Family history of reproductive cancers and ovarian cancer risk: an Italian case-control study.

The relation between family history of ovarian, breast, and endometrial cancer and risk of epithelial ovarian carcinoma was analyzed within the framework of a case-control study conducted from 1983 to 1989. The study included 755 cases of ovarian cancer and 2,023 controls in hospital for a spectrum of acute nongynecologic, hormonal, or neoplastic conditions in the Greater Milan area, Italy. Eighteen cases (2%) and 24 controls (1%) reported a history of ovarian cancer in a first-degree relative: The corresponding multivariate adjusted odds ratio (OR) was 1.9 (95% confidence interval (CI) 1.1-3.6). The risk of ovarian cancer was elevated in women reporting a family history of breast cancer (OR = 1.6, 95% CI 1.1-2.3), but no significant association emerged with a family history of endometrial cancer (OR = 1.3, 95% CI 0.8-1.7). When the data were stratified by family history of breast cancer, a family history of ovarian cancer was over 10 times more frequent in both cases and controls who reported a family history of breast cancer than in cases and controls reporting no family history of breast cancer. The estimated odds ratio for ovarian cancer associated with a family history of the disease was 2.3 (95% CI 1.1-4.5) in women not reporting a family history of breast cancer, but no association emerged in the subgroup of women reporting a family history of breast cancer. These results confirm that a family history of ovarian cancer increases the risk of the disease, but the percentage of ovarian cancer cases explained by a family history of the disease is small: Less than 1% of observed cases in this study could be attributed to this "family risk factor."     

Aggregation of ovarian cancer with breast, ovarian, colorectal, and prostate cancer in first-degree relatives

Epidemiologic studies have demonstrated a tendency for common cancers to aggregate in families. The authors investigated the effects of family history of cancer at multiple sites, including the breast, ovary, colorectum, and prostate, on ovarian cancer risk among 607 controls and 558 ovarian cases in Hawaii and Los Angeles, California, in 1993-1999. A family history of cancer of the breast, ovary, colorectum, or prostate in first-degree relatives was associated with an increased risk of ovarian cancer (odds ratio (OR)=1.7, 95% confidence interval (CI): 1.1, 2.6; OR=3.2, 95% CI: 1.3, 7.9; OR=1.5, 95% CI: 0.9, 2.5; and OR=1.6, 95% CI: 1.0, 2.8, respectively). A greater risk of ovarian cancer was observed for women with parents rather than siblings with a history of breast or prostate cancer and for women with parental colorectal cancer diagnosed at an early age, suggesting a genetic predisposition among these women. The risk of nonmucinous tumors, but not mucinous tumors, was positively associated with a family history of cancer. No significant interaction effects on risk existed between oral contraceptive pill use or pregnancy and family history of breast and/or ovarian cancer. Study findings suggest that ovarian cancer aggregates with several common cancers in family members.     

Heterogeneity of the effect of family history on breast cancer risk

We studied the effects of family history on breast cancer risk among 2,908 cases and 3,180 controls, selected from participants in a nationwide screening project. First-degree family history was associated with a twofold risk increase. Second-degree family history effects were minimal, after adjusting for effects of first-degree relatives. Family history effects were not confounded by age at menarche, age at first full-term birth, age at natural menopause, or previous benign breast disease. Risks from mother's and sister's history were independent. The odds ratio (OR) from a maternal history, 1.9 (95% confidence interval [CI]: 1.6-2.3), varied little by the subject's age at diagnosis, menopause status, or disease laterality. Interactions of maternal history effects with multiple breast biopsies and age at menopause were greater than additive, indicating common mechanistic pathways. The OR from a sister's history was 2.3 (95% CI: 1.9-2.8) and was increased among women who were less than 45 (OR = 6.9), had bilateral disease (OR = 4.7), or were premenopausal (OR = 4.4). The effects from a mother's history and a sister's history are modified in different directions by different factors, providing further indication of the separate roles of a mother's and sister's history in breast cancer etiology.     

Hormone-related factors and risk of breast cancer in relation to estrogen receptor and progesterone receptor status

Risk factors were examined for subgroups of breast cancer characterized by estrogen receptor (ER) and progesterone receptor (PR) status. Data from the Carolina Breast Cancer Study, a population-based, North Carolina case-control study of 862 breast cancer cases aged 20-74 years diagnosed during 1993-1996 and 790 controls frequency matched on race and age, were obtained by personal interview. ER and PR status was retrieved from medical records (80%) or was determined in the authors' laboratory (11%) but was missing for 9% of cases. The receptor status distribution was as follows: 53% ER+PR+, 11% ER+PR-, 8% ER-PR+, and 28% ER-PR-. Several hormone-related factors were associated with stronger increased risks for ER+PR+ than for ER-PR- breast cancer: the elevated odds ratios were strongest for ER+PR+ breast cancer among postmenopausal women who had an early age at menarche (odds ratio (OR) = 1.6, 95% confidence interval (CI): 1.0, 2.4), nulliparity/late age at first full-term pregnancy (OR = 1.7, 95% CI: 0.9, 3.2 and OR = 1.6, 95% CI: 1.0, 2.7, respectively), or a high body mass index (OR = 1.6, 95% CI: 0.9, 3.0) and among pre-/perimenopausal women who had a high waist-hip ratio (OR = 1.9, 95% CI: 1.2, 3.1). In contrast, family history of breast or ovarian cancer and medical radiation exposure to the chest produced higher odds ratios for ER-PR- than for ER+PR+ breast cancer, especially among pre-/perimenopausal women.     

Risk of contralateral breast cancer: associations with factors related to initial breast cancer

A case-control study was conducted to assess the risk factors associated with the development of a contralateral primary breast cancer among women who had had a first primary breast cancer. Hospital records were reviewed for 292 women who had an incident contralateral breast cancer, diagnosed in one of eight Connecticut hospitals between July 1, 1975 and December 31, 1983, and for a comparison group of 264 surviving unilateral breast cancer patients previously diagnosed in the same hospitals. All subjects were identified through the records of the Connecticut Tumor Registry. A family history of breast cancer in any first- or second-degree relative was associated with an almost threefold increased risk of developing a contralateral cancer (adjusted odds ratio (OR) = 2.8, 95% confidence interval (CI) = 1.6-4.9). Further, this relation was modified by the time elapsed since the initial cancer diagnosis (ratio of OR = 1.9, 95% CI = 1.2-3.0 for a five-year differential in time since initial diagnosis). A delay of 10 years in first full-term pregnancy was associated with a 36% decrease in risk (adjusted OR = 0.6, 95% CI = 0.3-1.2); this estimate excluded the magnitude of increased risk usually observed in studies of initial breast cancer. A conceptual framework is presented for assessing the study findings in the context of previous studies that have examined the corresponding associations for initial primary breast cancers.     

A case-control study of the relationship between the risk of colon cancer in men and exposures to occupational agents

BACKGROUND: We conducted a population-based case-control study in Montreal, Canada, to explore associations between hundreds of occupational circumstances and several cancer sites, including colon. METHODS: We interviewed 497 male patients with a pathologically confirmed diagnosis of colon cancer, 1514 controls with cancers at other sites, and 533 population-based controls. Detailed job histories and relevant potential confounding variables were obtained, and the job histories were translated by a team of chemists and industrial hygienists into a history of occupational exposures. RESULTS: We found that there was reasonable evidence of associations for men employed in nine industry groups (adjusted odds ranging from 1.1 to 1.6 per a 10-year increase in duration of employment), and in 12 job groups (OR varying from 1.1 to 1.7). In addition, we found evidence of increased risks by increasing level of exposures to 21 occupational agents, including polystyrene (OR for "substantial" exposure (OR(subst)) = 10.7), polyurethanes (OR(subst) = 8.4), coke dust (OR(subst) = 5.6), mineral oils (OR(subst) = 3.3), polyacrylates (OR(subst) = 2.8), cellulose nitrate (OR(subst) = 2.6), alkyds (OR(subst) = 2.5), inorganic insulation dust (OR(subst) = 2.3), plastic dusts (OR(subst) = 2.3), asbestos (OR(subst) = 2.1), mineral wool fibers (OR(subst) = 2.1), glass fibers (OR(subst) = 2.0), iron oxides (OR(subst) = 1.9), aliphatic ketones (OR(subst) = 1.9), benzene (OR(subst) = 1.9), xylene (OR(subst) = 1.9), inorganic acid solutions (OR(subst) = 1.8), waxes, polishes (OR(subst) = 1.8), mononuclear aromatic hydrocarbons (OR(subst) = 1.6), toluene (OR(subst) = 1.6), and diesel engine emissions (OR(subst) = 1.5). Not all of these effects are independent because some exposures occurred contemporaneously with others or because they referred to a group of substances. CONCLUSIONS: We have uncovered a number of occupational associations with colon cancer. For most of these agents, there are no published data to support or refute our observations. As there are few accepted risk factors for colon cancer, we suggest that new occupational and toxicologic studies be undertaken focusing on the more prevalent substances reported herein.     

Associations between several sites of cancer and nine organic dusts: results from an hypothesis-generating case-control study in Montreal, 1979-1983

A multi-cancer site, multi-factor case-control study was undertaken to generate hypotheses about possible occupational carcinogens. Probing interviews were carried out with over 2,000 subjects. All incident cases of 19 sites of cancer in males aged 35-70 and resident in Montreal were eligible. The interview was designed to obtain detailed lifetime job histories, and information on potential confounders. Each job history was reviewed by a team of chemists who translated it into a history of occupational exposures. These occupational exposures were then analyzed as potential risk factors in relation to the sites of cancer included. For each site of cancer analyzed as a case series, controls were selected from among the other cancer sites in the study. This report concerns the associations between sites of cancer for which there were over 100 cases processed (stomach; colorectal, also analyzed by subsites; lung; prostate; bladder; kidney; non-Hodgkin's lymphoma) and nine organic dusts (wood; paper; grain; flour; fabrics; cotton; wool; synthetics; fur). All site-exposure combinations were investigated. The ones that provided the most interesting leads were lung-wood dust (odds ratio (OR) = 1.5), stomach-wood dust (OR = 1.5), colorectal-synthetic fiber (OR = 1.5), bladder-synthetic fiber (OR = 1.8), non-Hodgkin's lymphoma-cotton dust (OR = 1.9), colon-grain dust (OR = 2.6), prostate-grain dust (OR = 2.2), and prostate-paper dust (OR = 2.0). Only the associations with wood dust, synthetic fibers and cotton dust showed some evidence of "dose-response" with duration of exposure. Because it is such a common exposure and appears to increase lung and stomach cancer risks, wood dust may be responsible for a great deal of occupational cancer.     

Relationship of epithelial ovarian cancer to other malignancies within families

The relationship of family history of cancer of the breast, colon/rectum, cervix, endometrium, lung, and thyroid to the risk of epithelial ovarian cancer was investigated in a large population-based case-control study. The data consisted of family histories from 493 epithelial ovarian cancer cases and 2,465 controls aged 20-54 years. After controlling for potential confounders, risk for epithelial ovarian cancer was found to be significantly elevated among women reporting breast cancer and colo/rectal cancer in a first-degree relative. Adjusted odds ratios were 1.5 (95% CI = 1.1-2.1) and 1.9 (95% CI = 1.1-3.3), respectively. None of the remaining four types of cancer was found to be statistically associated with the risk of epithelial ovarian cancer. However, when histologic subtypes of epithelial ovarian cancer were considered, a family history of breast cancer was found to be associated with an elevated risk of endometrioid ovarian cancer (odds ratio = 2.3; 95% CI = 1.1-4.7), as was a family history of endometrial cancer (odds ratio = 2.7; 95% CI = 1.0-6.9). The results are considered in the context of other studies of familial patterns of cancer and are compared with published findings concerning the occurrence of multiple primary cancers in the same individual. The findings indicate that further study is warranted regarding possible genetic relationships between epithelial ovarian cancer and cancers arising in other organs.     

A pooled analysis of second primary pancreatic cancer

Studies of pancreatic cancer in the setting of second primary malignant neoplasms can provide etiologic clues. An international multicenter study was carried out using data from 13 cancer registries with a registration period up to year 2000. Cancer patients were followed up from the initial cancer diagnosis, and the occurrence of second primary malignant neoplasms was compared with expected values derived from local rates, adjusting for age, sex, and period of diagnosis. Results from individual registries were pooled by use of a fixed-effects model. People were at higher risk of developing pancreatic cancer within 10 years of a diagnosis of cancers of the pharynx, stomach, gallbladder, larynx, lung, cervix, corpus uteri, bladder, and eye and 10 years or later following a diagnosis of cancers of the stomach, colon, gallbladder, breast, cervix, placenta, corpus uteri, ovary, testis, bladder, kidney, and eye, as well as Hodgkin's and non-Hodgkin's lymphomas. Pancreatic cancer was connected with smoking-related cancers, confirming the etiologic role of tobacco. The associations with uterine and ovarian cancers suggest that reproductive factors might be implicated in pancreatic carcinogenesis. The elevated pancreatic cancer risk in young patients observed among several types of cancer implies a role of genetic factors. Radiotherapy is also suggested as a risk factor.     

Familial clustering of colon,breast, uterine,and ovarian cancers as assessed by family history

The aggregation of colon, endometrial, ovarian, and possibly breast cancers in families has been described as a “cancer family syndrome” (now called Lynch syndrome II). To determine if the familial clustering of these malignancies was more common in women with cancer than without, we analyzed data from the Iowa Women's Health Study (IWHS), a population-based sample of 41,837 women aged 55–69 years. Self-reported information was collected on history of colon, uterine, ovarian, and breast cancers in female first-degree relatives. A family history of cancer of the breast (odds ratio [OR] = 1.4), colon (OR = 1.3), and uterus (OR = 1.3), but not ovary (OR = 1.2), was significantly more common among women with a personal history of any of these four cancers (all P < 0.05); the pattern of the ORs suggested strongly that the clustering tended to be site-specific. Age-adjusted relative risks (RR) of incident colon cancer over 5 years of follow-up (N = 237) were calculated with regard to family history. Colon cancer incidence was increased among women with a family history of breast (RR = l.3), uterine (RR = 1.4), colon (RR = l.5), and ovarian (RR = 1.3) cancers, although none of the risk estimates achieved statistical significance. RR was, however, significantly related to the number of different cancer sites reported among family members (P_trend = 0.008). These data on a representative sample of postmenopausal women suggest that family histories of colon, breast, uterine, and ovarian cancers are associated with an increased risk of cancer at the same site, but provide little support for the hypothesis that Lynch syndrome II is a non-random occurrence. © 1993 Wiley-Liss, Inc.     

Fat from different foods show diverging relations with breast cancer risk in postmenopausal women

The aim was to explore previous findings within the Malm? Diet and Cancer cohort (Sweden) that omega6-fatty acid intakes are positively associated with breast cancer risk among women 50 yr of age and older and specifically examine relations between breast cancer risk and fat from different food groups. Incident breast cancer cases (n = 237) were matched to controls (n = 673) on age and screening date. A modified diet history method, a structured questionnaire, and anthropometric measurements provided data. Fat-food variables from 24 food groups were computed. Conditional logistic regression examined breast cancer risk associated with energy-adjusted exposure categories of fat-food variables. Fat from fermented milk products was negatively associated with breast cancer risk (trend, P = 0.003). The highest quartiles of vegetable oil-based dietary fats (odds ratio, OR = 1.74; confidence interval, CI = 1.12-2.72) and dried soup powders (OR = 1.59; CI = 1.04-2.43) showed positive associations. Dietary fiber did not influence associations.     

Risk of subsequent cancer following invasive or in situ squamous cell skin cancer

PURPOSE: Determine the risk of subsequent cancer following squamous cell skin cancer. METHODS: Using computerized surgical pathology records and membership data from a health maintenance organization, we retrospectively identified 822 individuals with primary squamous cell skin cancer (SCSC) and 3662 comparison subjects matched for age, sex, race, residence area, and length of membership. Patients were included in the study if they had no prior history of cancer, and received at least one multiphasic health checkup and questionnaire (MHC). Patients were followed for subsequent invasive cancer up to 24 years, with a mean follow-up time of 7.8 years. RESULTS: SCSC patients had a significantly greater risk [adjusted for body mass index (BMI) and education] for subsequent cancer overall (excluding non-melanoma skin cancer) [risk ratio (RR) = 1.4, 95% confidence interval (CI) = 1.2-1.6], and for basal cell skin cancer (RR = 13.8, 95% CI = 8.8-21.9), digestive (RR = 1.6, 95% CI = 1.1-2.4), and genitourinary cancers (RR = 1.5, 95% CI = 1.0-2.0). An increased, but not statistically significant, adjusted risk (RR > or = 1.4) was also observed for lip, oral cavity, and pharynx cancer (RR = 3.9, 95% CI = 0.6-25.0); non-cutaneous squamous cell cancer (RR = 1.9, 95% CI = 0.9-4.4); and respiratory and intrathoracic cancer (RR = 1.4, 95% CI = 0.8-2.6). The addition of alcohol consumption, combined occupational exposure, marital status, and smoking history to the multivariate model did not materially change any significant positive associations with SCSC. CONCLUSIONS: Our results suggest that patients diagnosed with SCSC may be at an increased risk of subsequent cancer at many sites, although several estimated risk estimates were within the limits of chance given no true association.     

The genetic epidemiology of second primary breast cancer.

It is well established that women with a family history of breast cancer run a higher risk of breast cancer than do women without a family history. The evidence, however, is less clear regarding a possible association between a family history of breast cancer and risk of second primaries. The purpose of this prospective study was to estimate the risk for second primary breast cancer associated with having a family history of breast, endometrial, and ovarian cancers. A cohort of 4,660 women with a first primary breast cancer diagnosed between 1980 and 1982 were interviewed as part of the Cancer and Steroid Hormone Study, a multi-center population-based case-control study, and followed through eight Surveillance, Epidemiology, and End Results (SEER) program registries for 4 to 6 years. Of these women, 136 developed a second primary breast cancer in the contralateral breast at least 6 months after diagnosis of the first primary. Cox proportional hazards modeling techniques were used to model the time to onset of second primary breast cancer while adjusting for multiple predictors. The risk of contralateral breast cancer was elevated among cohort members who reported a history of breast cancer in a first-degree relative (multivariable-adjusted rate ratio (RR) = 1.91, 95% confidence interval (CI) = 1.22-2.99). Early age at onset (< 46 years) in the relative further increased the risk of developing contralateral breast cancer (sister: multivariable-adjusted RR = 3.36, 95% CI 1.62-6.98; mother: multivariable-adjusted RR = 2.35, 95% CI 1.02-5.43). Bilateral breast cancer in mothers was also associated with more than a two and a half-fold increase in risk (multivariable-adjusted RR = 2.55, 95% CI 1.02-6.35). The association between family history of breast cancer and risk of contralateral breast cancer did not vary substantially according to age at onset of the first primary breast cancer. The age-adjusted rate ratio for development of a second primary breast cancer among women with a first-degree relative with endometrial cancer was 2.13 (95% CI 1.04-4.35), while the corresponding rate ratio among women with a family history of ovarian cancer was 1.69 (95% CI 0.42-6.83). There was little evidence that age at onset among the relatives with endometrial or ovarian cancer affected the risk. Some of these findings have not been previously reported and need replication in future studies.     

Coffee and alcohol intake and risk of ovarian cancer: an Italian case-control study

The relation between coffee and alcohol intake and ovarian cancer risk was analyzed in a case-control study conducted in Italy between 1992 and 1999. Cases were 1,031 women, aged 18-79 years, with incident, histologically confirmed invasive epithelial ovarian cancer, and controls were 2,411 women, aged 17-79 years, admitted to the hospital for acute nonneoplastic non-hormone-related diseases. Coffee intake (mostly espresso and mocha) was not associated with ovarian cancer risk, with an odds ratio (OR) of 0.93 [95% confidence interval (CI) = 0.69-1.27] in drinkers of > or = 4 cups/day compared with drinkers of < 1 cup/day. No meaningful relation was observed with cappuccino (OR = 1.06, 95% CI = 0.85-1.32 for drinkers compared with nondrinkers), decaffeinated coffee (OR = 0.64, 95% CI 0.42-0.96), and tea intake (OR = 0.90, 95% CI = 0.75-1.08). Total alcohol intake was not associated with ovarian cancer risk (OR = 1.09, 95% CI = 0.76-1.57 in drinkers of > or = 36 g/day compared with never drinkers). No relationship was found with wine (OR = 1.03, 95% CI = 0.70-1.50 for > 39 g/day compared with never drinkers), beer, amari, grappa, and spirits. No significant heterogeneity was found for coffee or total alcohol intake across strata of age, education, parity, oral contraceptive use, family history of ovarian/breast cancer, body mass index, and calorie intake. This study, based on a large data set; provides no support for a causal association between invasive epithelial ovarian cancer risk and coffee and alcohol intake.     

Risk Factors for Pancreatic Cancer in China: A Multicenter Case-Control Study

Background

Despite having one of the highest mortality rates of all cancers, the risk factors of pancreatic cancer remain unclear. We assessed risk factors of pancreatic cancer in China.

Methods

A case-control study design was conducted using data from four hospital-based cancer registries (Henan Provincial Cancer Hospital, Beijing Cancer Hospital, Hebei Provincial Cancer Hospital, and Cancer Hospital of Chinese Academy of Medical Sciences). Controls were equally matched and selected from family members of non-pancreatic cancer patients in the same hospitals. Face-to-face interviews were conducted by trained staff using questionnaires. Conditional logistic regression models were used to assess odd ratios (ORs) and 95% confident intervals (CIs).

Results

Among 646 recruited participants, 323 were pancreatic cancer patients and 323 were controls. Multivariate logistic analysis suggested that pancreatic cancer family history (adjusted OR 1.23; 95% CI, 1.11–3.70), obesity (adjusted OR 1.77; 95% CI, 1.22–2.57), diabetes (adjusted OR 2.96; 95% CI, 1.48–5.92) and smoking (adjusted OR 1.78; 95% CI, 1.02–3.10) were risk factors for pancreatic cancer, but that drinking tea (adjusted OR 0.49; 95% CI, 0.25–0.84) was associated with reduced risk of pancreatic cancer.

Conclusions

Cigarette smoking, family history, obesity, and diabetes are risk factors of pancreatic cancer, which is important information for designing early intervention and preventive strategies for pancreatic cancer and may be beneficial to pancreatic cancer control in China.Key words: pancreatic cancer, multicenter, case-control study, risk factor, China     

Complex ovarian cysts in postmenopausal women are not associated with ovarian cancer risk factors. Preliminary data from the plco cancer screening trial

PURPOSE: We assessed whether ovarian abnormalities detected on ultrasound in postmenopausal women are precursors to ovarian cancer.METHODS: We compared the transvaginal ultrasound findings from the initial examination of twenty thousand postmenopausal women enrolled to date in an ongoing randomized trial of cancer screening to data on the established risk factors for ovarian cancer obtained from self-administered questionnaires. We distinguished cysts with the suspicious characteristics of a septum, solid component, irregular or thick wall ("complex cysts") from simple sonolucent cysts with none of those features.RESULTS: High parity, protective for cancer, was negatively associated with complex cysts (Odds Ratio ["OR"] for five or more births versus no births = 0.72, 95% CI = 0.53-0.97), but long-term oral contraceptive use was not (OR = 0.96, 95% CI = 0.76-1.20). A family history of ovarian cancer or multiple breast cancers, a strong risk factor for cancer, was not associated with complex cysts (OR = 0.99, 95% CI = 0.68-1.44). Other abnormalities found on ultrasound (including simple cysts, bilateral cysts, or all abnormalities combined) also did not share the established risk factors for ovarian malignancy. We formed no combination of features of abnormalities (septum, echogenicity, size, or papillary projection) with the cancer risk factor profile.CONCLUSIONS: Although a very small proportion of the clinically silent ovarian abnormalities found on ultrasound are found to be ovarian cancers, the remaining complex cysts and other clinically suspicious abnormalities do not appear to be the immediate precursors of ovarian cancer.     

Association of incident lung cancer with family history of female reproductive cancers: the Iowa Women's Health Study

A number of studies have documented the familial aggregation of lung cancer; there is at least one report that female reproductive cancers are also increased in these families. To determine if the risk exists for all reproductive cancer sites, we conducted a nested case-control study of lung cancer incidence in a cohort of 41,837 women ages 55-69 years. Women were recruited by mail and asked to provide information on education, occupation, smoking habits, physical activity, and family history of specific cancer sites among female relatives. Four year follow-up for cancer incidence was conducted using a state-wide tumor registry. Compared to random controls (n = 1900), cases (n = 152) were more likely to have reported at baseline a sister affected with cancer of the uterus [crude odds ratio (OR) = 3.4, 95% Cl = 1.7-7.0, P less than 0.01], cervix (OR = 3.2, 95% Cl 1.2-8.6, P less than 0.05), or cancer at any site (OR = 1.6, 95% Cl 1.1-2.4, P less than 0.05). A family history of an affected mother with a female reproductive cancer was also more common among the cases, but not statistically significant. Cases were less educated, more likely to work in a technical/industrial setting, less physically active, more likely to smoke, and to smoke for a longer period of time than the controls (all P less than 0.01). These differences reduced the magnitude of the family history risk indicators; only the combined category of reproductive cancer at all sites among sisters remained statistically significant. Additional family studies should be done to assess environmental factors in the relatives of the cases and controls to disentangle the influence of shared genes and shared environmental factors in these associations.     

Intakes of selected nutrients and food groups and risk of ovarian cancer

In a hospital-based case-control study, we examined dietary intakes of selected nutrients and food groups and ovarian cancer risk among 496 women with primary, histologically confirmed epithelial ovarian cancer and 1,425 women with nonneoplastic diagnoses, ages 20-87 years, admitted to Roswell Park Cancer Institute between 1982 and 1998. Data on diet and other relevant risk factors in the few years before admission were collected with a self-administered questionnaire. Odds ratios (OR) and 95% confidence intervals (CI) were estimated by unconditional logistic regression adjusting for age, education, region of residence, regularity of menstruation, family history of ovarian cancer, parity, age at menarche, oral contraceptive use, and energy intake. Women in the highest vs. the lowest quartile of total energy had a weak increase in risk (OR = 1.25, 95% CI = 0.90-1.73). Significantly reduced risks were associated with higher intakes of dietary fiber (OR = 0.57, 95% CI = 0.38-0.87), vitamin A (OR = 0.66, 95% CI = 0.45-0.98), carotenoid (OR = 0.64, 95% CI = 0.43-0.93), vitamin E (OR = 0.58, 95% CI = 0.38-0.88), beta-carotene (OR = 0.68, 95% CI = 0.46-0.98), and total fruit and vegetable intake (OR = 0.62, 95% CI = 0.42-0.92). Our findings suggest that a diet high in plant foods may be important in reducing risk of ovarian cancer.     

Cancer risks among iron and steel workers in Anshan,China, part II: Case-control studies of lung and stomach cancer

Nested case-control interview studies of lung cancer (610 incident cases), stomach cancer (292 incident cases), and 959 controls were conducted to follow up leads from a proportional mortality analysis of deaths among male workers in a large integrated iron-steel complex in Anshan, China. For lung cancer, after adjusting for the significant non-occupational risk factors (smoking, other pulmonary disease, family history of lung cancer, and low consumption of fruit or tea), risks were significantly elevated for those employed for 15 or more years in smelting and rolling (OR = 1.5, CI = 1.1–2.2), in the fire-resistant brick factory (OR = 2.9, CI = 1.4–5.9), in general loading (OR = 2.5, CI = 1.0–6.1), and as coke oven workers (OR = 3.4; CI = 1.4–8.5). For stomach cancer, after adjusting for consumption of pickled vegetables, prior gastric diseases, family history of stomach cancer, low intake of fruits and vegetables, and education, risks were significantly elevated for those employed for 15 or more years in ore sintering and transportation (OR = 2.1, CI = 1.0–4.4), in the fire-resistant brick factory (OR = 2.5, CI = 1.1–5.8), in general loading (OR = 3.2, CI = 1.2–8.9), as boilerworkers and cooks (OR = 2.6, CI = 1.2–5.6), and as coke oven workers (OR = 5.4, CI = 1.8–16.0). For both lung and stomach cancers, significant dose-response gradients were observed for exposure to total dust and benzo(a)pyrene, but not for specific chemical components of dust. Overall, long-term steel workers with exposure to workplace pollutants had a 40% increased risk of both lung and stomach cancers. These case-control studies confirm many of the occupational findings reported in the proportionate mortality analysis, and suggest avenues for further work to evaluate the carcinogenicity of individual components of dust. (This article is a US Government work and, as such, is in the public domain in the United States of America.) © 1996 Wiley-Liss, Inc.