Effects of alpha-tocopherol and beta-carotene supplementation on gastric cancer incidence in male smokers (ATBC Study,Finland)

Objectives: This study investigated the effects of alpha-tocopherol and beta-carotene supplementation on the incidence of gastric cancer. Methods: A total of 29,133 male smokers, aged 50–69 years, participated in a placebo-controlled prevention trial, the Alpha-Tocopherol, Beta-Carotene Cancer Prevention (ATBC) Study in southwestern Finland between 1985 and 1993. The men were randomly assigned to receive alpha-tocopherol (50 mg/day) or beta-carotene (20 mg/day) supplementation in a 2 × 2 factorial design. We identified 126 gastric cancer cases during the median follow-up of six years. Of these, 122 were adenocarcinomas: 75 of intestinal type, 30 of diffuse type, and 17 of mixed type. Results: There was no significant effect for either supplementation on the overall incidence of gastric cancer: relative risk (RR) 1.21, 95% confidence interval (CI) 0.85–1.74 for alpha-tocopherol, and RR 1.26, 95% CI 0.88–1.80 for beta-carotene. Subgroup analyses by histologic type suggested an increased risk for beta-carotene on intestinal type cancers, RR 1.59, 95% CI 0.99–2.56. There were no differences across anatomic locations (cardia/noncardia) in the effects of alpha-tocopherol or beta-carotene supplementation. Conclusions: Our study found no overall preventive effect of long-term supplementation with alpha-tocopherol or beta-carotene on gastric cancer in middle-aged male smokers.     

Effects of beta-carotene supplementation on cancer incidence by baseline characteristics in the Physicians' Health Study (United States)

Objectives: The Physicians' Health Study (PHS) was a randomized trial of beta-carotene (50 mg, alternate days) and aspirin in primary prevention of cancer and cardiovascular disease among 22,071 US male physicians. This report updates results for beta-carotene and examines effect modification by baseline characteristics. Methods: Beta-carotene's effect on cancer over nearly 13 years was examined overall and within subgroups defined by baseline characteristics using proportional-hazards models. Results: 2667 incident cancers were confirmed, with 1117 prostate, 267 colon, and 178 lung cancers. There were no significant differences with supplementation in total (relative risk (RR) = 1.0, 95% confidence interval (CI) = 0.9–1.0); prostate (RR = 1.0, 95% CI = 0.9–1.1); colon (RR = 0.9, 95% CI = 0.7–1.2); or lung (RR = 0.9, 95% CI = 0.7–1.2) cancer, and no differences over time. In subgroup analyses, total cancer was modestly reduced with supplementation among those aged 70+ years (RR = 0.8, 95% CI = 0.7–1.0), daily drinkers of alcohol (RR = 0.9, 95% CI = 0.8–1.0), and those in the highest BMI quartile (RR = 0.9, 95% CI = 0.7–1.0). Prostate cancer was reduced with supplementation among those in the highest BMI quartile (RR = 0.8, 95% CI = 0.6–1.0), and colon cancer was reduced among daily drinkers of alcohol (RR = 0.5, 95% CI = 0.3–0.8). Conclusions: The PHS found no overall effect of beta-carotene on total cancer, or the three most common site-specific cancers. The possibility of risk reduction within specific subgroups remains.     

A multicenter case–control study of diet and lung cancer among non-smokers

Objective: We have examined the role of dietary patterns and specific dietary nutrients in the etiology of lung cancer among non-smokers using a multicenter case–control study.Methods: 506 non-smoking incident lung cancer cases were identified in the eight centers along with 1045 non-smoking controls. Dietary habits were assessed using a quantitative food-frequency questionnaire administered by personal interview. Based on this information, measures of total carotenoids, beta-carotene and retinol nutrient intake were estimated.Results: Protective effects against lung cancer were observed for high consumption of tomatoes, (odds ratio (OR) = 0.5; 95% confidence interval (CI) 0.4–0.6), lettuce (OR = 0.6; 95% CI 0.3–1.2), carrots (OR = 0.8; 95% CI 0.5–1.1), margarine (OR = 0.7; 95% CI 0.5–0.8) and cheese (OR = 0.7; 95% CI 0.5–1.0). Only weak protective effects were observed for high consumption of all carotenoids (OR = 0.8; 95% CI 0.6–1.0), beta-carotene (OR=0.8; 95% CI 0.6–1.1) and retinol (OR = 0.9; 95% CI 0.7–1.1). Protective effects for high levels of fruit consumption were restricted to squamous cell carcinoma (OR = 0.7; 95% CI 0.4–1.2) and small cell carcinoma (OR = 0.7; 95% CI 0.4–1.2), and were not apparent for adenocarcinoma (OR = 0.9; 95% CI 0.6–1.3). Similarly, any excess risk associated with meat, butter and egg consumption was restricted to squamous and small cell carcinomas, but was not detected for adenocarcinomas.Conclusions: This evidence suggests that the public health significance of increasing vegetable consumption among the bottom third of the population would include a reduction in the incidence of lung cancer among lifetime non-smokers by at least 25%, and possibly more. A similar protective effect for increased fruit consumption may be present for squamous cell and small cell lung carcinomas.     

Cancer incidence among marine engineers,a population-based study (Iceland)

Objectives: Marine engineers are in their occupation exposed to different chemicals, organic solvents, exhaust gases, oils, and petroleum products, and were formerly exposed to asbestos. The aim was to study the cancer pattern, with particular attention to lung and bladder cancer, in an Icelandic cohort of marine engineers, indirectly controlling for their smoking habits. Methods: A cohort of 6603 male marine engineers was followed up from 1955 to 1998, a total of 167,715 person-years. The cohort was record linked by the engineers' personal identification numbers to population-based registers containing the vital and emigration status and cancer diagnosis. Standardized incidence ratios (SIRs) were calculated for all cancers and different cancer sites in relation to different lag time and year of graduation. Information on smoking habits was obtained by administering a questionnaire to a sample of the cohort (n = 1501). Results: In the total cohort 810 cancers were observed, whereas 794 were expected (SIR 1.0, 95% CI 1.0–1.1), and significantly increased risk of stomach cancer (SIR 1.3, 95% CI 1.0–1.5) and lung cancer (SIR 1.2, 95% CI 1.0–1.5) was found. Increased risk of all cancers (SIR 1.2, 95% CI 1.1–1.3), stomach cancer (SIR 1.5, 95% CI 1.1–1.9), lung cancer (SIR 1.4, 95% CI 1.2–1.8), pleural mesothelioma (SIR 4.8, 95% CI 1.3–12.3), and urinary bladder cancer (SIR 1.3, 95% CI 1.0–1.8) were observed when a 40-year lag time was applied. The engineers' smoking habits were similar to those in a sample of the general population. The predictive value for lung cancer was 1.03. Conclusions: The increased risk for mesothelioma is possibly attributable to the previous asbestos exposure. The excess of lung cancer could also be related to asbestos exposure. The high incidence of stomach cancer, lung cancer, and bladder cancer may be related to exposure to chemical risk factors, such as oils and petroleum products, as confounding due to smoking seems to be ruled out. In the light of the limited exposure information in the present study the importance of the different occupational exposures needs to be evaluated in further studies.     

Micronutrients and ovarian cancer: A case-control study in Italy

Background:The role of selected micronutrients, vitaminsand minerals in the aetiology of epithelial ovarian cancer wasinvestigated using data from a case-control study conducted between 1992and 1999 in five Italian areas. Patients and methods:Cases were 1031 patients with histologically confirmed incidentepithelial ovarian cancer. Controls were 2411 subjects admitted foracute, non-neoplastic diseases to major hospitals in the same catchmentareas. Dietary habits were elicited using a validated food frequencyquestionnaire including 78 food groups and recipes. Odds ratios (OR) and95% confidence intervals (95% CI) were computed byquintiles of intake of nutrients. Results:Inverseassociations emerged for vitamin E (OR = 0.6; 95% CI:0.5–0.8), beta-carotene (OR = 0.8; 95% CI: 0.6–1.0),lutein/zeaxanthin (OR = 0.6; 95% CI: 0.5–0.8 for thehighest vs. the lowest quintile of intake), and calcium intake (OR =0.7; 95% CI: 0.6–1.0). When the combined effect of calciumand vitamin E was considered, the OR reached 0.4 (95% CI:0.3–0.7) for subjects in the highest compared to those in thelowest intake tertile of both micronutrients. Results were consistentacross strata of menopausal status, parity and family history of ovarianor breast cancer. Conclusions:The intake of selectedmicronutrients, which were positively correlated to a diet rich invegetables and fruits, was inversely associated with ovarian cancer.     

Acromegaly and cancer risk: a cohort study in Sweden and Denmark

Objective: Several studies have suggested that patients with acromegaly have an increased risk of benign and malignant neoplasms, especially of the colon. To further investigate this relationship we evaluated cancer risk in population-based cohorts of acromegaly patients in Sweden and Denmark. Methods: Nationwide registry-based cohorts of patients hospitalized for acromegaly (Denmark 1977–1993; Sweden 1965–1993) were linked to tumor registry data for up to 15–28 years of follow-up, respectively. Standardized incidence ratios (SIR) and 95% confidence intervals (CI) were calculated to estimate cancer risk among 1634 patients with acromegaly. Results: The patterns of cancer risk in Sweden and Denmark were similar. After excluding the first year of follow-up, 177 patients with acromegaly had a diagnosis of cancer compared with an expected number of 116.5 (SIR = 1.5, 95% CI = 1.3–1.8). Increased risks were found for digestive system cancers (SIR = 2.1, 95% CI = 1.6–2.7), notably of the small intestine (SIR = 6.0, 95% CI = 1.2–17.4), colon (SIR = 2.6, 95% CI = 1.6–3.8), and rectum (SIR = 2.5, 95% CI = 1.3–4.2). Risks were also elevated for cancers of the brain (SIR = 2.7, 95% CI = 1.2–5.0), thyroid (SIR = 3.7, 95% CI = 1.8–10.9), kidney (SIR = 3.2, 95% CI = 1.6–5.5), and bone (SIR = 13.8, 95% CI = 1.7–50.0). Conclusions: The increased risk for several cancer sites among acromegaly patients may be due to the elevated proliferative and anti-apoptotic activity associated with increased circulating levels of insulin-like growth factor-1 (IGF-1). Pituitary irradiation given to some patients may have contributed to the excess risks of brain tumors and thyroid cancer. Our findings indicate the need for close medical surveillance of patients with acromegaly, and further studies of the IGF-1 system in the etiology of various cancers.     

Hormonal risk factors for endometrial cancer: modification by cigarette smoking (United States)

Objectives: To evaluate whether smoking modifies the risk of endometrial cancer associated with body mass index (BMI), postmenopausal hormone use, and other hormonal factors. Methods: Using multivariate adjusted models we examined interview data from a population-based case–control study of Wisconsin women (n = 740 cases, n = 2372 controls). Results: The relative risk for endometrial cancer associated with current smoking was 0.8 (95% CI: 0.6–1.0) compared to never smokers. No clear dose–response relationship was evident for pack-years smoked. When examined according to smoking status the risk associated with the highest quartile of BMI seemed to be greater among non-smokers (OR = 3.6, 95% CI: 2.4–5.3) than among current smokers (OR = 2.8, 95% CI: 1.4–5.6). Among postmenopausal women the risk associated with current use of postmenopausal hormones appeared to be greater among non-smokers (OR = 3.3, 95% CI: 2.3–4.9) than among current smokers (OR = 2.7, 95% CI: 1.3–5.5). Risk for long-term use (10 or more years) compared with never users was 8.3 (95% CI: 4.6–15.1) among never smokers and 2.5 (95% CI: 0.8–7.9) among current smokers. The risk associated with non-insulin-dependent diabetes was greater among non-smokers (OR = 2.5, 95% CI: 1.7–3.6) than current smokers (OR = 1.1, 95% CI: 0.4–3.1). There was no modifying effect of smoking on the risk associated with parity. Conclusion: These results suggest that smoking moderates the risk associated with endometrial cancer among women at greatest risk, specifically women who are obese or who use postmenopausal hormones.     

A prospective study of lifestyle factors and the risk of pancreatic cancer in Nord-Trøndelag, Norway

Objectives: Cancer of the pancreas is highly fatal and, despite extensive scrutiny, only cigarette smoking stands out as a likely causal agent in epidemiological studies. To explore to what extent different lifestyle factors are associated with the risk of pancreatic cancer, data from a large health screening survey in a county in Norway were analyzed. Methods: Our study included 31,000 men and 32,374 women initially free from any diagnosed cancer, and during 12 years of follow-up, 166 incident cases of pancreatic cancer were diagnosed at the Cancer Registry. Results: Compared with never smokers, we found a two-fold increased risk among current smokers, and a dose–response association with number of cigarettes (p for trend = 0.02 for both men and women) and with number of pack-years (p for trend = 0.02 for men and 0.01 for women). The risk among former smokers quitting more than 5 years before study entry was close to the risk of never smokers. Compared with persons who reported never or infrequently to be physically worn out after a day's work, the relative risk (RR) among those who nearly always became worn out was 2.9 (95% confidence interval (CI) = 1.4–5.8) for men and 3.8 (95% CI = 1.6–9.2) for women. Divorced or separated men had a risk of 3.1 (95% CI = 1.3–7.2) compared with married men. We observed a higher risk among women in occupations of high socioeconomic status (RR = 2.5; 95% CI = 1.2–5.2), and among men occupied in farming, agriculture or forestry (RR = 2.1; 95% CI = 1.1–4.0), compared with persons in occupations of low socioeconomic status. Conclusions: Our results confirm the findings of previous studies that indicate a causal role of cigarette smoking in pancreatic cancer. Moreover, we found that the risk of former smokers may approach the risk of never smokers within a few years subsequent to quitting.     

Cigarette smoking and risk of epithelial ovarian cancer (Australia)

Objectives: We studied the association between cigarette smoking and ovarian cancer in a population-based case–control study. Methods: A total of 794 women with histologically confirmed epithelial ovarian cancer who were aged 18–79 years and resident in one of three Australian states were interviewed, together with 855 controls aged 18–79 years selected at random from the electoral roll from the same states. Information was obtained about cigarette smoking and other factors including age, parity, oral contraceptive use, and reproductive factors. We estimated the relative risk of ovarian cancer associated with cigarette smoking, accounting for histologic type, using multivariable logistic regression to adjust for confounding factors. Results: Women who had ever smoked cigarettes were more likely to develop ovarian cancer than women who had never smoked (adjusted odds ratio (OR) = 1.5; 95% confidence interval (CI) = 1.2–1.9). Risk was greater for ovarian cancers of borderline malignancy (OR = 2.4; 95% CI = 1.4–4.1) than for invasive tumors (OR = 1.7; 95% CI = 1.2–2.4) and the histologic subtype most strongly associated overall was the mucinous subtype among both current smokers (OR = 3.2; 95% CI = 1.8–5.7) and past smokers (OR = 2.3; 95% CI = 1.3–3.9). Conclusions: These data extend recent findings and suggest that cigarette smoking is a risk factor for ovarian cancer, especially mucinous and borderline mucinous types. From a public health viewpoint, this is one of the few reports of a potentially avoidable risk factor for ovarian cancer.     

A prospective study of obesity and cancer risk (Sweden)

Objective: We evaluated the relation between obesity and the risks for various forms of cancer. Methods: In a population-based cohort of 28,129 hospital patients (8165 men, 19,964 women) with any discharge diagnosis of obesity (9557 only diagnosis, 5266 primary, 13,306 secondary) during 1965–1993, cancer incidence was ascertained through 1993 by record linkage to the nationwide Swedish Cancer Registry. Cancer risk was estimated using the standardized incidence ratio (SIR, with 95% confidence interval), which is the ratio of the observed number of cancers to that expected. Results: Overall, a 33% excess incidence of cancer was seen in obese persons, 25% in men and 37% in women. Significant risk elevations were observed for cancers of the small intestine (SIR = 2.8; 95% CI 1.6–4.5), colon (1.3; 1.1–1.5), gallbladder (1.6; 1.1–2.3), pancreas (1.5; 1.1–1.9), larynx (2.1; 1.1–3.5), renal parenchyma (2.3; 1.8–2.8), bladder (1.2; 1.0–1.6), cervix uteri (1.4; 1.1–1.9), endometrium (2.9; 2.5–3.4), ovary (1.2; 1.1–1.5), brain (1.5; 1.2–1.9), and connective tissue (1.9; 1.1–3.0), and for lymphomas (1.4; 1.0–1.7), with higher risk observed for Hodgkin's disease only in men (3.3; 1.4–6.5) and for non-Hodgkin's lymphoma only in women (1.6; 1.2–2.1). The association of obesity with risk of breast, prostate and pancreas cancers was modified by age. Conclusions: Obesity is associated with more forms of cancer than previously reported.     

Alcoholism and cancer risk: a population-based cohort study

The incidence of cancer was studied in a population-based cohort of 9,353 individuals (8,340 men and 1,013 women) with a discharge diagnosis of alcoholism in 1965–83, followed up for 19 years (mean 7.7). After exclusion of cancers in the first year of follow-up, 491 cancers were observed cf 343.2 expected through 1984 (standardized incidence ratio [SIR] = 1.4,95 percent confidence interval [CI] = 1.3–1.6). A similar excess risk of cancer was seen among men (SIR = 1.4, CI = 1.3–1.6) and among women (SIR = 1.5, CI = 1.1–2.0). We observed the established associations with cancers of the oral cavity and pharynx (SIR = 4.1, CI = 2.9–5.7), esophagus (SIR = 6.8, CI = 4.5–9.9), larynx (SIR = 3.3, CI = 1.7–6.0), and lung (SIR = 2.1, CI = 1.7–2.6), although confounding by smoking likely increased these risk estimates. While there was evidence of increased risk for pancreatic cancer (SIR = 1.5, CI = 0.9–2.3), alcoholism did not elevate the incidence of cancer of the stomach (SIR = 0.9, CI = 6–1.4), large bowel (SIR = 1.1, CI = 0.8–1.5), prostate (SIR = 1.0, CI = 0.8–1.3), urinary bladder (SIR = 1.0, CI = 0.6–1.5), or of malignant melanoma (SIR = 0.9, CI = 0.3–1.9). Among women, the number of breast cancers observed was close to expected (SIR = 1.2, CI = 0.6–2.2), although a significant excess number of cervical cancers occurred (SIR = 4.2, CI = 1.5–9.1). The results of this study, one of the first to evaluate the incidence of cancer in a population-based cohort of alcoholics of both sexes, are consistent with smaller previous studies, which were usually limited to cancer mortality and of short follow-up.Dr Adami is with the Cancer Epidemiology Unit, University Hospital, Uppsala, Sweden. Drs McLaughlin and Hsing are with the Biostatistics Branch, National Cancer Institute, Bethesda, MD, USA. Dr Wolk is with the Cancer Epidemiology Unit, University Hospital, Uppsala, Sweden. Dr Ekbom is with the Department of Surgery and with the Cancer Epidemiology Unit, University Hospital, Uppsala, Sweden. Dr Persson is with the Department of Obstetrics and Gynaecology and with the Cancer Epidemiology Unit, University Hospital, Uppsala, Sweden. Address correspondence to Dr Adami, Cancer Epidemiology Unit, University Hospital, S-751 85 Uppsala, Sweden. The work was performed at the Cancer Epidemiology Unit, Uppsala University, Sweden; the research was supported by grants from the Swedish Cancer Society.     

Nutrient intake and ovarian cancer: an Italian case-control study

Objective: The role of selected macronutrients, cholesterol, and fatty acids in the etiology of epithelial ovarian cancer was analyzed using data from a case–control study carried out in five Italian areas between January 1992 and December 1999. Methods: Cases comprised 1031 women with incident, histologically confirmed epithelial ovarian cancer, admitted to the major teaching and general hospitals of the study areas. Controls comprised 2411 women admitted for acute, non-neoplastic conditions to the same network of hospitals. Information on dietary habits was elicited using a validated food-frequency questionnaire including 78 food groups and recipes. Odds ratios (OR) and their corresponding 95% confidence intervals (CI) were computed by subsequent quintiles of nutrient intake. Results: Direct associations with ovarian cancer emerged for starch intake (OR = 1.4 in the highest vs the lowest quintile of intake; 95% CI 1.1–1.8), while inverse associations emerged for monounsaturated (OR = 0.7; 95% CI 0.5–0.9), and polyunsaturated (OR = 0.7; 95% CI 0.5–0.9) fatty acids. Among fatty acids, oleic (OR = 0.7; 95% CI 0.5–0.9), linoleic (OR = 0.7; 95% CI 0.5–0.9), and linolenic (OR = 0.8; 95% CI 0.6–1.0) acids were inversely related to ovarian cancer. When, however, six macronutrients were included in the same model, only the adverse effect of high starch intake remained significant. Results were consistent in separate strata of menopausal status, parity, and energy intake. Conclusions: Starch was directly associated, and unsaturated fatty acids were inversely associated, with ovarian cancer risk.     

Double primary cancers of the breast and thyroid in women: molecular analysis and genetic implications

Multiple primary cancers are characteristic of hereditary cancer syndromes. A familial association between breast and thyroid cancer has been suggested, but a genetic basis for this association has not yet been established. To determine the extent to which double primary cancers of the breast and thyroid are due to common hereditary factors, we conducted a registry- and hospital-based study in Ontario and Quebec. We obtained family histories of 74 women diagnosed with both cancer of the breast and thyroid before 70 years of age. Cancer histories were obtained for the 533 first-degree relatives of these women. The observed cancer rate in the relatives was compared with the expected number, based on age-standardized Canadian cancer incidence rates, and relative risks were estimated. A total of 87 cancers were observed in the relatives, compared to 93.7 expected cancers, giving a relative risk of 0.9 (95% confidence interval (CI): 0.7–1.1). The risk for breast cancer was 1.1 (95% CI: 0.6–1.7) and the risk for thyroid cancer was 0.7 (95% CI: 0–3.8). Blood samples were collected on 53 patients for mutational analysis of the BRCA1, BRCA2, and PTEN genes. One woman was found to be a carrier of a BRCA1 mutation (exon 11 3227delT). Our findings do not support the hypothesis that a significant proportion of double primary cancers of the breast and thyroid are due to hereditary factors.     

Visual impairment and cancer: a population-based cohort study in Finland

Objectives: To describe the cancer risk pattern of Finnish persons with visual impairment.Methods: A cohort of 17,557 persons identified from the Finnish Register of Visual Impairment was followed-up for cancer through the Finnish Cancer Registry from 1983–95. The degree of visual impairment ranged from moderate low vision with visual acuity less than 0.3, to total blindness with no perception of light. The standardized incidence ratios (SIR) and 95% confidence intervals (CI) were calculated by primary site; the expected rates were based on national cancer incidence rates.Results: The SIR for overall cancer among totally blind men was 2.2 (CI=1.3–3.5) while in the entire cohort the incidence was increased by only 15% (1,255 cancers observed cf 1,093 expected). Excesses were observed inboth genders in cancers of the liver (SIR=1.8, CI=1.2–2.5) and lung (SIR=1.5, CI=1.3–1.7); in females in cancers of the stomach (SIR=1.5, CI=1.2–1.9) and the colorectum (SIR=1.3, CI=1.1–1.6); and in males incancers ofthe kidney (SIR=1.8, CI=1.1–2.6) and the eye (5.8, CI=1.9–13). The excess in lung cancer was entirely attributable to age-related macular degeneration (which is most common among smokers).Conclusions: Cancer incidence among the visually impaired tended to be increased for most cancer types. Attention should be paid to lifestyle factors underlying the observed risk increases, such as unbalanced diet.     

Diet and prostate cancer risk in a cohort of smokers, with a specific focus on calcium and phosphorus (Finland)

Background:Calcium, phosphorus, fructose, and animal protein are hypothesized to be associated with prostate cancer risk, potentially via their influence on 1,25-dihydroxyvitamin D₃. We examined these nutrients and overall diet and prostate cancer risk in the Alpha-Tocopherol Beta-Carotene Cancer Prevention Study (ATBC Study). Materials and methods:The ATBC Study was a randomized 2 × 2 trial of alpha-tocopherol and beta-carotene on lung cancer incidence conducted among Finnish male smokers; 27,062 of the men completed a food-use questionnaire at baseline, and comprise the current study population. There were 184 incident clinical (stage 2–4) prostate cancer cases diagnosed between 1985 and 1993. We used Cox proportional hazards models to examine associations between dietary intakes and prostate cancer. Results:We did not observe significant independent associations for calcium and phosphorus and prostate cancer risk. However, men with lower calcium and higher phosphorus intake had a multivariate relative risk of 0.6 (95% CI 0.3–1.0) compared to men with lower intakes of both nutrients, adjusting for age, smoking, body mass index, total energy, education, and supplementation group. Of the other foods and nutrients examined, none was significantly associated with risk. Discussion:This study provides, at best, only weak evidence for the hypothesis that calcium and phosphorus are independently associated with prostate cancer risk, but suggests that there may be an interaction between these nutrients.     

Risk factors for local recurrence after conservative treatment in stage I breast cancer. Definition of a subgroup not requiring radiotherapy

Background: Risk factors for local recurrence after breast-conservingtreatment of early breast cancer have not previously been evaluated insettings where mammography has been a major pathway to diagnosis of bothprimary tumour and recurrences, or in patients treated surgically by a formalsector resection.Patients and methods: Three hundred eighty-one women with stage Iprimary breast cancer were randomised after a standardised sector resectionto either a course of postoperative radiotherapy to 54 Gy to the breast (XRTgroup) or to surgery alone (non XRT group). At five years, 43 localrecurrences, six of them in the XRT group, appeared. Patient characteristicscollected from the medical records, histopathological characteristicsdetermined by re-examination of slides, and mammographic characteristcs fromthe pre-operative mammograms were evaluated as risk factors for recurrence byunivariate and multivariate Cox proportional hazards models. Results arereported as relative hazards (RH) with 95% confidence intervals(95% CI).Results: In the univariate analysis comedo cancer, RH 3.5 (95%CI 1.8–6.7), lobular cancers RH 2.8 (95% CI 1.1–7.1),mammographic appearance as circular/oval shaped density, RH 2.3 (95%CI 1.1–4.5), and mammographic appearance as a stellate lesion withmicrocalcifications inside the lesion, RH 3.8 (95% CI 1.1–13.0)were identified as risk factors for local recurrence. Age, with a RH of 0.97(95% CI 0.94–0.99) for each increasing year was inverselyassociated with risk. A multivariate analysis, which also took postoperativeradiotherapy into account, only showed comedo cancers with a RH 2.6(95% CI 1.3–5.0) and mammographic appearance of a stellate lesionwith microcalcification inside the lesion RH 4.5 (95% CI1.1–17.6) to be statistically significant. The estimates for age RH 0.98(95% CI 0.95–1.0) and lobular cancers RH 2.5 (95% CI0.98–6.6) were marginally changed, with widened CIs. Patients > 60years of age, without comedo or lobular carcinomas were found to be at lowrisk (5.9% at five years in Kaplan–Meyer estimate) of localrecurrence, even without postoperative radiotherapy.Conclusion: Low age, comedo and lobular cancers and mammographicappearance of the tumour as a stellate lesion with microcalcifications insidethe lesion indicate an increased risk for local recurrence after sectorresection in stage I tumours at five years. Patients >60 years of agewithout comedo or lobular cancers are at low risk for local recurrence at fiveyears even without postoperative radiotherapy.     

Employment as butcher and cancer risk in a record-linkage study from Sweden

Objective: To investigate the risk of cancer among butchers and other meat workers in a large record-linkage study from Sweden. Methods: The Swedish Cancer Environment Register III contains nationwide data on cancer incidence during 1971–1989 for all residents, by occupation and industry of employment as reported at the 1960 and 1970 censuses. We identified 25,049 men classified as butchers or meat workers at either census. We used as a comparison group the remaining part of the active male population, after exclusion of workers with direct contact with animals. Results: Butchers in the meat industry had a slight increase in the risk of cancer (relative risk [RR] 1.1, 95% confidence interval [CI] 1.0–1.3), which was due to an increased risk of cancers of the oral cavity and pharynx (RR 1.6, 95% CI 1.0–2.7), stomach (RR 1.6, 95% CI 1.1–2.7), larynx (RR 1.4, 95% CI 0.6–3.4), and lung (RR 1.4, 95% CI 1.1–1.9). The risk of stomach cancer was highest during the first 5 years of the study, and among butchers from urban areas. No temporal or geographic variations were seen for lung cancer risk, with elevations restricted to squamous cell carcinoma. An increased risk of stomach, laryngeal and lung cancers was present in butchers and meat workers outside the meat industry. There was no clear indication of an increased risk of other neoplasms. Conclusions: The increased risk of oral, laryngeal, lung and stomach cancers among Swedish butchers may be at least partly due to confounding by tobacco smoking, alcohol drinking, and other lifestyle factors. However, exposures in the meat industry (e.g., viruses, nitrosamines, polycyclic aromatic hydrocarbons) may contribute the elevated cancer risks.     

Diet in the epidemiology of endometrial cancer in Western New York (United States)

Objectives: We examined diet and risk of endometrial cancer among women in the Western New York Diet Study (1986–1991). Methods: Self-reported frequency of use of 172 foods and beverages during the 2 years before the interview and other relevant data were collected by detailed interviews from 232 endometrial cancer cases and 639 controls, frequency-matched for age and county of residence. Odds ratios (OR) and 95% confidence intervals (CI) were estimated by unconditional logistic regression, adjusting for age, education, body mass index (BMI), smoking history, hypertension, diabetes, age at menarche, parity, oral contraceptive use, menopausal status, menopausal estrogen use, and energy. Results: Risks were reduced for women in the highest quartiles of intake of protein (OR 0.4, 95% CI: 0.2–0.9), dietary fiber (OR 0.5, 95% CI: 0.3–1.0), phytosterols (OR 0.6, 95% CI: 0.3–1.0), vitamin C (OR 0.5, 95% CI: 0.3–0.8) folate (OR 0.4, 95% CI: 0.2–0.7), alpha-carotene (OR 0.6, 95% CI: 0.4–1.0), beta-carotene (OR 0.4, 95% CI: 0.2–0.6), lycopene (OR 0.6, 95% CI: 0.4–1.0), lutein + zeaxanthin (OR 0.3, 95% CI: 0.2–0.5) and vegetables (OR 0.5, 95% CI: 0.3–0.9), but unrelated to energy (OR 0.9, 95% CI: 0.6–1.5) or fat (OR 1.6, 95% CI: 0.7–3.4). Conclusions: Our results support previous findings of reduced endometrial cancer risks associated with a diet high in plant foods.     

Second primary cancers following cancers of the kidney and prostate in New South Wales (Australia), 1972–91

Data from the New South Wales (NSW) (Australia) Central Cancer Registry for the period 1972–91 were examined to determine the risk of second primary cancers following an initial invasive cancer of the renal parenchyma (ICD-9 code 189.0), renal pelvis (code 189.1), or prostate (code 185). Eligible cases were restricted to those who had survived for at least two months after diagnosis of the first primary cancer. Expected numbers of cancers were obtained by assuming that subjects experienced the same cancer incidence as prevailed in the corresponding general population and applying gender-, age-, and calendar-specific rates to the appropriate person-years at risk. The relative risk (RR) of a second primary cancer was taken to be the ratio of observed to expected numbers of second cancers. Following prostatic cancer, there was an overall deficit of cancers at all sites combined (RR=0.79, 95 percent confidence interval [CI]=0.75–0.84), and no site had a significantly raised RR. Taking this into consideration, there appeared to be a reciprocal relationship of increased risk of prostatic cancer (RR=1.7, CI=1.2–2.3) following an initial cancer of the renal parenchyma and of renal parenchymal cancer (RR=1.2, CI=0.8–1.7) after cancer of the prostate. An increased risk of bladder cancer occurred following renal parenchymal (RR=3.4, CI=1.1–8.0, for women only) as well as after renal pelvic cancer (men:RR=8.7, CI=5.4–13; women:RR=39, CI=26–56). A tobacco-related pattern of excess risk was seen after renal pelvic cancer but not after cancer of the renal parenchyma. These data illustrate that an excess of second primary cancers may reflect shared etiologic factors or increased medical surveillance.Dr McCredie and Ms Coates are with the New South Wales Cancer Council in the Cancer Epidemiology Research Unit (Dr McCredie) and NSW Central Cancer Registry (Ms Coates). Dr Stewart is with the Western Clinical School, University of Sydney, Australia. Dr Macfarlane is with the ARC Epidemiology Unit, University of Manchester, UK. Address correspondence to Dr McCredie, Cancer Epidemiology Research Unit, NSW Cancer Council, PO Box 572, Kings Cross 2011, New South Wales, Australia.