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."     

Association of parity and ovarian cancer risk by family history of breast or ovarian cancer in a population-based study of postmenopausal women.

Although parity is associated with a decreased risk of ovarian cancer in the general population, this association among women with a family history is less clear. We examined this question in a prospective cohort of 31,377 Iowa women 55-69 years of age at baseline. Relative risks (RRs) and 95% confidence intervals (CIs) were estimated through Cox regression. We identified 181 incident epithelial ovarian cancers through 13 years of follow-up. At baseline, 14% of the women reported breast or ovarian cancer in a first-degree relative, and an additional 12% reported a family history in a second-degree relative. Among women without a family history of breast or ovarian cancer in a first-degree relative, nulliparous women were at slightly increased risk of ovarian cancer (RR = 1.4, 95% CI = 0.9-2.4) compared with parous women, whereas among women with a family history, nulliparous women were at a much higher risk (RR = 2.7, 95% CI = 1.1-6.6) than parous women. Similar results were seen when family history included first- or second-degree relatives with breast or ovarian cancer or a first- or second-degree relative with ovarian cancer only. Nulliparity may be more strongly associated with an increased risk of ovarian cancer among women with a family history of breast or ovarian cancer, compared with women who do not have a family history of those cancers.     

Breast cancer incidence in women with abnormal cytology in nipple aspirates of breast fluid.

This is a prospective study of breast cancer risk in relation to nipple aspirate fluid cytology in 2,701 volunteer white women from the San Francisco Bay Area first enrolled between 1973 and 1980. The women were not pregnant or lactating and were free of breast cancer within 6 months of entry into the study. The breast cancer status of this cohort was determined between June 1988 and April 1991. Follow-up was complete for 87% (n = 2,343) of the cohort, representing 29,961 person-years and an average of 12.7 years of follow-up. The overall breast cancer incidence was 4.4% (104 of 2,343) and rose with fluid cytology findings as follows: no fluid obtained, 2.6% (9 of 352); unsatisfactory specimen, 4.8% (15 of 315); normal cytology, 4.3% (56 of 1,291); epithelial hyperplasia, 5.5% (18 of 327); and atypical hyperplasia, 10.3% (6 of 58). Relative risks for breast cancer and their 95% confidence intervals were estimated by Cox regression, adjusting for age and year of entry. Compared with the relative risk for women who yielded no fluid, relative risks were: unsatisfactory specimen, relative risk (RR) = 1.4 (95% confidence interval (CI) 0.6-3.3); normal cytology, RR = 1.8 (95% CI 0.9-3.6); epithelial hyperplasia, RR = 2.5 (95% CI 1.1-5.5); and atypical hyperplasia, RR = 4.9 (95% CI 1.7-13.9). These findings were strongest for and were mainly confined to women aged 25-54 years. Women with atypical hyperplasia and a first-degree family history of breast cancer were six times more likely to develop breast cancer than were women with atypical hyperplasia but without a family history of breast cancer (95% CI 1.0-30.2). These findings provide strong support for our hypothesis that hyperplasia and atypical hyperplasia diagnosed in nipple aspirates of breast fluid are associated with an increased risk of breast cancer.     

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.     

Association between family history of cancer and breast cancer defined by estrogen and progesterone receptor status

There are recent data to suggest that risk factors for breast cancer may differ according to whether the tumor expresses detectable levels of the estrogen receptor (ER) and progesterone receptor (PR). While a family history of breast cancer is one of the most consistent predictors of the disease, we recently reported a modest inverse association with ER+PR− tumors. However, the definition of a family history of cancer did not consider second-degree relatives or cancer sites that may be etiologically related. The current report presents additional data analysis from the Iowa Women's Health Study, a prospective population-based cohort study conducted among 41,837 postmenopausal women. At baseline in 1986, respondents provided information on family history of cancers of the breast, ovaries, or uterus/endometrium in their mothers, sisters, daughters, maternal and paternal grandmothers, and maternal and paternal aunts. Data on family history of prostate cancer in fathers and brothers and age at onset of breast cancer in mothers and sisters were collected in 1992. Cohort members were followed for cancer incidence through the statewide tumor registry. After 7 years and more than 235,000 person-years of follow-up, 939 incident cases of breast cancer were identified. Information was obtained from the tumor registry on ER (+/−) and PR (+/−) status for 610 cases (65.0%). A family history of breast cancer in first-degree relatives was associated with increased risk (relative risk [RR] = 1.4; 95% confidence interval [CI]: 1.1–1.6) for all receptor-defined subtypes of breast cancer except ER+PR− tumors (RR = 0.7; 95% CI: 0.3–1.4). These results were unchanged when data on second-degree relatives were included. When the onset of breast cancer in relatives occurred at or before the age of 45 years, increased risks were evident only for ER−PR+ and ER−PR− tumors (RR = 2.3 and 3.3, respectively). Conversely, when relatives were affected with breast cancer after the age of 45 years, increased risks were most apparent for ER+PR+ and ER−PR+ tumors (RR = 1.3 and 3.2, respectively). A family history of prostate cancer in first-degree relatives was associated with a 1.2-fold increased risk of breast cancer (95% CI: 0.98–1.50), largely a reflection of the association with ER−PR− tumors (RR = 1.5; 95% CI: 0.8–3.0). The small numbers of cases in some categories and the corresponding wide CIs preclude definitive conclusions, but these data are at least suggestive that joint stratification of breast tumors on ER and PR status may be useful in partitioning breast cancer families into more homogeneous subsets. © 1996 Wiley-Liss, Inc.     

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.     

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.     

Health effects of dioxin exposure: a 20-year mortality study

Follow-up of the population exposed to dioxin after the 1976 accident in Seveso, Italy, was extended to 1996. During the entire observation period, all-cause and all-cancer mortality did not increase. Fifteen years after the accident, mortality among men in high-exposure zones A (804 inhabitants) and B (5,941 inhabitants) increased from all cancers (rate ratio (RR) = 1.3, 95% confidence interval (CI): 1.0, 1.7), rectal cancer (RR = 2.4, 95% CI: 1.2, 4.6), and lung cancer (RR = 1.3, 95% CI: 1.0, 1.7), with no latency-related pattern for rectal or lung cancer. An excess of lymphohemopoietic neoplasms was found in both genders (RR = 1.7, 95% CI: 1.2, 2.5). Hodgkin's disease risk was elevated in the first 10-year observation period (RR = 4.9, 95% CI: 1.5, 16.4), whereas the highest increase for non-Hodgkin's lymphoma (RR = 2.8, 95% CI: 1.1, 7.0) and myeloid leukemia (RR = 3.8, 95% CI: 1.2, 12.5) occurred after 15 years. No soft tissue sarcoma cases were found in these zones (0.8 expected). An overall increase in diabetes was reported, notably among women (RR = 2.4, 95% CI: 1.2, 4.6). Chronic circulatory and respiratory diseases were moderately increased, suggesting a link with accident-related stressors and chemical exposure. Results support evaluation of dioxin as carcinogenic to humans and corroborate the hypotheses of its association with other health outcomes, including cardiovascular- and endocrine-related effects.     

Familial aggregation of breast cancer with early onset lung cancer.

Site-specific familial aggregation and evidence supporting Mendelian codominant inheritance have been shown in lung cancer. In characterizing lung cancer families, a number of other cancers have been observed. The current study evaluates whether first-degree relatives of early onset lung cancer cases are at increased risk of breast cancer. Families were identified through population-based lung cancer cases and controls under 40 years of age. Cases were ascertained through the Metropolitan Detroit SEER registry; controls through random-digit dialing. Data were available for 384 female relatives of 118 cases and 465 female relatives of 161 controls. Breast cancer in relatives was evaluated after adjusting for age, race, sex, and smoking status of each family member and the sex and age of the probands. A positive family history of early onset lung cancer increased breast cancer risk among first-degree relatives 5. 1-fold (95% CI, 1.7-15.1). Relatives of cases with adenocarcinoma of the lung were at highest risk (RR = 6.3, 95% CI 2.0-20). Mean age of breast cancer diagnosis among relatives of cases was 52.2 years and not statistically different from relatives of controls. Three case families also reported early ovarian cancers (mean age of diagnosis of 35 years). These findings suggest that shared susceptibility genes may act to increase risk of early onset lung and breast cancer in families.     

Retrospective cohort mortality study of workers engaged in motion picture film processing

OBJECTIVE: To assess potential health risks associated with work in a large motion picture film-processing facility. METHODS: A retrospective cohort mortality study was conducted during 1960-2000 among 2646 film workers. Job family categories, created from detailed employee work history information, were used to evaluate chemical exposure patterns. RESULTS: Overall mortality was as expected (standardized mortality ratio [SMR] = 1.1; 95% confidence interval [CI] = 1.0-1.2). Statistically significant associations were found for suicides (SMR = 2.0; 95% CI = 1.2-3.0) among the hourly workers and AIDS (SMR = 5.3; 95% CI = 1.7-12.3) among the administrative workers. Film developers had increases of respiratory cancer (SMR = 1.9; 95% CI = 1.1-3.0) and suicides (SMR = 2.4; 95% CI = 1.0-4.7), whereas film assemblers had an increase in suicides (SMR = 2.4; 95% CI = 1.2-4.4) only. CONCLUSIONS: Excess deaths resulting from suicides and AIDS among the workforce suggest that nonoccupational influences may be involved in the mortality of this cohort and warrant further investigations.     

Validation of family history data in cancer family registries

BACKGROUND: Although family history information on cancer is used to infer risk of the disease in population-based, case-control, cohort, or family-based studies, little information is available on the accuracy of a proband's report. In this study, we sought to determine the validity of the reporting of family history of cancer by probands in population-based and clinic-based family registries of breast, ovarian, and colorectal cancers. METHODS: To assess the accuracy of probands' reported family history of cancer in their relatives, we compared the family history from the personal interview of each proband to a reference standard that included pathology reports, self-reports, or death certificates on the relatives. Our study included 1111 families that accounted for 3222 relatives who were verified. To account for within-family correlations in the responses, we used a generalized estimating equation approach. RESULTS: The probability of agreement between the proband-reported cancer status in a relative with the reference standard varied by cancer site and by degree of relationship to the proband. This probability for first-degree relatives was 95.4% (95% confidence interval [CI]=92.6-98.3) for female breast cancer; 83.3% (95% CI=72.8-93.8) for ovarian cancer; 89.7% (95% CI=85.4-94.0) for colorectal cancer; and 79.3% (95% CI=70.0-88.6) for prostate cancer. CONCLUSIONS: We found high reliability of probands' reporting on most cancer sites when they reported on first-degree relatives and moderate reliability for their reporting on second- and third-degree relatives. Overreporting of cancer was rare (2.4%). Race or ethnicity and gender of the proband did not influence the accuracy of reporting. However, degree of relationship to the proband, type of cancer, age at diagnosis of the proband, and source of ascertainment of probands were statistically significant predictors of accuracy of reporting.     

A prospective study of the development of breast cancer in 16,692 women with benign breast disease

The authors studied the relation between benign breast disease and subsequent breast cancer in 16,692 women with biopsy-diagnosed benign breast disease who had participated in the Breast Cancer Detection Demonstration Project throughout the United States. Women were classified into one of five benign breast disease categories: atypical hyperplasia, proliferative disease without atypia, nonproliferative disease, fibroadenoma, and other benign breast disease. A total of 485 incident cases of breast cancer were identified in the women from August 1973 to February 1986 after a median follow-up period of 8.3 years from the diagnosis of benign breast disease. Age-adjusted incidence rates were calculated for benign breast disease types stratified by family history and calcification status. Relative risk (RR) estimates of breast cancer for women in the five benign breast disease categories, compared with the screened women who did not develop recognizable breast disease (normal subjects), were computed using the proportional hazards model. Results indicated that risk was associated with the degree of epithelial atypia. Over all age groups, women with nonproliferative disease, proliferative disease without atypia, and atypical hyperplasia displayed progressively increasing risks of 1.5, 1.9, and 3.0, respectively, compared with normal subjects, with 95% confidence intervals (CI) exceeding unity. Particularly high risk was seen among women under age 46 years with atypical hyperplasia (RR = 5.7, 95% CI 3.0-10.6). Women with fibroadenoma as the only indication of their benign breast disease had a relative risk of 1.7, with a lower 95% confidence limit of 1.0. No increased risk was seen for women with other benign breast disease. Positive family history (RR = 1.8) and calcification (RR = 1.2) significantly increased a woman's risk proportionately over the risk associated with each benign breast disease subtype. The authors conclude that the risk of developing breast cancer varies by category of benign breast disease and is directly related to the degree of epithelial atypia.     

Cancer risk assessment: quality and impact of the family history interview

BACKGROUND: Identification of individuals at high risk for colon and breast cancer requires an adequate family history assessment and can influence cancer screening and genetic testing decisions. Little data exist that evaluate the completeness of the family history interview in primary care. METHODS: Retrospective chart review of 995 new patient visits to 28 primary care physicians evaluating the completeness of the family cancer history for colon or breast cancer. Family history information was evaluated for inclusion of age at diagnosis, degree of kinship, and specification of disease of interest. RESULTS: Family history information on cancer diagnoses was collected on 679 (68%) of the patients. Specific information regarding the individual affected and the cancer diagnosis was present in 414 (61%) of the records. Affected first-degree relatives were more likely to have their age of cancer diagnosis recorded than second-degree relatives (39%, 95% confidence interval [CI]=34%-44% vs 16%, 95% CI=12%-20%). Age at diagnosis of cancer in first-degree relatives was documented in 51% of colon cancers, 38% of breast cancers, and 27% of ovarian cancers. Only 17% of individuals who meet criteria for early-onset breast cancer genetic testing were referred for genetic services. CONCLUSIONS: Adequate cancer risk assessment using family history information requires age at cancer diagnosis and specification of a cancer diagnosis. Age at diagnosis was frequently missing from family history assessments, which could have a potential impact on identification of high-risk individuals. When family history information does identify high-risk individuals, only the minority are referred for genetic services.     

Family breast cancer history and mammography: Framingham Offspring Study.

The authors examined mammography use according to family cancer history and identified predictors of recent use (相似文献   

Cancer incidence in a cohort of infertile women

To explore further the relation between infertility and breast and female reproductive cancers, cancer incidence among 2,632 Israeli women treated for infertility between 1964 and 1974 was evaluated. Cancer incidence through December 1981 was determined by matching the study cohort to the Israel Cancer Registry. The observed number of cancers was compared with sex-age-ethnic and calendar-year, site-specific national cancer rates. There were 42 cancers observed compared with 37.4 expected, yielding a standardized incidence ratio of 1.1 (95% confidence interval (CI) = 0.8-1.5). Analysis by infertility diagnosis demonstrated no significant excess of total cancer incidence; the standardized incidence ratio was 1.3 (95% CI = 0.8-1.8) for infertility due to hormonal deficiency, 0.7 (95% CI = 0.3-1.4) for mechanical infertility, 1.6 (95% CI = 0.6-3.6) for infertility of the male partner, and 1.1 (95% CI = 0.5-2.2) for unclassified diagnosis. Site-specific analyses revealed a significantly increased risk (8.0; 95% CI = 2.5-19.3; four cases observed, 0.50 expected) of endometrial cancer for the hormonal group and a nonsignificant excess of breast cancer and melanoma. Although numbers were small, women with disorders causing unopposed estrogen production had a risk of 1.4 (95% CI = 0.8-2.2) for all cancer sites, which reached 10.3 (95% CI = 2.6-28.2; three cases observed, 0.29 expected) for endometrial cancer and 1.8 (95% CI = 0.8-3.4; eight cases observed, 4.43 expected) for breast cancer. Among women with nonhormonal infertility, there was a suggestion of increased risks of carcinoma of the ovary (3.2; 95% CI = 0.3-32.9; two cases observed, 0.63 expected) and thyroid (3.0; 95% CI = 0.3-24.6; two cases observed; 0.67 expected). No evidence of an association between ovulation-inducing drugs and cancer was found. This study supports the hypothesis that infertility caused by hormone deficiency is a risk factor for uterine cancer, but is inconclusive regarding breast cancer.     

Mammographic parenchymal patterns as indicators of breast cancer risk

Mammographic parenchymal patterns have been suggested as indicators of breast cancer risk. However, few well-controlled studies have used prediagnostic mammograms to determine the pattern classification. The authors studied 266 cases of breast cancer and 301 controls from 25 screening centers of the Breast Cancer Detection and Demonstration Project, a nationwide screening program conducted between 1973 and 1980 to evaluate the risk associated with mammographic patterns using mammograms taken four years before the detection of breast cancer. Mammograms of the cancerous breast of cases and of the ipsilateral breast in the control matched to each case were blindly assessed by one of the investigators (J.N.W.), originator of the mammographic pattern classification. The breast cancer odds ratio among women with the combined P2 + DY patterns, compared with women with the N1 pattern, was 2.8 (95% confidence interval (CI): 1.6-5.1). This estimate of relative risk was comparable with the risk associated with other recognized breast cancer risk factors. The odds ratio among P2 + DY women with a first-degree family history of breast cancer was 5.5 (95% CI: 2.6-11.8) compared with N1 women without a family history. These data provide additional evidence that mammographic patterns are indicators for subsequent development of breast cancer, particularly among women with a first-degree family history of this malignancy.     

Breast cancer risk associated with proliferative disease, age at first birth, and a family history of breast cancer

The authors reevaluated 10,542 consecutive breast biopsies of women who presented at three Nashville hospitals. Median follow-up was 17 years for 3,398 women (84.4% of patients originally selected for follow-up). Breast cancer relative risks associated with no proliferative disease, proliferative disease without atypia, and atypical hyperplasia were 0.80, 1.4, and 4.0 times that for women from the Cancer in Connecticut data base, respectively (adjusted for age at biopsy, year of biopsy, and length of follow-up). Nulliparous women were at increased risk of breast cancer (relative risk = 1.6; 95% confidence interval (CI) = 1.1-2.2). Women who gave birth to their first child before age 21 years had a relative risk of 0.80, with higher cancer risks associated with later age at first birth. The effect of age at first birth on cancer risk followed a similar pattern within the no proliferative disease, proliferative disease without atypia, and atypical hyperplasia groups. Nulliparous women with atypical hyperplasia had a relative risk of 4.9 (95% CI = 2.7-8.9), while women with no proliferative disease who gave birth before age 21 years had a relative risk of 0.50 (95% CI = 0.19-1.3). Nulliparous women with a family history of breast cancer had a relative risk of 2.7 (95% CI = 1.4-5.2). Women with a family history who first gave birth by age 20, between ages 21 and 29, and after age 30 years had relative risks of 0.53, 2.1, and 4.0, respectively (95% CI = 0.08-3.8, 1.1-3.9, and 1.8-9.6, respectively). Breast size had no effect on cancer risk in women without proliferative disease. However, in women with proliferative disease, small, medium, and large breasts were associated with relative risks of 1.2, 1.4, and 2.1, respectively.     

Active and passive smoking and risk of breast cancer by age 50 years among German women

Recent studies suggest that both active and passive smokers have an increased risk of breast cancer compared with women who have never been either actively or passively exposed. Data on lifetime active and passive smoking were collected in 1999-2000 from 468 predominantly premenopausal breast cancer patients diagnosed by age 50 years and 1,093 controls who had previously participated in a German case-control study conducted in 1992-1995. Compared with never active/passive smokers, former smokers and current smokers had odds ratios of 1.2 (95% confidence interval (CI): 0.8, 1.7) and 1.5 (95% CI: 1.0, 2.2), respectively, and ever active smokers had an odds ratio of 1.3 (95% CI: 0.9, 1.9). The risk increased with duration of smoking and decreased after cessation of smoking. Among never active smokers, ever passive smoking was associated with an odds ratio of 1.6 (95% CI: 1.1, 2.4). Exposure to environmental tobacco smoke during childhood or before the first pregnancy did not appear to increase breast cancer risk. At greatest risk were women who had a high level of exposure to both passive and active smoking (odds ratio = 1.8, 95% CI: 1.2, 2.7). This study strengthens the hypothesis of a causal relation between active and passive smoke exposures and breast cancer risk.     

Cancer risk at sites other than the breast following augmentation mammoplasty

PURPOSE: There has been limited investigation of cancer risk other than breast cancer among patients with breast implants, despite some clinical and laboratory evidence suggesting links with certain cancer sites, including hematopoietic and connective tissue malignancies. METHODS: A retrospective cohort study of 13,488 patients who received cosmetic breast implants at 18 plastic surgery practices in six geographic areas was conducted to assess long-term health effects. After an average of 12 years of follow-up, questionnaires were administered to subjects located and alive (78% of eligible population). Attempts were made to obtain death certificates for deceased subjects and medical verification for all reported cancers. Expected numbers of cancers were derived using general population cancer incidence rates and an internal comparison series of 3936 patients who received other types of plastic surgery at the same practices as the implant patients. RESULTS: A total of 359 malignancies was observed versus 295.95 expected based on general population rates, resulting in a standardized incidence ratio (SIR) of 1.21 [95% confidence interval (CI) 1.1-1.4]. Individual malignancies for which incidence was significantly elevated included cancers of the stomach (SIR = 2.65), cervix (SIR = 3.18), vulva (SIR = 2.51), brain (SIR = 2.16), and leukemia (SIR = 2.19). No excess risks were observed for other hematopoietic malignancies, including multiple myeloma. The internal analyses, however, based on cancer rates derived among the comparison patients, showed no increased cancer risk among the implant patients [relative risk (RR) = 1.00, 95% CI 0.8-1.2], as well as no statistically significant elevations for most individual sites. Cervical cancer continued to be elevated (RR = 1.78), although to a lesser extent than in the external analyses, while the risk for respiratory cancers was higher (RR = 2.40). Non-significant elevations in risk persisted in this analysis for liver cancer (RR = 2.65), brain cancer (RR = 2.83), and leukemia (RR = 1.83). Many of the cancers showing excesses were defined on the basis of death certificates, requiring caution in interpretation. The histologies of the leukemias were quite varied, which makes a biologic relationship appear unlikely. However, respiratory cancers showed some evidence of increasing risk with follow-up time and both respiratory and brain cancers were elevated in the mortality analyses. CONCLUSIONS: Although excesses of cervical and vulvar cancer among implant patients might be attributable to lifestyle factors, reasons for excesses of respiratory and brain cancers were less apparent.     

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.