Vasectomy and risk of prostate cancer.

Most studies do not support an association between vasectomy and prostate cancer, but a few have suggested a link. Vasectomy is a common birth control method, and prostate cancer is the most frequently diagnosed solid tumor in men, making this a major public health question. This study was specifically designed to determine whether or not vasectomy is associated with risk of prostate cancer. To examine this issue, we conducted a population-based case-control study in King County, Washington. Interviews were completed with men ages 40-64 years newly diagnosed with prostate cancer between January 1993 and December 1996 who were ascertained through the Seattle-Puget Sound Surveillance, Epidemiology, and End Results (SEER) cancer registry (n = 753) and with comparison men without prostate cancer identified from the same general population (n = 703). The odds ratio (OR) for prostate cancer in relation to vasectomy was assessed. The prevalence of vasectomy was similar in cases (39.4%) and controls (37.7%), resulting in no association (adjusted OR, 1.10; 95% confidence interval, 0.9-1.4). There was no consistent evidence that risk varied by the age at which vasectomy was performed, the time since vasectomy, or the calendar period when the vasectomy was performed. The OR in relation to vasectomy was higher in men with less aggressive prostate cancer. Risk estimates did not differ according to age, race, or family history of prostate cancer. This study suggests that vasectomy is not associated with the risk of developing prostate cancer. It also provides evidence that vasectomized men may be more likely to present with earlier-stage, lower-grade prostate tumors.     

Sexually transmitted diseases and other urogenital conditions as risk factors for prostate cancer: a case–control study in Wayne County,Michigan

Objective To investigate associations between prostate cancer and sexually transmitted diseases (STDs), prostatitis, benign prostatic hyperplasia (BPH), and vasectomy in a population-based case–control study in Wayne County, Michigan, among African American and white men aged 50–74 years.Methods: Incident prostate cancer cases (n=700) from 1996–1998 were identified from the Metropolitan Detroit Cancer Surveillance System. Controls (n=604) were identified through random digit dialing and Medicare recipient lists, and frequency matched to cases on age and race. History of potential prostate cancer risk factors was ascertained through in-person interview.Results: Prostate cancer was not associated with STD or vasectomy history. History of prostatitis was associated with prostate cancer among all subjects (odds ratio [OR]=1.8, 95% confidence interval [CI]: 1.1, 2.9) and in African American men (OR=2.2, 95% CI: 1.1, 4.6). History of BPH was associated with prostate cancer among all subjects (OR=2.4, 95% CI: 1.8, 3.3); significant associations were observed in both African American (OR=2.7, 95% CI: 1.6, 4.4) and white (OR=2.3, 95% CI: 1.5, 3.4) men.Conclusions: Among all subjects, prostate cancer was associated with prostatitis and BPH history, but not with STD or vasectomy history. Prevention efforts could be enhanced if inflammatory or infectious etiologies are found to be of importance in the subsequent development of prostate cancer.     

Alcohol consumption,smoking, and other risk factors and prostate cancer in a large health plan cohort in California (United States)

Alcohol consumption and cigarette smoking have been suggested as possible causes of prostate cancer. We therefore examined this relation in a cohort of 43,432 men who were members of a prepaid health plan in northern California (United States) and who had received a health examination in the period from 1979 through 1985. Detailed information on demographic variables, alcohol consumption, smoking habits, medical complaints and conditions, occupation, and surgery (including vasectomy) was assessed. Symptoms of prostatism and a history of sexually transmitted diseases were abstracted from the medical records of all prostate cancer patients and of a matched subsample of randomly selected control-subjects. Alcohol consumption was associated with no elevated prostate cancer risk for the 238 men in our study in whom prostate cancer developed, but smoking one or more packs of cigarettes per day was associated with an adjusted relative risk (RR) of 1.9 (95 percent confidence interval [CI]=1.2–3.1). Prostate cancer risk for Black men was 2.2 (CI=1.6–3.1) when compared with that for White men, and education level was associated positively in an increasing trend (P<0.02) up to an RR of 1.4 (CI=0.9–2.1) among men with postgraduate education. Symptoms of prostate hypertrophy were not associated with elevated risk of prostate cancer if they occurred two or more years before the diagnosis. The finding that smoking increased the risk of prostate cancer confirms the observations of others but needs cautious interpretation because we were unable to adjust for the potential confounding effect of dietary and hormonal factors.Presented in abstract form at the 118th annual meeting of the American Public Health Association and related organizations, New York City, September 30–October 4, 1990. The research was supported by US National Cancer Institute Contract N01-CP-95606 and by the Alcoholic Beverage Medical Research Foundation, Baltimore, Maryland, USA.     

Vasectomy, cigarette smoking, and age at first sexual intercourse as risk factors for prostate cancer in middle-aged men

A population-based case-control study was conducted in men aged 60 or less to assess the risk of prostate cancer associated with vasectomy and other factors. Data were obtained from 216 case-control pairs by telephone interviews; this number represented 55% of all eligible cases. The matched pairs relative risk (RR) for vasectomy in ever married men was 1.4 with a 95% confidence interval (CI) of 0.9-2.3. There was a positive association between the number of years since vasectomy and prostate cancer risk (1-sided P = 0.01). Early age at first sexual intercourse was associated with increased prostate cancer risk (age less than 17 vs. 21+, RR = 2.3, 95% CI = 1.3, 4.0) but there were no consistent associations with number of sexual partners or frequency of sexual intercourse. Cigarette smoking was also associated with increased risk of prostate cancer (RR = 1.9, 95% CI = 1.2, 3.0) and there was a positive dose-response relationship with years of smoking (1-sided P = 0.001). We discuss the possible implication of the low response rate on each of these findings. To determine whether the association with vasectomy might have a hormonal basis, we compared levels of testosterone (T) and testosterone binding globulin-binding capacity (TeBG-bc) in 33 of the vasectomized control men with levels in 33 non-vasectomized controls of the same age, weight and height. T levels were higher in vasectomized than in non-vasectomized controls (1-sided P = 0.06). The ratio of T to TeBG-bc (an index of bioavailable T) was 13.5% higher in vasectomized men (1-sided P = 0.03).     

Daily aspirin use and prostate cancer risk in a large,multiracial cohort in the US

Objective: To examine the relationship between daily aspirin use and risk of prostate cancer in a large, racially diverse cohort of men followed for up to 32 years. Methods: The study population included 90,100 male subscribers to the Kaiser Permanente Medical Care Program who had received one or more multiphasic health checkups between 1964 and 1973. This general health checkup included a self-completed questionnaire that requested men to record if they took more than six aspirin almost every day during the previous year. Subjects were followed for the development of prostate cancer using the local tumor registry. Cox regression was used to estimate relative risks (RR) and 95% confidence intervals (CI). Results: A total of 2574 men developed prostate cancer. Of these, 1617 had local stage disease and 719 had either regional or distant disease at diagnosis. A total of 2466 men (2.7%) reported taking more than six aspirin almost every day during the past year at one or more health checkups. After adjusting for birth year, education, race, and the number of health checkups, the relative risk of prostate cancer associated with this amount of aspirin use was 0.76 (95% CI 0.60–0.98). Relative risks did not differ by race and were similar for both local stage and regional or distant stage prostate cancer. Conclusion: Results from our large, multiracial cohort study support a modest inverse relationship between daily consumption of more than six aspirin and prostate cancer risk.     

Is it Reporting Bias Doubled the Risk of Prostate Cancer in Vasectomised Men in Mumbai,India?

Background: Vasectomy is a common method of family planning in India and worldwide. The objective of the ‍present study was to assess the association of vasectomy with prostate cancer in a low risk population of a developing ‍country. A population based case control study was conducted in Mumbai, India, for this purpose. Methods: Included ‍in this study were microscopically proved cases of prostate cancer diagnosed during 1998 to 2000 and registered by ‍Bombay Population Based Cancer Registry (n=594). The controls were healthy men belonging to the resident general ‍population of Mumbai, India. Two controls for each case matched by age and place of residence were selected as the ‍comparison group. Data on vasectomy and potential confounding factors were obtained by structured face to face ‍interviews. After exclusions, 390 cases and 780 controls were available for final analysis and confounding was controlled ‍by multiple logistic regression. Results: Overall 14.9% of cases and 10.0% of controls had undergone vasectomy. ‍Compared with no vasectomy the OR with ever having undergone vasectomy was 1.9 (95% CI: 1.3-2.9), after ‍controlling for age and other possible confounding factors. The risk for those who had had a vasectomy before the ‍age of 45 years was 2.1 fold (95% CI: 1.2-3.9) and for those who underwent the procedure at a later age was 1.8 fold ‍(95% CI: 1.1-2.9). The linear trend for an increase in risk with a decrease in age at vasectomy was statistically ‍significant (p for trend= 0.01). The risk for those who completed 25 years or more time since undergoing vasectomy ‍was 3.8 fold (95% CI: 1.9-7.6) and for those who completed less than 25 years it was 1.2 fold (95% CI: 0.7-2.1). The ‍linear trend for an increase in risk with an increase in time since vasectomy was highly significant (p for trend = ‍0.001). Conclusion: There are major public health and birth control implications on vasectomy increases the risk for ‍prostate cancer. It is likely, however, that biases identified in this study result in high estimates of risk and the true ‍risk due to vasectomy is substantially less than the estimated one. Due to the several limitations and possibilities for ‍reporting biases in this study, the evidence for the estimates of the higher odds ratio for prostate cancer in vasectomised ‍men may not be a strong one. In view of the importance of vasectomy for fertility control, further studies with good ‍design and conduct (the information on vasectomy need to be collected with better reliability) are required to clarify ‍the issue of vasectomy associations with prostate cancer.     

Tobacco use and prostate cancer in Blacks and Whites in the United States

Prostate cancer occurs more frequently in Blacks than Whites in the United States. A population-based case-control study which investigated the association between tobacco use and prostate cancer risk was carried out among 981 pathologically confirmed cases (479 Blacks, 502 Whites) of prostate cancer, diagnosed between 1 August 1986 and 30 April 1989, and 1,315 controls (594 Blacks, 721 Whites). Study subjects, aged 40 to 79 years, resided in Atlanta (GA), Detroit (MI), and 10 counties in New Jersey, geographic areas covered by three, population-based, cancer registries. No excesses in risk for prostate cancer were seen for former cigarette smokers, in Blacks (odds ratio [OR]=1.1, 95 percent confidence interval [CI]=0.7–1.5) and in Whites (OR=1.2, CI=0.9–1.6), or for current cigarette smokers, in Blacks (OR=1.0, CI=0.7–1.4) and in Whites (OR=1.2, CI=0.8–1.7). Increases in risk were noted for smokers of 40 or more cigarettes per day, among former (OR=1.4, CI=1.0–1.5) and current (OR=1.5, CI=1.0–2.4) smokers. Duration of cigarette use and cumulative amount of cigarette use (pack-years) were not associated with prostate cancer risk for Blacks or Whites. By age, only the youngest subjects, aged 40 to 59 years, showed excess risk associated with current (OR=1.5, CI=1.0–2.3) and former (OR=1.7, CI=1.1–2.6) use of cigarettes, but there were no consistent patterns in this group according to amount or duration of smoking. Risks also were not elevated for former or current users of pipes, cigars, or chewing tobacco, but the risk associated with current snuff use was OR=5.5 (CI=1.2–26.2). This subgroup finding may have been due to chance. The results of the present study may be consistent with a small excess risk for prostate cancer associated with tobacco use, but the lack of consistent findings in population subgroups and the lack of a clear dose-response relationship argue more strongly that no causal association exists. The data do not indicate that the Black-White difference in prostate cancer risk is related to tobacco use.This research was performed under contracts: NO1-CP-51090, NO1-CN-0522, NO1-CP-51089, NO1-CN-31022, NO1-CP-51092, and NO1-CN-5227.     

Risk of prostate cancer associated with a family history in an era of rapid increase in prostate cancer diagnosis (Australia)

Objective: We conducted a case–control study of prostate cancer and familial risk of the disease in Australia between 1994 and 1998, a period during which the incidence of prostate cancer increased dramatically with widespread use of prostate-specific antigen (PSA) testing. Methods: 1475 cases and 1405 controls were asked about prostate cancer in their first-degree relatives. Odds ratios (OR) were calculated using logistic regression. Results: Cases were more likely to report a family history of prostate cancer than controls (OR 3.0; 95% confidence interval (CI) 2.3–3.9) and cases reporting an affected relative were younger (58.8 versus 60.9 years, p < 0.0001). The OR for an affected first-degree relative increased with increasing number of affected relatives and decreased with increasing age of the case. The OR for more than one affected first-degree relative was 6.9 (95% CI 2.7–18). The OR for an affected brother was 3.9 (95% CI 2.5–6.1) and for an affected father was 2.9 (95% CI 2.1–3.9) but these were not significantly different (p = 0.2). When analyses were repeated including only diagnoses made in relatives prior to 1992, the risks were generally similar except that the OR for an affected brother decreased to 3.1 (95% CI 1.2–3.9). When only relatives' diagnoses made after 1991 were included results were again similar to those for all relatives, although the effect for brothers was greater and the attenuation with age at diagnosis dissipated. Conclusions: The recent introduction of PSA testing that has resulted in a greater prevalence of apparent prostate cancer, does not appear to have substantially altered familial risks of disease, although effects associated with brothers may be inflated.     

Relatives of Prostate Cancer Patients have an Increased Risk of Prostate and Stomach Cancers: A Population-Based, Cancer Registry study in Finland

Objective: Five to ten percent of prostate cancers may be caused by inherited genetic defects. In order to explore the nature of inherited cancer risks in the genetically homogeneous Finnish population, we investigated the incidence of prostate cancer and other cancers in first-degree relatives of prostate cancer patients by linking the population-based parish records on relatives with the Finnish Cancer Registry (FCR) data. Methods: The study population was composed of first-degree relatives of two groups of prostate cancer patients diagnosed in Finland during 1988–1993: (1) all early-onset (60years) patients (n=557) from the entire country, (2) a sample (n=989) of prostate cancer patients diagnosed at an age of >60years. A total of 11,427 first-degree relatives were identified through parish records, and their cancer incidence was determined based on a total of 299,970 person-years. Standardized incidence ratios (SIR) were calculated based on expected cancer rates in the general population. Results: The SIR of prostate cancer was increased in both Cohort 1 (2.5, 95% CI 1.9–3.2) and Cohort 2 (1.7, 95% CI 1.4–2.1). The risk of prostate cancer was high for relatives of patients diagnosed at an early age, and then leveled off for patients in the median age of prostate cancer diagnosis (70–79 years). However, the prostate cancer risk for relatives of patients diagnosed 80years was again statistically significantly elevated (SIR 1.8, 95% CI 1.3–2.6), suggesting a contribution of genetic factors to prostate cancer also at a late age of onset. Gastric cancer was the only other cancer type with a significantly elevated risk among the relatives. Increased risk of gastric cancer was seen only in male relatives of prostate cancer patients diagnosed at an early age, with the highest risk detected for the male relatives of prostate cancer patients diagnosed at an age of 55 years or less (SIR 5.0, 95% CI 2.8–8.2). Conclusions: Our population-based study indicates that hereditary factors may play an important role in the development of prostate cancer among the relatives of men diagnosed both at younger and older ages. This finding is relevant in the context of our observations that HPCX (hereditary prostate cancer susceptibility locus on Xq27-28) linkage in Finland is found exclusively among families with late age of onset. The association of gastric cancer with prostate cancer has not been reported previously, and may reflect the effects of a novel predisposition locus, which increases the risk to both of these common tumor types.     

Risk of breast cancer in relation to blood lipids: a prospective study of 31,209 Norwegian women

In this prospective study, the relationship between blood lipids and breast cancer risk was examined. Between 1977 and 1983, 31,209 Norwegian women, 20 to 54 years of age, attended a health screening carried out by the Norwegian National Health Screening Services. The screening consisted of a questionnaire, anthropometric measurements, and nonfasting blood drawn for analysis of total serum cholesterol (TC), triglyceride (TG), and high density lipoprotein (HDL) cholesterol. Low density lipoprotein (LDL) cholesterol was calculated by the Friedewald's formula. During the seven to 13 years of follow-up, 302 breast cancer cases were identified by linkage to the Norwegian Cancer Registry. After adjustment for some of the known risk factors of breast cancer, the relative risk of women in the highest quartile of TC compared with women in the lowest quartile was 0.87 (95 percent confidence interval [CI]=0.61–1.23). The corresponding relative risks and CIs were 0.82 (CI=0.58–1.16) for TG, 1.02 (CI=0.73–1.42) for HDL, and 0.93 (CI=0.67–1.29) for LDL. No association between breast cancer risk and blood lipids was found in the total population, nor when the data were divided into those diagnosed before or after the age of 50 as a dividing line between pre- and postmenopausal diagnosis.This work is funded by grant no. 93020/002 from the Norwegian Cancer Society and supported by a grant from Dr Nils Helsingen's Foundation.     

Are the known bladder cancer risk-factors associated with more advanced bladder cancer?

Risk factors for superficial and invasive bladder cancer were examined in a case-control study of 470 cases Identified in 1967–68 in the Brockton and Boston Standard Metropolitan Areas (MA, United States) and of 500 population-based controls. Histologic specimens were reviewed and classified as superficial or invasive, following a standardized protocol. The tobacco-associated risk for superficial bladder cancer was odds ratio (OR)=2.6 (95 percent confidence interval [CI]=1.7–4.1) and the risk for invasive bladder cancer was OR=1.7 (CI=1.1–2.5). For subjects less than 60 years of age, the risks were greater for invasive tumors (OR=4.3, CI=1.2–15) than for superficial tumors (OR=0, CI=0.9–4.2), but this pattern for tobacco use was not found in older subjects. A strong trend of increased risk with increased amount of cigarettes smoked was shown only for invasive bladder tumors. No clear pattern of excess risk for invasive bladder tumors was seen for age at first use and years since last use of tobacco. The risk associated with occupational exposure to aromatic amine bladder carcinogens was OR=1.7 (CI=0.8–3.3) for superficial and OR=1.5 (CI=0.8–3.0) for invasive bladder cancer. For subjects less than 60 years of age, the risks were greater for invasive (OR=12.0, CI=2.1–65) than for superficial tumors (OR=4.3, CI=0.8–24), but this pattern for occupational exposure was not found in older subjects. Risk by age at first exposure to occupational aromaticamine, bladder carcinogens was similar for superficial and invasive tumors. Overall, there was no association between known bladder-cancer risk-factors and more advanced bladder cancer. The relative risk associated with cigarette smoking and occupational exposure to aromatic amines was higher for invasive than superficial cancer only for men less than 60 years of age.Drs Hayes and Zahm are with the Environmental Epidemiology Branch, National Cancer Institute, Bethesda, MD, USA. Authors are affiliated also with the Lucille P. Markey Cancer Center, Lexington, KN, USA (Dr Friedell) and the Department of Epidemiology, University of Alabama, Birmingham, AL, USA (Dr Cole). Address correspondence to Dr Hayes, Environmental Epidemiology Branch, National Cancer Institute, EPN 418, Bethesda, MD 20892, USA.     

Prospective study of plasma enterolactone and prostate cancer risk (Sweden)

Objectives: Enterolactone, a phytoestrogen produced by the intestinal microflora from precursors in plant foods, has been postulated to protect against hormone-dependent cancers. We studied the association between plasma enterolactone and risk of prostate cancer. Methods: In the Northern Sweden Health and Disease Cohort, enterolactone concentrations were measured by time-resolved fluoroimmunoassay in plasma taken from 265 men who were diagnosed with prostate cancer at a mean time of 5 years after blood collection, and in plasma from 525 control men, matched for age and date of blood collection. Results: There was no significant association between quartiles of plasma enterolactone and risk of prostate cancer. Odds ratios for prostate cancer, estimated by conditional logistic regression for increasing concentrations of enterolactone in quartiles were 1.00 (referent), 0.81 (95% confidence interval 0.52–1.27), 1.03 (0.67–1.58), and 1.22 (0.80–1.86). Adjustments for body mass index (BMI), smoking status and stratification for age, lag time, storage time and tumour characteristics did not materially alter risk estimates. Men with very low enterolactone levels, however, had significantly higher risk of prostate cancer, odds ratio for bottom decile versus all other deciles was 1.68 (1.03–2.74). Conclusions: Our results do not support the hypothesis that enterolactone formed from dietary lignans protects against prostate cancer.     

Case-control study of alcohol consumption and prostate cancer risk in Montréal, Canada

Objectives: to estimate the risk of prostate cancer associated with alcohol consumption. Methods: Between 1979 and 1985 a population-based case–control study was carried out in Montréal, which accrued over 4000 men in total, including cases of prostate cancer, other cancers, and population controls. The present analysis was restricted to the subset, aged 45–70 years, who underwent face-to-face interviews, in which aspects of lifelong alcohol consumption were ascertained. The cancer control series was further restricted to men whose tumor types were considered unrelated to alcohol consumption. There were 399 incident cases of prostate cancer, 476 population controls, and 674 cancer controls. Results: When using the population controls, risk increased with increasing cumulative consumption of alcohol. There was no decrease in risk after quitting. Risk was particularly high among those who reported having started before age 15 years (odds ratio = 3.8; 95% confidence interval: 1.6–9.3). The results obtained using the cancer controls were less pronounced, but still indicated an excess risk associated with alcohol consumption. Beer was the most prevalent type of alcohol consumed in this population and showed the strongest association with prostate cancer. Conclusions: The results are consistent with an increase in the risk of prostate cancer due to alcohol consumption.     

Incidence of thyroid cancer in Scandinavia following fallout from atomic bomb testing: an analysis of birth cohorts

Objectives: The occurrence relation between radioactive fallout from nuclear testing at Novaja Semlja in north-west Russia and the incidence of thyroid cancer in Norway and Sweden was studied following a birth cohort approach.Methods: Birth cohorts with presumably different levels of exposure were identified according to calendar year of atomic tests and previous Norwegian estimates of the population dose (born 1947–1950 received low exposure in late childhood, born 1951–1962 received the highest exposure in early childhood, born 1963–1970 were not exposed). For each one-year birth cohort the incidence rates were calculated, with denominators based on exact population figures for each year of follow-up.Results: In a stratified analysis, the relative risk for the highest exposed cohorts born 1951–1962, compared to those not exposed born 1963–1970, was found to decrease with increasing age from a borderline significant relative risk (RR) of 1.7 (95 percent confidence interval, 95% CI: 1.0–3.0) for children in the age-group 7–14 years to no excess risk among those 20–24 years of age (RR: 0.9; 95% CI: 0.7–1.2). The mean age at diagnosis of thyroid cancer in the age-group 7–14 years was lowest in the birth cohorts with the highest exposure. The Poisson regression analysis showed essentially the same results, with an improved fit when adding an interaction term between age and birth-cohort to a basic model with age, gender, birth-cohort and country.Conclusion: These results are compatible with an increased risk of thyroid cancer during childhood and adolescence for subjects exposed to radioactive fallout early in life. Alternative explanations for the pattern of incidence are discussed.     

Diabetes mellitus and ovarian cancer (Sweden)

OBJECTIVE: We present results from a large, population-based cohort study in Sweden, where we assessed ovarian cancer risk among patients hospitalized for diabetes mellitus.METHODS: The cohort was composed of patients identified in the Swedish In-Patient Register as having a hospital discharge diagnosis of diabetes mellitus in 1965–1994. The follow-up was done by linkages with the national cancer register and other population-based registers. Standardized incidence ratios (SIR) were used as a measure of relative risk.RESULTS: After exclusion of the first year of follow-up (to avoid selection bias), 141,627 women remained in the cohort, contributing 865,746 years of follow-up to the study. The overall SIR for ovarian cancer was 0.97 (95% confidence interval (CI) 0.87–1.08). We found no difference in the risk estimates among women who had been hospitalized for classic complications of diabetes and for those who had not, or according to the duration of follow-up. Women above 40 years of age at first hospitalization presented a SIR of 0.96 (95% CI 0.85–1.07).CONCLUSIONS: Our study provides evidence of lack of an association between diabetes mellitus and ovarian cancer.     

Risks of breast and endometrial cancer after estrogen and estrogen–progestin replacement

Objective: We studied the risk of breast and endometrial cancer in a cohort of 11,231 Swedish women prescribed different replacement hormone regimens.Methods: All 10,472 women at risk of developing breast cancer and 8,438 women at risk of endometrial cancer were followed up from the time of the questionnaire in 1987–88 through 1993, by record-linkages to the National Swedish Cancer Registry. Using data from a questionnaire we analyzed the relationships between hormone exposures and cancer risk, with non-compliers and users of less than 1 year as a reference group.Results: For breast cancer, women reporting use of estrogens combined with progestins had evidence of an increased risk relative to women denying intake or taking hormones for less than 1 year; relative risk (RR) = 1.4 (95% confidence interval 0.9–2.3) after 1–6 years of intake, and RR=1.7 (95% CI 1.1–2.6) after more than 6 years. This excess risk seemed confined to recent exposure. We found no association with intake of estrogens alone using non-compliers and short-term takers as the reference group. The risk of invasive endometrial cancer was increased four-fold in women using medium-potency estrogens alone for 6 years or longer, RR = 4.2 (95% CI 2.5–8.4). Women on such long-term progestin-combined treatment had a lower, non-significant, excess risk (RR = 1.4; 95% CI 0.6–3.3).Conclusions: We conclude that long-term recent use of estrogen–progestin combined replacement therapy may increase the risk of breast cancer. Exposure to estrogen alone substantially elevates the risk of endometrial cancer, an increase that can be reduced or perhaps avoided by adding progestins.     

The association of height,weight, menstrual and reproductive events with breast cancer: results from two prospective studies on the island of Guernsey (United Kingdom)

The association with breast cancer of menstrual and reproductive events, family history of breast cancer, and body size have been studied on two cohorts of 6,706 volunteers on the island of Guernsey (United Kingdom), 168 of whom had breast cancer detected during follow-up. The median follow-up time of the non-cases was 21 years in the first study and 10 years in the second. A time-dependent Cox regression model was fitted to the data with age as the time-dependent variable in order to represent the effect of changing menopausal status. Other variables examined in the model were age at menarche, parity, age at first birth, family history of breast cancer, height, weight (both directly measured), relative weight (weight [kg]/height[m]), and Quetelet's body mass index (weight[kg]/height[m]²). Interactions between age and all other covariates also were examined. Family history was found to be the most important risk factor for women aged less than 51 years (relative risk [RR]=3.5, 95 percent confidence interval [CI]=2.0–6.0), and intervals between menarche and first birth longer than 14 years were found to increase significantly the risk of breast cancer in women older than 61 years (RR=2.4, CI=1.3–4.4). Height was the only indicator of body size which was associated significantly with risk of breast cancer, the estimated regression coefficient indicating an increase in risk of about 70 percent for women on the 90th centile of height relative to those on the 10th centile. A survey of the literature showed that the association between risk of breast cancer and height was found in those studies which used direct measurements of height but not in others which used self-reported values.     

Followup after 11 years – update of mortality results in the Stockholm mammographic screening trial

Results from several randomised mammography screening trials haveshown that it is possible to reduce mortalityin breast cancer by mammographic screening at leastfor women above 50 years of age. Thepurpose of this article is to present dataon mortality in breast cancer in study andcontrol groups of the Stockholm trial after 11years of followup, to analyse which age groupbenefits most from screening. In March 1981, 40,318women in Stockholm, aged 40 through 64 years,entered a randomized trial of breast cancer screeningby single view mammography alone, versus no interventionin a control group of 20 000 women.Two screening rounds were performed and the attendancerate was over 80% in the two rounds.During 1986 the control group was invited onceto screening. Totally 428 and 217 cases ofbreast cancer were diagnosed in the study andcontrol groups respectively. After a mean follow-up of11.4 years a nonsignificant mortality reduction of 26%was observed for the whole study group, witha relative risk (RR) of death in breastcancer of 0.74 (CI(confidence interval)=0.5–1.1). Forwomen aged 50–64 years a significant 38% mortalityreduction was observed with a RR of 0.62(CI=0.38–1.0). For women aged 40–49 yearsno effect on mortality was found, with aRR of death in breast cancer of 1.08(CI=0.54–2.17). The breakpoint for benefit inthis study seemed to be at 50 yearsof age when 5-year age groups were analysed,but this tendency is uncertain because of thelow statistical power in the analysis of theyounger age groups. Long screening intervals, the useof single-view mammography, and the fact that morethan 50% of the women in age group40–49 years were still below 50 years ofage when the study was closed, were allfacts that could have influenced the results inage group 40–49 years. Larger studies are neededto answer the question whether mammographic screening canbe successful in younger age groups.     

Randomized study of mammography screening — preliminary report on mortality in the stockholm trial

Summary In March 1981, 40,318 women in Stockholm, aged 40–64, entered a randomized trial of breast cancer screening by single-view mammography alone versus no intervention in a control group of 20,000 women. The attendance rate during the first screening round was 81 per cent and the cancer detection rate was 4.0 per 1000 women. The detection the rate fell to 3.1 per 1000 in the second round, which was completed in October 1985. During 1986 the controlled design of the study was broken and the contro women were invited once to screening which was completed the same year. A total of 428 cases of breast cancer were thus diagnosed in the study group and 439 in the adjusted control group. After a mean follow-up of 7.4 years the number of breast cancer deaths in the study and control groups was 39 and 30 respectively. The relative risk of breast cancer death (screening versus control) was 0.71 (95 per cent confidence interval: 0.4–1.2). Among women older than 50 years at entry the relative risk was 0.57 (95 per cent confidence interval: 0.3–1.1). Cancer deaths among women under 50 were few and perhaps because of this no mortality reduction was seen in this age group. The estimate of mortality reduction lies between the results from two earlier Swedish randomized controlled trials.     

Age and risk factors for colon cancer (United States and Australia): Are there implications for understanding differences in case-control and cohort studies?

Data from two population-based case-control studies were used to investigate the effect of age on colon cancer risk. Dietary intake data were assessed from a study conducted in Utah (United States) between 1979 and 1983; reproductive data were assessed from a study conducted in Adelaide (Australia) between 1979 and 1980. Data from both studies were assessed for their impact on those less than 65 years of age and those 65 or more years of age. Intake of energy, fat, and protein had a greater impact on risk among older men than among younger men. Risk estimates for the upper quartile of intake relative to the lowest quartile of intake were 8.5 (95 percent confidence interval [CI]=1.7–43.0) for energy, 8.2 (CI=1.6–41.3) for protein, and 7.2 (CI=1.6–31.4) for total fat for older men, while comparable risk estimates were 2.4 (CI=0.6–9.1) for energy, 3.0 (CI=0.7–13.6) for protein, and 1.9 (CI=0.5–7.1) for total fat among younger men. Similar trends were seen for older women for energy and protein. -carotene decreased colon cancer risk among younger men (odds ratio [OR]=0.4, CI=0.1–1.2) and women (OR=0.1, CI=0.1–0.5), although not among older men (OR=1.2, CI=0.3–4.9) and women (OR=1.9, CI=0.6–64). Calcium decreased risk of colon cancer among older men (OR=0.1, CI=<0.1–0.8) and younger women (OR=0.2, CI=<0.1–0.7). Women who were diagnosed at age 65 or older and were nulliparous had a tenfold increase in colon cancer risk (CI=2.4–47.9) relative to women who had an early age at first birth. Women diagnosed with colon cancer before age 65 did not experience an increase of colon cancer risk associated with being nulliparous. These data suggest that age at diagnosis may interact with other factors to alter risk of colon cancer.This study was supported by grant number R01 CA48998 and P01 CA50305 from the US National Cancer Institute. Its contents are solely the responsibility of the authors and do not necessarily represent the official views of the National Cancer Institute.