particularly prevalent or severe in specific subgroups of women.
View details for Web of Science ID A1996VQ68400009
View details for PubMedID 8915472
Breast cancer incidence rates have historically been four to seven times higher in the United States than in China or Japan, although the reasons remain elusive. When Chinese, Japanese, or Filipino women migrate to the United States, their breast cancer risk rises over several generations and reaches that for white women in the United States, indicating that modifiable exposures are involved. In a previous report on this case-control study of breast cancer in Asian-American women, designed to take advantage of their diversity in risk and lifestyle, we demonstrated a sixfold gradient in risk by migration history, comparable to the international differences in breast cancer incidence rates.In this analysis, we have examined the roles of adult height, adiposity, and weight change in breast cancer etiology.A population-based, case-control study of breast cancer was conducted among women of Chinese, Japanese, and Filipino ethnicities, aged 20-55 years, living in San Francisco-Oakland (CA), Los Angeles (CA), and Oahu (HI) during the period from April 1, 1983, through June 30, 1987. We successfully interviewed 597 (70%) of 852 eligible case subjects and 966 (75%) of 1287 eligible control subjects from August 1985 through February 1989. Subjects were asked about current height, usual adult weight, and usual weight in each decade of life, excluding the most recent 3 years and any periods of pregnancy.Height, recent adiposity (weight in the current decade of life/height 1.5), and recent weight change (between the current and preceding decades of life) were strong predictors of breast cancer risk after adjustment was made for accepted breast cancer risk factors. Risk doubled (relative risk [RR] = 2.01; 95% confidence interval [CI] = 1.16-3.49) over the 7-inch (17.8-cm) range in height (two-sided P for trend = .003), with comparable effects in both premenopausal and postmenopausal women. Except for reduced risk in the heavy, younger women (weight/height 1.5 > 29 kg/m 1.5 and < 40 years old), risk was positively associated with usual adult adiposity. Trends in risk became more striking as adiposity in each succeeding decade of adult life was considered. Women in their 50s and in the top quintile for their age group had twice the breast cancer risk (RR = 2.13; 95% CI = 1.17-3.87) of women in the bottom quintile (two-sided P for trend = .004). Women in their 50s, above the median adiposity for their age group, and with a recent gain of more than 10 pounds had three times the risk (RR = 3.01; 95% CI = 1.45-6.25) of women below the median adiposity and with no recent weight change. Recent weight loss was consistently associated with reduced risk (RRs of approximately 0.7) relative to no recent weight change.Adult adiposity, weight change, and height are critical determinants of breast cancer risk. Increased adiposity and weight gain in the decade preceding diagnosis are especially influential, suggesting that excess weight may function as a late stage promoter.Weight maintenance and/or reduction as an adult, possibly accompanied by specific changes in diet and physical activity, may have a significant and rapid impact on breast cancer risk.
View details for Web of Science ID A1996UK18600010
View details for PubMedID 8627641
We conducted a population-based case-control study of breast cancer among Chinese-, Japanese- and Filipino-American women in Los Angeles County Metropolitan Statistical Area (MSA), San Francisco-Oakland MSA and Oahu, Hawaii. One objective of the study was to quantify breast cancer risks in relation to menstrual and reproductive histories in migrant and US-born Asian-Americans and to establish whether the gradient of risk in Asian-Americans can be explained by these factors. Using a common study design and questionnaire in the three study areas, we successfully conducted in-person interviews with 597 Asian-American women diagnosed with incident, primary breast cancer during the period 1983-87 (70% of those eligible) and 966 population-based controls (75% of those eligible). Controls were matched to cases on age, ethnicity and area of residence. In the present analysis, which included 492 cases and 768 controls, we observed a statistically non-significant 4% reduction in risk of breast cancer with each year delay in onset of menstruation. Independent of age at menarche risk of breast cancer was lower (odds ratio; OR=0.77) among women with menstrual cycles greater than 29 days. Parous Asian-American women showed a significantly lower risk of breast cancer then nulliparous women (OR=0.54). An increasing number of livebirths and a decreasing age at first livebirth were both associated with a lower risk of breast cancer, although the effect of number of livebirths was no longer significant after adjustment for age at first livebirth. Women with a pregnancy (spontaneous or induced abortions) but no livebirth had a statistically non-significant increased risk (OR=1.84), but there was no evidence that one type of abortion was particularly harmful. A positive history of breastfeeding was associated with non-significantly lower risk of breast cancer (OR=.78). There are several notable differences in the menstrual and reproductive factors between Asian-Americans in this study and published data on US whites. US-born Asian Americans had an average age at menarche of 12.12 years-no older than has been found in comparable studies of US whites, but 1.4 years earlier than Asian women who migrated to the US. Asian-American women, particularly those born in the US and those who migrated before age 36, also had a later age at first birth and fewer livebirths than US whites. A slightly higher proportion of Asian-American women breastfed, compared with US whites. The duration of breastfeeding was similar in US-born Asians and US whites, but was longer in Asian migrants, especially those who migrated at a later age. Menstrual and reproductive factors in Asian-American women are consistent with their breast cancer rates being at least as high as in US whites, and they are. However, the effects of these menstrual and reproductive factors were small and the ORs for migration variables changed only slightly after adjustment for these menstrual and reproductive factors. These results suggest that the lower rates of breast cancer in Asians must be largely as a result of other environmental/lifestyle factors.
View details for Web of Science ID A1996TV82700022
View details for PubMedID 8605107
Differences in endogenous androgen levels have been hypothesized to explain ethnic differences in prostate cancer risk. To examine this hypothesis, we gathered data on serum concentrations of androgens and sex hormone-binding globulin (SHBG) in healthy older men from four ethnic groups at different levels of prostate cancer risk. As part of a population-based case-control study of prostate cancer we conducted in California, Hawaii, and Vancouver, Canada, 1127 African-American, white, Chinese-American, and Japanese-American control men, mostly ages 60 years or older (mean age, 69.9 years) provided information on various lifestyle factors and donated an early morning fasting blood sample between March 1990 and March 1992. We used these data to examine the distributions of serum androgens [testosterone (total, free, and bioavailable), dihydrotestosterone (DHT)], the ratio of DHT to total testosterone (DHT:testosterone ratio), and SHBG in these four ethnic groups. We also assessed correlations between concentrations of these measures with age, body size, physical activity, and other personal characteristics, and we evaluated ethnic differences in concentrations of androgens and SHBG after adjusting for these characteristics. In each of the four ethnic groups, concentrations of free and bioavailable testosterone declined with age, whereas SHBG concentrations increased with age. Age-adjusted concentrations of all androgen measures and SHBG decreased with increasing levels of Quetelet's index. After adjustment for age and Quetelet's index, androgens and SHBG showed no clear and consistent relationships to physical activity, alcohol consumption, or tobacco use. DHT:testosterone ratio was higher in men reporting a history of benign prostate disease than in men without such a history, and higher in vasectomized men than in nonvasectomized men. SHBG concentrations were higher in men reporting one or more first-degree relatives with prostate cancer than in men without such a family history. After adjustment for age and Quetelet's index, the levels of total and bioavailable testosterone were highest in Asian-Americans, intermediate in African-Americans, and lowest in whites. However, the DHT:testosterone ratio was highest in African-Americans, intermediate in whites, and lowest in Asian-Americans, corresponding to the respective incidence rates in these groups and providing indirect evidence for ethnic differences in 5alpha-reductase enzyme activity.
View details for Web of Science ID A1995RZ11000007
View details for PubMedID 8672990
Vasectomy, a widely used form of contraception, has been associated in some studies with increased prostate cancer risk.We assessed this association on the basis of data collected in a large multiethnic case-control study of prostate cancer that was conducted in the United States (Los Angeles, San Francisco, and Hawaii) and Canada (Toronto and Vancouver).In home interviews conducted with newly diagnosed prostate cancer case patients and population control subjects, we obtained information on the participants' medical history, including a history of vasectomy and the age at which the procedure was performed, as well as other potential risk factors. Blood samples were collected from control subjects only and were assayed for concentration of sex hormones and sex hormone-binding globulin.The present analysis was based on 1642 prostate cancer patients and 1636 control subjects. A history of vasectomy was not significantly associated with prostate cancer risk among all racial/ethnic groups combined (odds ratio [OR] = 1.1; 95% confidence interval [CI] = 0.83-1.3), whites (OR = 0.94; 95% CI = 0.69-1.3), blacks (OR = 1.0; 95% CI = 0.59-1.8), or Chinese-Americans (OR = 0.96; 95% CI = 0.42-2.2). Among Japanese-Americans, the OR was 1.8 (95% CI = 0.97-3.4), but the statistically nonsignificant elevation in risk was limited to more educated men and those with localized cancers. ORs did not vary significantly by age at vasectomy or years since vasectomy. We found a lower serum concentration of sex hormone-binding globulin and a higher ratio of dihydrotestosterone to testosterone among vasectomized control subjects than among nonvasectomized control subjects.The findings of this study do not support previous reports of increased prostate cancer risk associated with vasectomy. However, the altered endocrine profiles of vasectomized control subjects seen in this cross-sectional comparison warrant further evaluation in longitudinal studies.
View details for PubMedID 7538594
International and interethnic differences in prostate cancer incidence suggest an environmental, potentially modifiable etiology for the disease.We conducted a population-based case-control study of prostate cancer among blacks (very high risk), whites (high risk), and Asian-Americans (low risk) in Los Angeles, San Francisco, Hawaii, Vancouver, and Toronto. Our aim was to evaluate the roles of diet, physical activity patterns, body size, and migration characteristics on risk in these ethnic groups and to assess how much of the interethnic differences in risk might be attributed to interethnic differences in such lifestyle characteristics.We used a common protocol and questionnaire to administer personal interviews to 1655 black, white, Chinese-American, and Japanese-American case patients diagnosed during 1987-1991 with histologically confirmed prostate carcinoma and to 1645 population-based control subjects matched to case patients by age, ethnicity, and region of residence. Sera collected from 1127 control subjects were analyzed for levels of prostate-specific antigen (PSA) to permit comparison of case patients with control subjects lacking serological evidence of prostate disease. Odds ratios were estimated using conditional logistic regression. We estimated the proportion of prostate cancer attributable to certain risk factors and the proportion of interethnic risk differences attributable to interethnic differences in risk-factor prevalence.A positive statistically significant association of prostate cancer risk and total fat intake was found for all ethnic groups combined. This association was attributable to energy from saturated fats; after adjusting for saturated fat, risk was associated only weakly with monounsaturated fat and was unrelated to protein, carbohydrate, polyunsaturated fat, and total food energy. Saturated fat intake was associated with higher risks for Asian-Americans than for blacks and whites. In all ethnic groups combined, the risk tended to be higher when only case patients with advanced disease were compared with control subjects with normal PSA levels. Among foreign-born Asian-Americans, risk increased independently with years of residence in North America and with saturated fat intake. Crude estimates suggest that differences in saturated fat intake account for about 10% of black-white differences and about 15% of white-Asian-American differences in prostate cancer incidence. Risk was not consistently associated with intake of any micronutrients, body mass, or physical activity patterns.These data support a causal role in prostate cancer for saturated fat intake but suggest that other factors are largely responsible for interethnic differences in risk.
View details for PubMedID 7752270
Increased risk of prostate cancer in men with a family history of the disease has been observed consistently in epidemiologic studies. However, most studies have been confined to white men; little is known about familial aggregation of prostate cancer in populations with unusually high incidence, such as African Americans, or in populations with low incidence, such as Asian-Americans. The authors report results from a population-based case-control study of prostate cancer among blacks, whites, and Asian-Americans in the United States and Canada. Controls were matched to cases on age (5-year groups), ethnicity (black, white, Chinese-American, Japanese-American), and region of residence (Los Angeles, San Francisco, Hawaii, Vancouver, Toronto). In the combined group of participants, 5% of controls and 13% of cases reported a father, brother, or son with prostate cancer. These prevalences were somewhat lower among Asian-Americans than among blacks or whites. A positive family history was associated with a statistically significant two- to threefold increase in risk in each of the three ethnic groups. The overall odds ratio associated with such a family history, adjusted for age and ethnicity, was 2.5 (95% confidence interval 1.9-3.3). This odds ratio varied by neither ethnicity nor age of the participants. Sera from 1,087 controls were used to examine the relations between family history and serum concentrations of androgens and prostate-specific antigen. The concentrations of sex hormone-binding globulin were slightly higher in men with than without a positive family history. Prostate-specific antigen concentrations were unrelated to family history.
View details for PubMedID 7535977
Breast cancer incidence rates have historically been 4-7 times higher in the United States than in China or Japan, although the reasons remain elusive. When Chinese, Japanese, or Filipino women migrate to the United States, breast cancer risk rises over several generations and approaches that among U.S. Whites.Our objective was to quantify breast cancer risks associated with the various migration patterns of Asian-American women.A population-based, case-control study of breast cancer among women of Chinese, Japanese, and Filipino ethnicities, aged 20-55 years, was conducted during 1983-1987 in San Francisco-Oakland, California, Los Angeles, California, and Oahu, Hawaii. We successfully interviewed 597 case subjects (70% of those eligible) and 966 control subjects (75%).A sixfold gradient in breast cancer risk by migration patterns was observed. Asian-American women born in the West had a breast cancer risk 60% higher than Asian-American women born in the East. Among those born in the West, risk was determined by whether their grandparents, especially grandmothers, were born in the East or the West. Asian-American women with three or four grandparents born in the West had a risk 50% higher than those with all grandparents born in the East. Among the Asian-American women born in the East, breast cancer risk was determined by whether their communities prior to migration were rural or urban and by the number of years subsequently lived in the West. Migrants from urban areas had a risk 30% higher than migrants from rural areas. Migrants who had lived in the West for a decade or longer had a risk 80% higher than more recent migrants. Risk was unrelated to age at migration for women migrating at ages less than 36 years. Ethnic-specific incidence rates of breast cancer in the migrating generation were clearly elevated above those in the countries of origin, while rates in Asian-Americans born in the West approximated the U.S. White rate.Exposure to Western lifestyles had a substantial impact on breast cancer risk in Asian migrants to the United States during their lifetime. There was no direct evidence of an especially susceptible period, during either menarche or early reproductive life.Because heterogeneity in breast cancer risk in these ethnic populations is similar to that in international comparisons and because analytic epidemiologic studies offer the opportunity to disentangle correlated exposures, this study should provide new insights into the etiology of breast cancer.
View details for Web of Science ID A1993MG53000011
View details for PubMedID 8230262
Data from a population-based study of newly diagnosed cases of prostate cancer (n = 362) and age-matched controls (n = 685) conducted in Utah (United States) between 1983 and 1986 were used to determine if cigarette smoking, alcohol, coffee, tea, caffeine, and theobromine were associated with prostate cancer risk. These factors were examined since their use differs in the Utah population, which is comprised predominantly of members of the Church of Jesus Christ of Latter-day Saints (LDS or Mormon), from most other populations. Pack-years of cigarettes smoked, alcohol intake, and consumption of alcohol, coffee, tea, and caffeine were not associated with prostate cancer risk. Compared with men with very low levels of theobromine intake, older men consuming 11 to 20 and over 20 mg of theobromine per day were at increased risk of prostate cancer (odds ratio [OR] for all tumors = 2.06, 95 percent confidence interval [CI] = 1.33-3.20, and OR = 1.47, CI = 0.99-2.19, respectively; OR for aggressive tumors = 1.90, CI = 0.90-3.97, and OR = 1.74, CI = 0.91-3.32, respectively). We present biological mechanisms for a possible association between prostate cancer and theobromine. This finding needs further exploration in studies with a wider range of theobromine exposures and more men with aggressive tumors.
View details for Web of Science ID A1993MJ06200008
View details for PubMedID 8280834
Cystic fibrosis (CF) is the commonest, fatal, autosomal recessive disorder and is associated with lung sepsis, pancreatic failure and elevated sweat electrolytes. The CF gene on chromosome 7 encodes a protein identified as CF transmembrane conductance regulator (CFTR) which regulates chloride ion transport in epithelial cell membranes. Almost 100 mutations have been identified in this gene which cause defective chloride-channel control. Recently, this abnormality has been reversed in affected CF cells in vitro by retrovirus-mediated transfer of a normal gene. Fifty years ago, most cases died in childhood, but now up to 80% reach adulthood. Chronic lung sepsis is the principal cause of death, and intensive antibiotic therapy with chest physiotherapy is used to control this. Advanced lung disease can be successfully treated by heart-lung transplantation. Nebulised recombinant DNase and antineutrophil elastase agents such as alpha-1-antitrypsin and secretory leucoprotease inhibitor are potentially promising new therapies. Pancreatic insufficiency is managed by high-calorie diets and enteric coated enzyme supplements. Other prominent gastrointestinal complications include meconium ileus equivalent, biliary cirrhosis and cholelithiasis. Specially dedicated CF centres have led to improved survival rates and allow experienced staff to treat the many complications of CF while promoting research in this multisystem disorder.
View details for Web of Science ID A1992HF82200004
View details for PubMedID 1551244
Beginning in 1985, a sudden and sustained doubling of salivary gland cancer incidence, among men only, is observed in the San Francisco-Oakland Metropolitan Statistical Area. Registry data are examined to determine the nature of this increase and its possible association with the AIDS epidemic. Changes in patient characteristics are assessed by comparing their distribution among recently diagnosed cases (1985-1988) to an expectation based on population growth and the age-specific incidence among patients diagnosed earlier (1973-1984). Based on the observed patterns, it is unlikely that the temporal increase in these tumours is a direct result of the AIDS epidemic or solely the result of a shift in the prevalence of established risk factors. The increase is predominantly seen in men over the age of 75 at diagnosis (O/E = 2.3, p = 0.02) and is observed among both those with and without a prior cancer (O/E = 2.7, p = 0.02 and O/E = 1.5, p = 0.06, respectively). Radiation for the prior cancer was not associated with increased occurrence. Military exposure is crudely approximated by examining birth cohorts. However, the cohort data do not support a hypothesis of military exposure.
View details for Web of Science ID A1991GJ74000007
View details for PubMedID 1955246
A population-based case-control study in Utah of 358 cases diagnosed with prostate cancer between 1984 and 1985, and 679 controls categorically matched by age and county of residence, were interviewed to investigate the association between dietary intake of energy (kcal), fat, protein, vitamin A, beta-carotene, vitamin C, zinc, cadmium, selenium, and prostate cancer. Dietary data were ascertained using a quantitative food-frequency questionnaire. Data were analyzed separately by age (45-67, 68-74) and by tumor aggressiveness. The most significant associations were seen for older males and aggressive tumors. Dietary fat was the strongest risk factor for these males, with an odds ratio (OR) of 2.9 (95 percent confidence interval [CI] 1.0-8.4) for total fat; OR = 2.2 (CI = 0.7-6.6) for saturated fat; OR = 3.6 (CI = 1.3-9.7) for monounsaturated fat; and OR = 2.7 (CI = 1.1-6.8) for polyunsaturated fat. Protein and carbohydrates had positive but nonsignificant associations. Energy intake had an OR of 2.5 (CI = 1.0-6.5). In these older men, no effects were seen for dietary cholesterol, body mass, or physical activity. There was little association between prostate cancer and dietary intake of zinc, cadmium, selenium, vitamin C, and beta-carotene. Total vitamin A had a slight positive association with all prostate cancer (OR = 1.6, CI = 0.9-2.4), but not with aggressive tumors. No associations were found in younger males, with the exception of physical activity which showed active males to be at an increased but nonsignificant risk for aggressive tumors (OR = 2.0, CI = 0.8-5.2) and beta-carotene which showed a nonsignificant protective effect (OR = 0.6, CI = 0.3-1.6). The findings suggest that dietary intake, especially fats, may increase risk of aggressive prostate tumors in older males.
View details for Web of Science ID A1991FC76000004
View details for PubMedID 1873441
Cholesterol ester hydrolase activity has been studied in mammary glands of rats. Subcellular fractionation of the glands obtained in mid-lactation indicated that around 80% of the recovered activity was associated with particulate fractions. Two distinct cholesterol ester hydrolase activities were identified, one with an optimum pH of 7.5-9.0 and the second (approximately 5% of the total activity) with a more acidic pH optimum. Although the neutral cholesterol ester hydrolase had some properties in common with the lipoprotein lipase in mammary tissue, it was shown to be a separate entity by several criteria. Its activity could be increased following treatment with Mg-ATP and cAMP-dependent protein kinase, suggesting identity with the hormone sensitive lipase of adipose tissue. The cholesterol ester hydrolase activity in mammary glands just after parturition was greater than in glands obtained either from late-pregnant or midlactating animals. The subcellular distribution of the neutral cholesterol ester hydrolase suggested that it may have a different function to the neutral cholesterol ester hydrolase of adrenals and other tissues. Nevertheless the fact that the activity of the enzyme can be modulated by cAMP-dependent protein kinase suggests the possibility that hormonal control of this enzyme may be involved in the regulation of cholesterol metabolism in the mammary gland.
View details for Web of Science ID A1991EU68100006
View details for PubMedID 1646925
A population-based, case-control study of prostate cancer in Utah was used to assess reported food-consumption patterns for the adolescent and adult years. Men reported eating eggs, whole milk, butter, white bread, cereals, and candy less frequently and red meat, fish, low-fat milk, cheese, yogurt, ice cream, margarine, fruits and vegetables, and whole-wheat bread more frequently as adults, indicating that diets changed in the hypothesized direction to correspond to national changes in food-consumption practices. Men who consumed a diet high in saturated fatty acids as adults were at a slightly increased risk of developing aggressive prostate cancer after adjusting for adolescent diet (odds ratio 1.8 comparing high with low intakes), whereas men who consumed a diet high in saturated fatty acids as adolescents were not at increased risk of developing these tumors after controlling for a diet high in saturated fatty acids as adults (odds ratio 1.1).
View details for Web of Science ID A1990DZ79500031
View details for PubMedID 2403069
A population-based case-control study was used to investigate associations between prostate cancer and cadmium exposure, longest industry held, and longest occupation held. The study included 358 men with newly diagnosed prostate cancer and 679 control men identified from the Utah population. Occupational exposures to cadmium were ascertained from self-reported data, through several a priori suspect industries and occupations, through an occupation-exposure linkage system, and through dietary food frequency questionnaires. Overall, cadmium exposure appeared to result in a small increased relative risk for prostate cancer, most apparent for aggressive tumors (OR = 1.7, CI = 1.0-3.1 for any occupational exposure, high dietary intake, or smoking cigarettes). Cases were more likely to have worked in the following industries: mining, paper and wood, medicine and science, and entertainment and recreation. Among men younger than 67, cases were also more likely to have worked in the food and tobacco industries (OR = 3.6, CI = 1.0-12.8). Cases were less likely to have worked in industries involved with glass, clay and stone, or rubber, plastics, and synthetics. Men employed as janitors and in other building service occupations showed increased relative risk for aggressive tumors (OR = 7.0, CI = 2.5-19.6). Agricultural occupations did not appear to be related to prostate cancer, although an increased relative risk for aggressive tumors was detected among younger men (OR = 2.6, CI = 0.6-12.1).
View details for PubMedID 2073496
We used data from a population-based case-control study to examine how use of tobacco products and consumption of alcohol, coffee, and caffeine relate to colon cancer in Utah. We hypothesized that low use of these substances is one factor contributing to the low colon cancer incidence in Utah and could help explain the low risk associated for colon cancer with being a member of the Church of Jesus Christ of Latter-day Saints. In females, we observed little or no increase in risk of colon cancer from smoking cigarettes or from consumption of alcohol, caffeine, or coffee. Males who used pipes, however, experienced an increased risk for colon cancer (OR = 4.1, 95% CI = 1.3-12.3). Risk for colon cancer associated with alcohol use was greatly attenuated after adjusting for caffeine and pipe use in males; males who consumed higher levels of caffeine during the two to three years prior to the interview were at higher risk than males who consumed low levels of caffeine (OR = 2.0, 95% CI = 1.0-4.2); similar associations were observed for coffee consumption. Nonuse of these substances could explain the low colon cancer incidence rates observed in members of the Church of Jesus Christ of Latter-day Saints and Utah males.
View details for PubMedID 2073501
The relation between cervical cancer and dietary intake of vitamins A, C, and E, beta-carotene, and selenium was examined in a population-based case-control study in Utah. Cervical cancer cases (n = 266) and population-based controls (n = 408) were interviewed between 1984 and 1987. Protective effects were observed for vitamins A, C, and E and beta-carotene but were attenuated by age, level of education, and lifetime cigarette use. Associated risk (comparing highest with lowest quartiles of intake) went from 0.53 (crude) to 0.71 (adjusted) for vitamin A; from 0.55 (crude) to 0.82 (adjusted) for beta-carotene; from 0.45 (crude) to 0.55 (adjusted) for vitamin C; from 0.58 (crude) to 0.60 (adjusted) for vitamin E; and from 0.95 (crude) to 0.70 (adjusted) for selenium. Adjustment for number of sex partners and church attendance, factors significantly related to cervical cancer risk, only slightly attenuated these adjusted risk estimates.
View details for PubMedID 2081246
A case-control study was conducted in Utah between July 1979 and June 1983 in which 231 cases of colon cancer identified through the Utah Cancer Registry and 391 controls identified through random digit dialing were interviewed. Odds ratios (OR) were calculated comparing the highest exposure categories with the lowest exposure categories. The highest quintile of body mass index (weight (kg)/height (m)2 for males; weight (kg)/height (m)1.5 for females) was associated with increased risk in both males (OR = 2.1) and females (OR = 2.3). In females, total dietary fat (OR = 1.9) and energy intake (OR = 1.5) were associated with an increased colon cancer risk after adjusting for age, body mass index, and crude fiber. Fiber was protective in females (OR = 0.5) after adjusting for age, body mass index, and energy intake, as was beta-carotene (OR = 0.5) after also adjusting for crude fiber. Adjusted risk estimates in males were 2.0 for total dietary fat, 3.8 for polyunsaturated fat, 2.1 for monounsaturated fat, 2.1 for energy intake, 2.5 for protein, 0.3 for fiber, 0.4 for beta-carotene, and 0.3 for cruciferous vegetables. Risk estimates differed by site of cancer within the colon. In males, protein (OR = 3.8) was a risk factor for cancer of the descending colon, while fats (OR = 2.7-8.8) increased the risk of cancer of the ascending colon. The hypotheses that dietary fat increases colon cancer risk while dietary fiber decreases colon cancer risk and that fat and protein may be independently associated with colon cancer risk are supported.
View details for Web of Science ID A1989AY60100004
View details for PubMedID 2554725
A case-control study was conducted in Utah between 1984 and 1987 to evaluate the effects of nutrient intake on risk of developing ovarian cancer. Detailed dietary intake information was available from 85 first primary ovarian cancer cases and 492 population-based controls. Calories, fat, protein, fiber, and vitamins A and C did not appreciably alter the risk of developing ovarian cancer. However, high intake of beta-carotene appears to confer protection against ovarian cancer (odds ratio = 0.5, 95% confidence interval 0.3-1.0) after adjusting for age, number of pregnancies, and the body mass index of weight/height.
View details for Web of Science ID A1989AL30500007
View details for PubMedID 2763995
The relationships between bladder cancer and occupation, industries, and occupational exposures in Utah were examined in a population-based, case-control study conducted between 1977 and 1983. Life-long occupational histories were obtained for 417 cases (332 men and 85 women) and 877 controls (685 men and 192 women). Although few positive findings emerged in this study, increased risks were detected among men for employment in the leather and textile industries which increased with duration of employment. The effects were most marked for employment beginning 45 or more years prior to interview (odds ratio [OR] for textiles = 1.92, confidence interval [CI] = 0.89-4.46; for leather OR = 2.95, CI = 0.63-13.76). Among men and women, increased risk was detected among clerical workers employed for less than 10 years (OR = 1.59, CI = 1.16-2.17) although the risk decreased with increased duration of employment (OR = 0.88, CI = 0.55-1.40 for greater than or equal to 10 years). A protective effect was seen among men and women for 10 or more years employment in professional, managerial, and technical occupations (OR = 0.68, CI = 0.50-0.92). Employment as a carpenter resulted in increased risk which increased with duration. Increased risk for bladder cancer was detected among carpenters who smoked but not among carpenters who never smoked. We used an occupation-exposure linkage system to identify workers exposed to aromatic amino compounds; such workers did not have increased risk of bladder cancer, although interaction between long-term exposure to aromatic amino compounds and smoking was detected. Interactions between smoking and other industrial or occupational exposures were not demonstrated, and for the most part, smoking did not confound the estimates of the bladder cancer-occupation relationships.
View details for Web of Science ID A1989AD74900009
View details for PubMedID 2750753
Smoking has been observed to affect plasma sex hormones and body mass index. The relationship between smoking, body mass index, and plasma concentration of sex hormones was studied in normal adult male twins. The analyses were performed for between 150 and 159 twin pairs for whom hormonal data were available on both twins. With bivariate analysis, neither body mass index nor smoking affected estrone, luteinizing hormone, follicle-stimulating hormone, ratio of testosterone to estradiol, or ratio of testosterone to dihydrotestosterone. Body mass index significantly (P less than 0.05) affected sex hormone binding globulin, whereas smoking had no effect. The plasma contents of testosterone and dihydrotestosterone and the luteinizing hormone/testosterone ratio were affected by both body mass index and smoking, although, after allowing for body mass, smoking was less significant (0.05 less than P less than 0.10). A path model was formulated to examine the relationship of body mass and sex steroid levels. Our results suggest that body mass index affects sex steroids, since common environmental factors do not account for the strength of the relationship. The bivariate analysis suggests that the smoking effect on sex hormones (except perhaps for dihydrotestosterone) is secondary to an effect on body mass index.
View details for Web of Science ID A1989AF05600002
View details for PubMedID 2753350
A population-based case-control study was used to assess the relations of physical activity and diet to the development of colon cancer in Utah. Data were obtained for a reference period of two years prior to interview for controls (204 females and 180 males) and two years prior to the date of diagnosis for cases (119 females and 110 males). Both leisure time and occupational activities were ascertained by level of intensity and were converted to calories expended per week for analysis. Dietary data were obtained from a quantitative food frequency questionnaire. Physical activity and dietary data were divided into quartiles based upon the distribution in the study population for analyses. Total physical activity was protective against the development of colon cancer for both males (odds ratio (OR) = 0.70) and females (OR = 0.48) when high and low quartiles of activity were compared. Intense physical activity was the component of activity that had the greatest protective effect for males (OR = 0.27); a similar relation was seen for females (OR = 0.55). The observed relation between physical activity and colon cancer was not confounded by dietary intake of calories, fat, or protein, nor was the diet and colon cancer relation confounded by physical activity (odds ratios for calories, protein, and fat in males were 2.40, 2.57, and 2.18, respectively). Assessment of the interrelations among physical activity, diet, and colon cancer suggests that physical activity modifies colon cancer risk associated with diet.
View details for Web of Science ID A1988Q806700004
View details for PubMedID 3189298
A population-based, incident case-control study was conducted in Utah to assess the relationship between fluid intake and bladder cancer. Cancer cases (n = 419) were identified through the Utah Cancer Registry, and controls (n = 889) were obtained through random digit dialing and the Health Care Financing Administration. After adjustment for cigarette smoking, age, sex, history of diabetes, and history of bladder infections using multiple logistic regression analysis, total fluid intake was not found to be related to bladder cancer development. Specific fluids related to bladder cancer risk were milk intake (OR = 0.64) and caffeinated coffee intake (OR = 1.60). A linear trend for a dose-response protective effect was observed for milk, while coffee increased risk only when 40 or more cups were consumed per week. Alcohol increased risk only when consumed at high levels (over 3.64 ounces or 103 g per week) by people who never smoked cigarettes (OR = 2.37). Likewise, tea consumption in non-cigarette smokers increased bladder cancer risk (OR = 2.25). Results from this study suggest that types of fluids consumed may play a role in the development of bladder cancer. Furthermore, it is hypothesized that the dietary components of these beverages may be related to the development of bladder cancer.
View details for Web of Science ID A1988P355600004
View details for PubMedID 3391705
A population-based, incidence case-control study was used to assess the effect of cigarette smoking on other risk factors for the development of bladder cancer. White men (n = 332) between the ages of 21 and 84 with bladder cancer were compared with 686 population-based controls. Cigarette smokers were classified by current smoking status as well as by amount, duration, inhalation patterns, age at first having smoked, and years since having stopped smoking. These variables were associated with a change in the risk for bladder cancer. The population-attributable risk associated with cigarette smoking was 48.5%. Risks from the use of other tobacco products such as cigars, pipes, snuff, and chewing tobacco, and from caffeinated coffee, tea, and alcoholic beverages were evaluated in light of cigarette smoking status. Cigarette smoking was shown to be both a confounder and an effect modifier. Risk estimates for bladder cancer associated with caffeinated coffee and alcoholic beverages were decreased after controlling for the effects of cigarette smoking. However, an increased risk of developing bladder cancer from cigar smoking (Odds ratio [OR] = 2.46) and tea drinking (OR = 3.14) was only seen in men who never smoked cigarettes. An increased but not significant risk was also seen for pipe, snuff, and chewing tobacco use in noncigarette smokers. The population-attributable risk from cigars and tea in the population of white men who had never smoked was 6.3% and 18.9%, respectively. Our results suggest that cigarette smoking may obscure other risk factors unless those who never smoked are separately studied.
View details for Web of Science ID A1988L671900032
View details for PubMedID 3334975
Dietary intake has been hypothesized as being associated with several hormonally related cancers including prostate, breast, ovarian, and endometrial cancer. Because diet may affect hormones directly, it is logical to examine the effects of dietary factors on hormone production and levels. Therefore, a set of 72 male MZ and 83 male DZ twin pairs was ascertained from the Utah birth certificates. A quantitative food frequency questionnaire was administered and blood samples were drawn for hormonal assays. Heritability estimates for hormonal levels were calculated indicating a range from no heritability for sex hormone binding globulin (SHBG), estrone, and testosterone glucuronide to 70% for androstanediol glucuronide and luteinizing hormone. To examine nutritional factors, the difference in hormone and SHBG levels between each MZ twin and his co-twin were correlated with the difference in nutrient intake. Weight and obesity were significantly correlated with plasma testosterone and follicle stimulating hormone. Fat intake showed a significant association with testosterone. Androstanediol glucuronide, a steroid that reflects tissue formation of dihydrotestosterone, was inversely correlated with caloric intake, theobromine and caffeine. Testosterone glucuronide exhibited significant correlations with calories and vitamin A. This study suggests that dietary intake affects plasma sex-steroid levels in men.
View details for Web of Science ID A1988M743900004
View details for PubMedID 3360302
View details for PubMedID 3365215
A case-control study was conducted to assess the role of diet in the etiology of colon cancer. Diet was measured by means of a comprehensive quantifiable food frequency history instrument in 246 cases and 484 controls drawn from the general population of Utah. Each subject's diet was described by major nutrient groups and total energy based on the nutritional content of foods reported. Cases reported higher daily food intake 5 years preceding diagnosis than controls [men, rate ratio (RR) = 2.5; women, RR = 3.6], as measured by total energy content of the diet. Higher risk of colon cancer with increasing energy intake was independent of stage of disease at diagnosis and obesity, as measured by body mass. Fat, protein, and carbohydrate intake all had elevated RRs but could not be assessed as risk factors independent of energy intake because of their strong correlations with total calories. Due to the higher energy intake of the cases, odds ratios for the daily intake of dietary fiber and vitamins A and C were also greater than 1. However, adjusting for caloric intake removed this effect, and dietary fiber showed a weak protective effect. Total energy intake must be evaluated before attempting to assign a causal role to any food or nutrient that may be postulated to play a role in colon cancer.
View details for Web of Science ID A1987H387800008
View details for PubMedID 3033383
Food frequency information from 762 Utahns, aged 24 to 80 years, selected from the general population using a random digit dialing technique was studied to determine the characteristics of diets that provide 18 mg iron/2,000 kcal, the Recommended Dietary Allowances (RDAs) of iron and energy for women aged 23 to 50 years. The diets were divided into three categories according to iron per 1,000 kcal: category 1, 9.0 mg or more iron; category 2, 6.0 to 8.99 mg iron; and category 3, 5.99 mg or less iron. Twenty-seven percent of the women and 16% of the men reported consuming diets containing more than 9 mg iron/1,000 kcal. Six percent of the women consumed 18 mg iron daily. Total energy intake decreased dramatically as iron density increased, as did intake of protein, carbohydrate, and fat. However, the percentage of energy consumed as protein and carbohydrate increased in the high-iron density categories. Individuals in the high-iron density categories consumed greater proportions of their iron and energy from vegetable, fruit, and cereal products; those in the low-iron density category consumed more pastries, beverages, sweets, and added fats, i.e., high-calorie foods. When fortified breakfast cereals were removed from the diets, only 14% of the women and 6% of the men consumed diets that provided at least 9 mg iron per 1,000 kcal. Women can meet the RDA for iron from their diets if they consume the recommended amount of energy distributed across food groups as follows: cereals, 14% to 16%; vegetables, at least 11%; meat, fish, poultry, and eggs, 16% to 18%.(ABSTRACT TRUNCATED AT 250 WORDS)
View details for Web of Science ID A1987G034900006
View details for PubMedID 3819237
Lifelong occupational histories obtained by interview prior to death were compared to death certificate data for 87 male bladder cancer patients in Utah. Agreement was defined as identical Bureau of Census codes, after predetermined groupings were made. Usual occupation, defined as that with the longest duration, agreed with the death certificate occupation for 54% of the individuals; usual industry agreed for 72%. Most recent occupation and industry agreed for 47% and 53%, respectively. For 69%, at least one interview occupation agreed with the death certificate occupation, and at least one industry agreed for 84%. Variables affecting agreement were duration of the job and education. Also examined were interview data about employment either during the last 15 years or prior to age 65 years, obtained from 112 male colon cancer patients. The Bureau of Census codes were in agreement for occupation in 63% and for industry in 65%. Duration of the job and education were related to percent agreement. We conclude that occupations and industries listed on death certificates reflect at least part of the work history of the majority of individuals.
View details for Web of Science ID A1987J284400002
View details for PubMedID 3661568
Whether familial factors affect the frequency of prostatic cancer and the plasma content of sex-steroids was investigated. Brothers (n = 257) of probands (n = 150) diagnosed with prostatic cancer before age 62 years had a fourfold higher risk for developing the disease than men in the general population in the State of Utah and their brothers-in-law (n = 202). Familial factors markedly affected the plasma content of sex steroids (testosterone, dihydrotestosterone, the ratio of testosterone to DHT, sex-hormone binding globulin, and the free fraction of testosterone) in nonendocrinologically treated probands and their brothers and sons and in normal men in the general populations. Index cases and their brothers and sons had a significantly lower mean plasma testosterone content than controls of comparable age. Preliminary data suggest that the metabolic clearance rate of testosterone and the conversion ratio of testosterone to estradiol are relatively high in probands. The observations indicate that familial factors are potent risk factors for the development of prostatic cancer. They also suggest that plasma androgen values in families with prostatic cancer cluster in the lower range of normal and that plasma sex-steroid content is more similar in each brothers with or without prostatic cancer than among nonbrothers.
View details for Web of Science ID A1985ADJ3400001
View details for PubMedID 3975174
A cross-sectional study was conducted in the Utah metropolitan area in which a random sample of white, married women with children 14 years of age or younger were interviewed by telephone. Information was obtained on possible risk factors for depression and depression was measured using the Beck Depression Inventory (BDI). Prevalence of depression was compared in Mormon women (N = 143) who have a high percentage of career homemakers and non-Mormon (N = 36) who have a high percentage of women working outside the home. No difference in prevalence of depression was noted. Risk factors for depression in Mormon women were also studied. After adjusting for confounding, the risk factors were: Less education, little perceived caring from spouse, perception of having less than good health and having a low income. These findings are compared to other studies.
View details for Web of Science ID A1984SJ47400006
View details for PubMedID 6608792
A hospital-based and population-based case-control study of cervical cancer (in situ and invasive) was conducted in urban Utah to determine if methods of respondent selection affect estimates of risk for variables thought to be associated with the disease. Population cases (N = 409) and cases from two large hospitals (N = 124) were identified through the Utah Cancer Registry. Population-based controls (N = 379) were identified through random-digit dialing; hospital-based controls (N = 150) with gynaecological disorders other than cancers and elective abortions were chosen from the same hospitals as the cases for the hospital study. Both control groups were frequency matched to cases by age. Approximately 79% of the identified cases and 85% of the selected controls completed interviews conducted in their homes. Most risk estimates were lower in the hospital-based study because of the more case-like attributes of this group. Stratified analysis for social class led to adjusted risk estimates which were lower than the unadjusted risk estimates for the population-based study, but not for the hospital-based study. The close social class matching in the hospital-based study seems to have led to concurrent overmatching on other risk factors since many of these are closely related to social class. Findings are discussed in terms of implications for case-control study design.
View details for Web of Science ID A1984SX32900016
View details for PubMedID 6735571
We review the goals of epidemiological nutritional studies and evaluate methods of dietary data collection in terms of these goals. Special problems for the cancer epidemiologist studying diet are then reviewed, including methods of data collection, quantification of food intake, and analysis of nutritional data. Food frequency methods are generally best for collection of dietary data in epidemiological studies, and the use of food data banks enables the study of specific dietary components. The major problems in analysis stem from the complex interrelationships among nutrients and their high correlation with each other.
View details for PubMedID 6831462
We carried out a case-control study of 217 cases of in situ carcinoma of the uterine cervix and 243 controls chosen from the general population of Utah. We found a relative risk of 3.0 for cigarette smoking after controlling for sexual and socioeconomic risk factors. The smoking association was strongest in the youngest age group (ages 20-29), reaching seventeenfold, and was weaker in the older age groups. These data suggest that cigarette smoking may be an independent risk factor for cancer of the uterine cervix, after considering sexual behavior and other well-established risk factors.
View details for Web of Science ID A1983QM44300012
View details for PubMedID 6837821
The relationship between coffee drinking and risk of bladder cancer was assessed with the use of data from a case-control study of bladder cancer. Incident cases (2,982) and general population controls (5,782) were interviewed. Overall, the relative risk (RR) of bladder cancer for subjects who had ever drunk coffee was estimated as 1.4 (95% confidence interval = 1.1-1.8). There was no consistent relation between the RR estimate and the current consumption level. Among men who drank coffee, those who drank more than 49 cupfuls of coffee per week had an apparent excess in risk, but women who drank that much had an apparent deficit in risk.
View details for Web of Science ID A1983QV32200007
View details for PubMedID 6574270
The relation between use of hair dyes and risk of bladder cancer was assessed using data from a case-control study of bladder cancer. Incident cases (2982) and general population controls (5782) were interviewed. The overall estimate of relative risk of bladder cancer for users of hair dyes was 1.0 (95%) confidence interval, 0.9 to 1.2) compared to nonusers. No consistent pattern of association was detected between bladder cancer risk and various indices of timing or intensity of exposure to hair dyes. Various explanations of the lack of association are discussed.
View details for Web of Science ID A1982PM03100075
View details for PubMedID 7127313
Data from the Utah Cancer Registry were used to compare cancer incidence in Mormons and non-Mormons in Utah for the period 1967--75. Church membership was identified for 97.8% of the 20,379 cases in Utah by a search of the central membership files of the Church of Jesus Christ of Latter-Day Saints (or Mormon Church). Sites associated with smoking (lung, larynx, pharynx, oral cavity, esophagus, and urinary bladder) showed an incidence in Mormons at about one-half that of non-Mormons. Rates of cancers of the breast, cervix, and ovary were low in Mormon women; the rate for cervical cancer was about one-half of that observed in non-Mormons. Cancers of the stomach, colon-rectum, and pancreas were about one-third lower in Mormons than in others who are not members of this religious group. Most of the differences seen in cancer incidence can be explained by Mormon teachings regarding sexual activity and alcohol and tobacco use, but some differences (e.g., colon and stomach) remain unexplained.
View details for Web of Science ID A1980KQ47600031
View details for PubMedID 6933238
In a comparison of Mormons and non-Mormons in Utah, more Mormon men and women married spouses of the same faith, were religiously active, were of Northern Europe ancestry, lived in rural areas, had fewer exposures to occupational hazards, were less likely to smoke cigarettes or drink coffee, tea, and alcohol, used fats in cooking, and were more often married that was the cohort of other religions. No differences existed in occupation, but Mormon men had completed more years of schooling. Mormon women were less likely to be college graduates, had fewer sexual partners, had more pregnancies, were older at first pregnancy, were less likely to use birth control pills, had fewer miscarriages and hysterectomies, examined their breasts more often, and had more breast X-rays. For women, there was only a small difference by religion for age at first intercourse and no difference for age at which they began using birth control pills. Religious activity was examined for Mormons, and in most instances inactive Mormons were more like the non-Mormon population in respect to the variables measured.
View details for Web of Science ID A1980KQ47600034
View details for PubMedID 6933240
An assessment of adaptation patterns among cancer patients with facial disfigurements was made by interviewing 152 patients in two head and neck clinics at Roswell Park Memorial Institute, Buffalo. It was found that 86.2% had adapted to their disfigurement. More specifically, disfigurement seldom was mentioned as a reason for not returning to work and for not participating in social activities with work mates, friends, relatives, and society in general. Disfigurement also seemed to have little effect on involvement in formal groups. Reactions from society toward disfigurement were perceived as being mostly positive (although staring was commonly reported). Reasons for this high level of adaptation are suggested. These include the need to maintain stability of self-concept, age as a stabilizing factor, the positive reaction from society, the nature of the disease itself (so that disfigurement may be seen as being more acceptable (positive) than the alternative of threat of death), the hospitalization experience as it prepares the patient for society's response, and the fact that this is an acquired disfigurement in a patient from a relatively normal population.
View details for Web of Science ID A1977EB78300002
View details for PubMedID 931585
After administration, a drug does not exert immediately all its actions. Rates of diffusion, fixation and excretion of drugs are depending from their nature as well as from the condition of the body to which they are given. The resultant of these mechanisms control the blood level of a drug, level which varies in function of time. The blood level reflects the pharmacodynamic activity of a drug. Information on kinetics and significance of the status of drug equilibrium are of major importance for rational drug administration.
View details for PubMedID 952595