Blood pressure,body size and prostate cancer risk in the Swedish Construction Workers cohort

Data from prospective studies on blood pressure and prostate cancer risk are limited, and results are inconclusive. Baseline measurements of height, weight and blood pressure were available in 336,159 men in the Swedish Construction Workers cohort. During an average of 22.2 years of follow‐up, 10,002 incident cases and 2,601 fatal cases of prostate cancer were identified in National registers. For 5,219 cases, tumor characteristics were available; 2,817 tumors were classified as nonaggressive and 2,402 as aggressive. Relative risks of disease were estimated from Cox regression models, using attained age as time‐scale, and adjusting for birth year, smoking status and body mass index (BMI). Top compared to bottom quintile level of systolic or diastolic blood pressure was associated with a significant 15–20% decreased risk of incident prostate cancer (p for trend: systolic < 0.0001, diastolic = 0.3), but blood pressure was not significantly associated with risk of fatal prostate cancer. BMI was not associated with prostate cancer incidence, but was positively associated with fatal prostate cancer; men in the top quintile had a 30% increased risk (p for trend = 0.0004). The associations between blood pressure and BMI and nonaggressive tumors were similar to those of incident prostate cancer, and associations with aggressive tumors were similar to those of fatal prostate cancer. Data from our study suggest that hypertension is associated with a decreased risk of incident prostate cancer, but the explanation for this finding is unclear. Our study support a positive association between overweight and risk of fatal prostate cancer.     

Risk factors for prostate cancer incidence and progression in the health professionals follow-up study

Risk factors for prostate cancer could differ for various sub-groups, such as for "aggressive" and "non-aggressive" cancers or by grade or stage. Determinants of mortality could differ from those for incidence. Using data from the Health Professionals Follow-Up Study, we re-examined 10 factors (cigarette smoking history, physical activity, BMI, family history of prostate cancer, race, height, total energy consumption, and intakes of calcium, tomato sauce and alpha-linolenic acid) using multivariable Cox regression in relation to multiple subcategories for prostate cancer risk. These were factors that we previously found to be predictors of prostate cancer incidence or advanced prostate cancer in this cohort, and that have some support in the literature. In this analysis, only 4 factors had a clear statistically significant association with overall incident prostate cancer: African-American race, positive family history, higher tomato sauce intake (inversely) and alpha-linolenic acid intake. In contrast, for fatal prostate cancer, recent smoking history, taller height, higher BMI, family history, and high intakes of total energy, calcium and alpha-linolenic acid were associated with a statistically significant increased risk. Higher vigorous physical activity level was associated with lower risk. In relation to these risk factors, advanced stage at diagnosis was a good surrogate for fatal prostate cancer, but high-grade (Gleason >/= 7 or Gleason >/= 8) was not. Only for high calcium intake was there a close correspondence for associations among high-grade cancer, advanced and fatal prostate cancer. Tomato sauce (inversely) and alpha-linolenic acid (positively) intakes were strong predictors of advanced cancer among those with low-grade cancers at diagnosis. Although the proportion of advanced stage cancers was much lower after PSA screening began, risk factors for advanced stage prostate cancers were similar in the pre-PSA and PSA era. The complexity of the clinical and pathologic manifestations of prostate cancer must be considered in the design and interpretation of studies.     

Alcohol consumption and prostate cancer risk: results from the Melbourne collaborative cohort study

Although there is little evidence to support an association between alcohol consumption and prostate cancer risk, questions remain concerning the effect on aggressive and nonaggressive tumours and the pattern and type of alcohol consumed. In a prospective cohort of 16,872 men aged 27-70 years at recruitment and followed-up from 1994 to the end of 2003, 732 incident prostate cancers were identified through the local population cancer registry, including 132 aggressive cases and 53 prostate cancer deaths. Detailed information on alcohol consumption was taken at baseline by trained interviewers using a structured questionnaire. Overall, alcohol intake was not associated with prostate cancer incidence. Compared to abstainers, men consuming 1-19 g/d of alcohol had a slightly reduced incidence of aggressive prostate cancers (hazard ratio 0.67; 95% confidence interval (CI) 0.43, 1.06) and prostate cancer mortality (hazard ratio 0.56; 95% CI 0.28, 1.14), but their risk of nonaggressive prostate cancers was close to unity (hazard ratio 1.09; 95% CI 0.85, 1.40). No significant association with pattern of drinking or type of alcoholic beverage was found. Our results show that alcohol consumption does not influence overall prostate cancer incidence but we found suggestive evidence that alcohol consumption might decrease the incidence of aggressive prostate cancer and mortality.     

A prospective study of calcium intake and incident and fatal prostate cancer.

Prostate cancer is the most common incident cancer and the second leading cause of cancer mortality in U.S. males. Higher milk intake has been relatively consistently associated with an increased risk of prostate cancer, especially advanced prostate cancer. Some data suggest that high intake of calcium might account for this association, but this relationship remains controversial. We hypothesized that high calcium intake, possibly by lowering 1,25(OH)2 vitamin D levels, is associated with poorer differentiation in prostate cancer and thereby with fatal prostate cancer. We examined calcium intake in relation to prostate cancer risk using data from the Health Professionals Follow-up Study, a prospective cohort study of 47,750 male health professionals with no history of cancer other than nonmelanoma skin cancer at baseline. We assessed total, dietary, and supplementary calcium intake in 1986, 1990, 1994, and 1998, using a validated food frequency questionnaire. We calculated the multivariable relative risk (RR) and 95% confidence intervals (95% CI) using Cox proportional hazards regression. Over 16 years of follow-up, we identified 3,544 total cases of prostate cancer, 523 advanced (extraprostatic) cases, and 312 fatal cases. Higher calcium intake was not appreciably associated with total or nonadvanced prostate cancer but was associated with a higher risk of advanced and fatal prostate cancer [for fatal prostate cancer, compared with men whose long-term calcium intake was 500-749 mg/d (excluding supplement use of <5 years); those with intakes of 1,500-1,999 mg/d had a RR, 1.87; 95% CI, 1.17-3.01; and those with > or = 2,000 mg/d had a RR, 2.43; 95% CI, 1.32-4.48; P(trend) = 0.003]. Dietary calcium and supplementary calcium were independently associated with an increased risk. For high-grade prostate cancer (Gleason > or = 7), an association was observed for high versus low calcium intake (RR, 1.89; 95% CI, 1.32-2.71; P(trend) = 0.005), but a nonsignificant, inverse association was observed for organ-confined, low-grade prostate cancer (RR, 0.79; 95% CI, 0.50-1.25; P(trend) = 0.09). In a sample of this cohort, higher calcium intake was associated with lower circulating 1,25(OH)2 vitamin D levels. Our findings suggest that calcium intakes exceeding 1,500 mg/d may be associated with a decrease in differentiation in prostate cancer and ultimately with a higher risk of advanced and fatal prostate cancer but not with well-differentiated, organ-confined cancers.     

Smoking and the risk of prostate cancer in the European Prospective Investigation into Cancer and Nutrition

Background:

Smoking is not associated with prostate cancer incidence in most studies, but associations between smoking and fatal prostate cancer have been reported.

Methods:

During 1992 and 2000, lifestyle information was assessed via questionnaires and personal interview in a cohort of 145 112 European men. Until 2009, 4623 incident cases of prostate cancer were identified, including 1517 cases of low-grade, 396 cases of high grade, 1516 cases of localised, 808 cases of advanced disease, and 432 fatal cases. Multivariable Cox proportional hazards regression models were used to examine the association of smoking status, smoking intensity, and smoking duration with the risk of incident and fatal prostate cancer.

Results:

Compared with never smokers, current smokers had a reduced risk of prostate cancer (RR=0.90, 95% CI: 0.83–0.97), which was statistically significant for localised and low-grade disease, but not for advanced or high-grade disease. In contrast, heavy smokers (25+ cigarettes per day) and men who had smoked for a long time (40+ years) had a higher risk of prostate cancer death (RR=1.81, 95% CI: 1.11–2.93; RR=1.38, 95% CI: 1.01–1.87, respectively).

Conclusion:

The observation of an increased prostate cancer mortality among heavy smokers confirms the results of previous prospective studies.     

Midlife metabolic factors and prostate cancer risk in later life

Metabolic syndrome is associated with several cancers, but evidence for aggressive prostate cancer is sparse. We prospectively investigated the influence of metabolic syndrome and its components on risk of total prostate cancer and measures of aggressive disease in a cohort of Icelandic men. Men in the Reykjavik Study (n = 9,097, enrolled 1967–1987) were followed for incident (n = 1,084 total; n = 378 advanced; n = 148 high‐grade) and fatal (n = 340) prostate cancer until 2014. Cox regression was used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for (1) measured metabolic factors at cohort entry (body mass index (BMI), blood pressure, triglycerides, fasting blood glucose) and (2) a metabolic syndrome score (range 0–4) combining the risk factors: BMI ≥30 kg/m²; systolic blood pressure (SBP) ≥130 or diastolic blood pressure (DBP) ≥85 mm Hg or taking antihypertensives; triglycerides ≥150 mg/dl; fasting blood glucose ≥100 mg/dl or self‐reported type 2 diabetes. Hypertension and type 2 diabetes were associated with a higher risk of total, advanced, high‐grade, and fatal prostate cancer, independent of BMI. Neither BMI nor triglycerides were associated with prostate cancer risk. Higher metabolic syndrome score (3–4 vs 0) was associated with a higher risk of fatal prostate cancer (HR 1.55; 95% CI: 0.89, 2.69; p trend = 0.08), although this finding was not statistically significant. Our findings suggest a positive association between midlife hypertension and diabetes and risk of total and aggressive prostate cancer. Further, metabolic syndrome as a combination of factors was associated with an increased risk of fatal prostate cancer.     

Cigarette smoking, elevated fasting serum glucose, and risk of pancreatic cancer in Korean men

Pancreatic cancer is one of the most fatal human cancers and continues to be a major unsolved health problem. The goal of this study was to estimate the independent effects and interactions between cigarette smoking and diabetes on the risk of pancreatic cancer in Korean male population. Cigarette smoking and the risk of incidence and death from pancreatic cancer were examined in a 10-year prospective cohort study of 446,407 Korean men aged 40 to 65 years who received health insurance from the National Health Insurance Corporation and who had a medical evaluation in 1992. Relative risks (RR) and 95% confidence intervals (CI) were calculated using a Cox proportional hazards model after adjusting for age, body mass index, exercise and alcohol use. Current smoking was associated with an increased risk of incidence (RR = 1.7, 95% CI = 1.6-1.9) and mortality (RR = 1.6, 95% CI = 1.4-1.7) from pancreatic cancer. The RR for pancreatic cancer increased with both duration and amount of smoking. Diabetes was also associated with an increased risk of both incidence (RR = 1.8, 95% CI = 1.5-2.2) and mortality (RR = 1.7, 95% CI = 1.4-2.1) from pancreatic cancer. There was no interaction between smoking and fasting serum glucose in terms of pancreatic cancer risk. Thus, our prospective study has demonstrated that cigarette smoking and elevated fasting serum glucose are independently associated with an increased risk of pancreatic cancer in a large cohort of Korean males.     

Body size across the life course and prostate cancer in the Health Professionals Follow‐up Study

Current evidence of an association between body size and prostate cancer is conflicting, possibly due to differential effects of body size across the lifespan and the heterogeneity of the disease. We therefore examined childhood and adult body size in relation to total incident prostate cancer and prognostic subtypes in a prospective cohort of 47,491 US men in the Health Professionals Follow‐up Study. We assessed adult height, body mass index (BMI) in early and middle‐to‐late adulthood, adult waist circumference, and body shape at age 10. With follow‐up from 1986 to 2010, we estimated the relative risk (RR) of prostate cancer using Cox proportional hazards models. We identified 6,183 incident cases. Tallness was associated with increased risk of advanced‐stage tumors, particularly fatal disease (RR = 1.66, 95% CI 1.23–2.23, highest vs. lowest quintile, p_trend < 0.001). High BMI at age 21 was inversely associated with total prostate cancer (RR = 0.89, 95% CI 0.80–0.98, BMI ≥26 vs. 20–21.9, p_trend = 0.01) and with fatal and advanced disease. The association for late adult BMI differed by age (p_interaction < 0.001); high BMI was inversely associated with total prostate cancer (RR = 0.64, 95% CI 0.51–0.78, BMI ≥30 vs. 21–22.9, p_trend<0.001) and with non‐advanced and less aggressive tumors among men ≤65 years, whereas no association was seen among men >65 years. Adult waist circumference was weakly inversely associated with less aggressive disease. Childhood obesity was unclearly related to risk. Our study confirms tall men to be at increased risk of fatal and advanced prostate cancer. The influence of adiposity varies by prognostic disease subtype and by age. The relationship between body size and prostate cancer is complex. Body size changes progressively throughout life and consequent effects on prostate cancer risk may be associated with related changes in hormonal and metabolic pathways. This large prospective study examined potential associations between the risk of various prostate cancer subtypes and multiple anthropometric measures at different ages in men. Tallness was confirmed to be associated with an elevated risk of advanced prostate cancer, particularly fatal disease. The extent to which body weight influenced risk varied according to factors such as age and disease subtype.     

Smoking at diagnosis and survival in cancer patients

The effect of smoking on survival in cancer patients is limited by the lack of structured prospective assessments of smoking at diagnosis. To assess the effect of smoking at diagnosis on survival, structured smoking assessments were obtained in a cohort of 5,185 cancer patients within 30 days of a cancer diagnosis between 1982 and 1998. Hazard ratios (HRs) or odds ratios were generated to analyze the effects of smoking at diagnosis on overall mortality (OM) and disease‐specific mortality (DSM) in a patient cohort from 13 disease sites containing at least 100 patients in each disease site. With a minimum of 12 years of follow‐up, current smoking increased OM risk versus recent quit (HR 1.17), former (HR 1.29) and never smokers (HR 1.38) in the overall cohort. Current smoking increased DSM risk versus former (HR 1.23) and never smokers (HR 1.18). In disease sites with proportionately large (>20%) recent quit cohorts (lung and head/neck), current smoking increased OM and DSM risks as compared with recent quit. Current smoking increased mortality risks in lung, head/neck, prostate and leukemia in men and breast, ovary, uterus and melanoma in women. Current smoking was not associated with any survival benefit in any disease site. Data using prospective structured smoking assessments demonstrate that current smoking increased long‐term OM and DSM. Standardized smoking assessment at diagnosis is an important variable for evaluating outcomes in cancer patients.     

Impact of prediagnostic smoking and smoking cessation on colorectal cancer prognosis: a meta-analysis of individual patient data from cohorts within the CHANCES consortium

BackgroundSmoking has been associated with colorectal cancer (CRC) incidence and mortality in previous studies and might also be associated with prognosis after CRC diagnosis. However, current evidence on smoking in association with CRC prognosis is limited.Patients and methodsFor this individual patient data meta-analysis, sociodemographic and smoking behavior information of 12 414 incident CRC patients (median age at diagnosis: 64.3 years), recruited within 14 prospective cohort studies among previously cancer-free adults, was collected at baseline and harmonized across studies. Vital status and causes of death were collected for a mean follow-up time of 5.1 years following cancer diagnosis. Associations of smoking behavior with overall and CRC-specific survival were evaluated using Cox regression and standard meta-analysis methodology.ResultsA total of 5229 participants died, 3194 from CRC. Cox regression revealed significant associations between former [hazard ratio (HR) = 1.12; 95 % confidence interval (CI) = 1.04–1.20] and current smoking (HR = 1.29; 95% CI = 1.04–1.60) and poorer overall survival compared with never smoking. Compared with current smoking, smoking cessation was associated with improved overall (HR_{<10 years} = 0.78; 95% CI = 0.69–0.88; HR_{≥10 years} = 0.78; 95% CI = 0.63–0.97) and CRC-specific survival (HR_{≥10 years} = 0.76; 95% CI = 0.67–0.85).ConclusionIn this large meta-analysis including primary data of incident CRC patients from 14 prospective cohort studies on the association between smoking and CRC prognosis, former and current smoking were associated with poorer CRC prognosis compared with never smoking. Smoking cessation was associated with improved survival when compared with current smokers. Future studies should further quantify the benefits of nonsmoking, both for cancer prevention and for improving survival among CRC patients, in particular also in terms of treatment response.     

Life-style and cancer: from epidemiological evidence to public behavior change to mortality reduction of target cancers.

Cigarette smoking, alcohol consumption, and diet are of essential importance in modulating risks of cancer of selected sites, as demonstrated by various epidemiological methods. Examples include demographic studies on changing cancer risk, correlation studies on dietary fat and cancers of breast and colon, and case-control studies on highly salted food and gastric cancer. Evidence was also obtained by cohort studies including a census-population-based large-scale prospective study in Japan. Results included elevated risk from cigarette smoking for cancers of most sites; from alcohol consumption for cancers of the upper and lower digestive tract, liver, and prostate; and from daily meat consumption for cancers of the pancreas, colon, lung, and breast. Daily consumption of green-yellow vegetables reduced risk for cancer of the stomach, colon, lung, cervix, and prostate. Reports of these results and intensive public education and public guidance by governmental and nongovernmental organizations such as cancer societies, consumer groups, and mass media resulted in a notable change in public behavior in most cases in Japan.     

The impact of dietary and lifestyle risk factors on risk of colorectal cancer: A quantitative overview of the epidemiological evidence

Colorectal cancer is a major cause of cancer mortality and is considered to be largely attributable to inappropriate lifestyle and behavior patterns. The purpose of this review was to undertake a comparison of the strength of the associations between known and putative risk factors for colorectal cancer by conducting 10 independent meta‐analyses of prospective cohort studies. Studies published between 1966 and January 2008 were identified through EMBASE and MEDLINE, using a combined text word and MESH heading search strategy. Studies were eligible if they reported estimates of the relative risk for colorectal cancer with any of the following: alcohol, smoking, diabetes, physical activity, meat, fish, poultry, fruits and vegetables. Studies were excluded if the estimates were not adjusted at least for age. Overall, data from 103 cohort studies were included. The risk of colorectal cancer was significantly associated with alcohol: individuals consuming the most alcohol had 60% greater risk of colorectal cancer compared with non‐ or light drinkers (relative risk 1.56, 95% CI 1.42–1.70). Smoking, diabetes, obesity and high meat intakes were each associated with a significant 20% increased risk of colorectal cancer (compared with individuals in the lowest categories for each) with little evidence of between‐study heterogeneity or publication bias. Physical activity was protective against colorectal cancer. Public‐health strategies that promote modest alcohol consumption, smoking cessation, weight loss, increased physical activity and moderate consumption of red and processed meat are likely to have significant benefits at the population level for reducing the incidence of colorectal cancer. © 2009 UICC     

Cigarette smoking and risk of prostate cancer among Singapore Chinese

Prospective epidemiologic studies conducted in Western populations support an association between current smoking and aggressive subtypes of prostate cancer. In Singapore, where prostate-specific antigen is not used for population-wide screening, prostate cancer incidence has tripled within the past two decades. Using Cox regression methods, we examined the relationship between smoking and prostate cancer established between 1993 and 1998 in a cohort of 27,293 Singapore Chinese men. As of December 2006, 250 incident prostate cancer cases were diagnosed. In our cohort, 42.2% reported never smoking cigarettes, 15.7% quit over 5 years ago (long-term former), 5.7% quit within the past 5 years (recent former), and 36.4% were current smokers. From multivariable models, we observed no association with smoking status, age at starting to smoke, years smoked, or number of cigarettes per day. Among recent former and current smokers combined, we observed a small positive association for earlier age at starting to smoke that was somewhat stronger for nonadvanced disease (hazard ratio = 1.63, 95% confidence interval: 0.85, 3.12, for <15 years versus nonsmokers). Smoking was not a major risk factor for prostate cancer in our Singapore Chinese cohort, a traditionally low risk population with parallel increases in incidence and mortality.     

Cigarette smoking and prostate cancer-specific mortality following diagnosis in middle-aged men

Objective The aim of this study was to examine associations of smoking at the time of diagnosis with the risk of prostate cancer death in a population-based cohort of men with prostate cancer. Methods Data were from 752 prostate cancer patients aged 40–64 years, who were enrolled in a case–control study and under long-term follow-up for mortality. Cox proportional hazards models were used to estimate hazard ratios (HR) and 95% confidence intervals (CI) for associations between smoking and prostate cancer-specific and other cause mortality. Results Compared to never smoking, smoking at the time of diagnosis was associated with a significant increase in risk of prostate cancer-specific mortality. After controlling for demographic characteristics, Gleason grade, stage at diagnosis, and primary treatment, the HR was 2.66 (95% CI: 1.10–6.43). Conclusions Smoking at the time of diagnosis, independent of key clinical prognostic factors, is associated with an increased risk of prostate cancer death.     

Body mass index, prostate cancer-specific mortality, and biochemical recurrence: a systematic review and meta-analysis

Increasing evidence suggested obesity, measured by body mass index (BMI), was associated with prostate cancer-specific mortality, and its impact on biochemical recurrence was also inconclusive. We systematically searched MEDLINE, EMBASE, and bibliographies of retrieved studies up to January 5, 2010. We used random-effects meta-analysis to assess the relative risks (RR) of prostate cancer-specific mortality and biochemical recurrence associated with a 5 kg/m(2) increase in BMI. Among the six population-based cohort studies in 1,263,483 initially cancer-free men, 6,817 prostate cancer deaths occurred; a 5 kg/m(2) increase in BMI was associated with 15% (RR: 1.15, 95% confidence interval (CI): 1.06-1.25, P < 0.01) higher risk of dying of prostate cancer. In the six postdiagnosis survival studies on 18,203 patients with 932 prostate cancer deaths, a 5 kg/m(2) increase in BMI was associated with 20% higher prostate cancer-specific mortality (RR: 1.20, 95% CI: 0.99-1.46, P = 0.06). In the sixteen studies which followed 26,479 prostate cancer patients after primary treatment, a 5 kg/m(2) increase in BMI was significantly associated with 21% increased risk of biochemical recurrence (RR: 1.21, 95% CI: 1.11-1.31 P < 0.01). Elevated BMI is associated with risk of prostate cancer-specific mortality in prospective cohort studies and biochemical recurrence in prostate cancer patients. Its association with prostate cancer-specific mortality in diagnosed patients needs to be further evaluated.     

Cigarette smoking and risk of prostate cancer in the physicians' health study (United States)

To assess whether cigarette smoking is associated with prostate cancer incidence or mortality, we analyzed a large cohort of 22,071 men, aged 40-84 at baseline, in the Physicians' Health Study. During an average of 12.5 years of follow-up, we documented 996 cases of prostate cancer, including 113 fatal cases. Men were categorized according to smoking status, total pack-years smoked, and duration of smoking. We used Cox proportional hazard models to estimate the relative risks associated with smoking. Compared to never smokers, the age-adjusted relative risks (RR) of total prostate cancer were 1. 14 (95% confidence interval [CI] = 1.00-1.30) for past smokers, 1.10 (95% CI = 0.78-1.55) for current smokers of less than 20 cigarettes per day, and 1.10 (95% CI = 0.84-1.44) for current smokers of 20 or more cigarettes per day. Adjustment for body mass index, height, alcohol intake, and physical activity did not materially alter these findings. No significant association was observed in analyses of total pack-years smoked or duration of smoking. The results were similar for non-fatal and fatal prostate cancer. These data indicate no material association between cigarette smoking and prostate cancer incidence or mortality.     

Smoking and survival after breast cancer diagnosis: a prospective observational study and systematic review

The association of smoking with outcomes following breast cancer prognosis is not well understood. In a cohort study called Life After Cancer Epidemiology (LACE), 2,265 women diagnosed with breast cancer were followed for a median of 12?years. We used multivariable proportional-hazards models to determine whether smoking, assessed approximately two years post-diagnosis, was associated with risk of death among these women. We also undertook a systematic review of all cohort studies to date that have examined the association between smoking and breast cancer mortality. Compared with never smokers, women who were current smokers had a twofold higher rate of dying from breast cancer [hazard ratio (HR)?=?2.01, 95?% confidence interval (CI) 1.27?C3.18] and an approximately fourfold higher rate of dying from competing (non-breast cancer) causes (HR?=?3.84, 95?% CI 2.50?C5.89). Among seven studies that met the inclusion criteria in the systematic review, three studies and our own reported significantly increased risk of breast cancer death with current smoking. We found little evidence of an association between former smoking and breast cancer mortality (HR?=?1.24, 95?% CI 0.94?C1.64). Consistent with findings from our prospective observational study, the systematic review of seven additional studies indicates positive association of current smoking with breast cancer mortality, but weak association with former smoking. Women who smoke following breast cancer diagnosis and treatment are at higher risk of death both from breast cancer and other causes.     

Cigarette smoking and the risk of incident and fatal melanoma in a large prospective cohort study

Objective  

Previous studies suggest that smoking may be inversely associated with risk of melanoma. We attempted to replicate this finding using data from the Cancer Prevention Study II (CPS-II) and CPS-II Nutrition cohort, two large prospective cohort studies of cancer mortality and incidence, respectively, with long-term follow-up.     

Serum calcium and incident and fatal prostate cancer in the National Health and Nutrition Examination Survey

We examined the association between serum calcium levels and the risk for prostate cancer using a prospective cohort, the National Health and Nutrition Examination Survey (NHANES) and the NHANES Epidemiologic Follow-up Study. Eighty-five incident cases of prostate cancer and 25 prostate cancer deaths occurred over 46,188 person-years of follow-up. Serum calcium was determined an average of 9.9 years before the diagnosis of prostate cancer. Comparing men in the top with men in the bottom tertile of serum calcium, the multivariable-adjusted relative hazard for fatal prostate cancer was 2.68 (95% confidence interval, 1.02-6.99; P(trend) = 0.04). For incident prostate cancer, the relative risk for the same comparison was 1.31 (95% confidence interval, 0.77-2.20; P(trend) = 0.34). These results support the hypothesis that high serum calcium or a factor strongly associated with it (e.g., high serum parathyroid hormone) increases the risk for fatal prostate cancer. Our finding of a >2.5-fold increased risk for men in the highest tertile of serum calcium is comparable in magnitude with the risk associated with family history and could add significantly to our ability to identify men at increased risk for fatal prostate cancer.     

Passive smoking exposure and female breast cancer mortality

BACKGROUND: Several studies have reported positive associations between environmental tobacco smoke (ETS) and increased risk of breast cancer. However, studies of active smoking and risk of breast cancer are equivocal and in general do not support a positive association. To try to resolve this paradox, we examined the association between breast cancer mortality and potential ETS exposure from spousal smoking in an American Cancer Society prospective study of U.S. adult women. METHODS: We assessed breast cancer death rates in a cohort of 146 488 never-smoking, single-marriage women who were cancer free at enrollment in 1982. Breast cancer death rates among women whose husbands smoked were compared with those among women married to men who had never smoked. Cox proportional hazards modeling was used to control for potential risk factors other than ETS exposure. RESULTS: After 12 years of follow-up, 669 cases of fatal breast cancer were observed in the cohort. Overall, we saw no association between exposure to ETS and death from breast cancer (rate ratio [RR] = 1.0; 95% confidence interval [CI] = 0.8-1.2). We did, however, find a small, not statistically significant increased risk of breast cancer mortality among women who were married before age 20 years to smokers (RR = 1. 2; 95% CI = 0.8-1.8). CONCLUSIONS: In contrast to the results of previous studies, this study found no association between exposure to ETS and female breast cancer mortality. The results of our study are particularly compelling because of its prospective design as compared with most earlier studies, the relatively large number of exposed women with breast cancer deaths, and the reporting of exposure by the spouse rather than by proxy.