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J R Daling

Publications and source records attributed to J R Daling.

At least 91 records · Page 5Linked to original sources
PubMed1996

BRCA1 mutations in a population-based sample of young women with breast cancer.

BACKGROUND: Inherited mutations in the BRCA1 gene are associated with a high risk of breast and ovarian cancer in some families. However, little is known about the contribution of BRCA1 mutations to breast cancer in the general population. We analyzed DNA samples from women enrolled in a population-based study of early-onset breast cancer to assess the spectrum and frequency of germ-line BRCA1 mutations in young women with breast cancer. METHODS: We studied 80 women in whom breast cancer was diagnosed before the age of 35, and who were not selected on the basis of family history. Genomic DNA was studied for BRCA1 mutations by analysis involving single-strand conformation polymorphisms and with allele-specific assays. Alterations were defined by DNA sequencing. RESULTS: Germ-line BRCA1 mutations were identified in 6 of the 80 women. Four additional rare sequence variants of unknown functional importance were also identified. Two of the mutations and three of the rare sequence variants were found among the 39 women who reported no family history of breast or ovarian cancer. None of the mutations and only one of the rare variants was identified in a reference population of 73 unrelated subjects. CONCLUSIONS: Alterations in BRCA1 were identified in approximately 10 percent of this cohort of young women with breast cancer. The risk of harboring a mutation was not limited to women with family histories of breast or ovarian cancer. These results represent a minimal estimate of the frequency of BRCA1 mutations in this population. Comprehensive methods of identifying BRCA1 mutations and understanding their importance will be needed before testing of women in the general population can be undertaken.

Adult↗
PubMed1996

Risk of breast cancer in a cohort of infertile women.

The purpose of this study was to assess: (1) the risk of breast cancer associated with use of ovulation-inducing agents (such as clomiphene citrate) as treatment for infertility; and (2) the risk associated with ovulatory abnormalities that result in infertility. We performed a case-cohort study among 3837 women evaluated for infertility at clinics in Seattle, Washington, at some time during 1974-1985. Computer linkage with a population-based tumor registry was used to identify women diagnosed with breast cancer before January 1, 1992. Data regarding infertility testing and treatment were abstracted from the infertility clinic medical records for women who developed breast cancer and a randomly selected subcohort. Twenty-seven women in the cohort developed in situ or invasive breast cancer, in comparison with an expected number of 28.8 cases (standardized incidence ratio, 0.9; 95% confidence interval (CI), ).6-1.4). Infertile women with evidence of an ovulatory abnormality were at a risk of breast cancer similar to that of women whose infertility was believed to be due to other causes. The risk among women who had taken clomiphene was reduced relative to infertile women who had not used this drug (adjusted relative risk, 0.5; 95% CI, 0.2-1.2), but the reduction in risk did not increase with duration of use. The possibility that use of clomiphene as treatment for infertility lowers the risk of breast cancer should be examined in other, larger studies.

Adolescent↗
PubMed1996

Incomplete pregnancies and risk of ovarian cancer (Washington, United States).

Because of the reduced risk of ovarian cancer related to prior full-term pregnancies, we sought to determine whether there was any association with a history of one or more incomplete pregnancies. White female residents of three counties in Washington State (United States) diagnosed with ovarian cancer during 1986-88 (n = 322), and a random sample of control women selected from these same counties (n = 426), were interviewed regarding their pregnancy and childbearing histories. Among women who had given birth to at least one child, an additional incomplete pregnancy was not associated with the risk of ovarian cancer (relative risk [RR] = 1.1, 95 percent confidence interval [CI] = 0.8-1.6, adjusting for age, oral contraceptive use, and number of births). For those who had never given birth, a somewhat smaller proportion of cases had a history of incomplete pregnancy than controls (RR = 0.8, CI = 0.4-1.7). In an analysis restricted to ever-pregnant women, a prior induced or spontaneous abortion was not found to be associated with the incidence of ovarian tumors (RR = 1.0, CI = 0.6-1.7, and RR = 1.3, CI = 0.8-1.9, respectively). Other studies of the possible relation between incomplete pregnancies and ovarian cancer generally have observed either a weak negative association or no association at all. It is possible that if incomplete pregnancies do affect the risk of ovarian cancer, their impact might be too small to be identified reliably through epidemiologic studies.

Abortion, Induced↗
PubMed1996

A population-based study of contralateral breast cancer following a first primary breast cancer (Washington, United States)

To evaluate predictors of contralateral breast cancer risk, we examined data from a nested case-control study of second primary cancers among a cohort of women in western Washington (United States) diagnosed with breast cancer during 1978 through 1990 and identified through a population-based cancer registry. Cases included all women in the cohort who subsequently developed contralateral breast cancer at least six months after the initial diagnosis, but prior to 1992 (n = 234). Controls were sampled randomly from the cohort, matched to cases on age, stage, and year of initial breast cancer diagnosis. Information on potential risk factors for second primary cancer was obtained through medical record abstractions and physician questionnaires. Women who were postmenopausal due to a bilateral oophorectomy (i.e., a surgical menopause) at initial breast cancer diagnosis had a reduction in contralateral breast cancer risk compared with premenopausal women (matched odds ratio [mOR] = 0.25, 95 percent confidence interval [CI] = 0.09-0.68), whereas no reduction in risk was noted among postmenopausal women who had had a natural menopause (mOR = 0.90, CI = 0.39-2.09). Among postmenopausal women, there was a suggestion of a lower risk associated with relatively high parity (2+). A family history of breast cancer was associated with an increased risk (mOR = 1.96, CI = 1.22-5.15) and varied little by menopausal status. Having an initial tumor with a lobular component (c.f. a ductal histology) was not related strongly to risk (mOR = 1.47, CI = 0.79-2.74). The results of the present and earlier studies argue that we have limited ability to predict the occurrence of a contralateral breast tumor. Better predictors will be required before diagnostic and preventive interventions can be targeted to subgroups of patients with unilateral breast cancer.

Adult↗
PubMed1996

Perinatal factors and risk of breast cancer.

A high level of endogenous estrogen in utero has been hypothesized to be a possible risk factor for breast cancer. We used information from two population-based case-control studies to investigate the relation between perinatal factors and risk of invasive breast cancer among women age 21-45 years (746 cases, 960 controls) and women age 50-64 years (401 cases, 439 controls). Breast cancer cases were ascertained through a population-based cancer registry, and controls were selected by random digit dialing. After adjustment for age, menopausal status, and maternal smoking, the birthweight-breast cancer association in women age 21-45 years followed a J-shaped curve, with women whose birthweight was less than 2,500 gm [odds ratio (OR) = 1.3; 95% confidence interval (CI) = 0.9-2.0] and 4,000 gm or more (OR = 1.7; 95% CI = 1.1-2.5) at increased risk. Women age 50-64 years who were 4,000 gm or more at birth appeared to be at slightly reduced risk of breast cancer (OR = 0.6; 95% CI = 0.3-1.1). With the exception of maternal smoking, there was little effect of other perinatal factors on breast cancer risk in either group. These results support the hypothesized association between intrauterine estrogen exposure and subsequent risk of breast cancer.

Adult↗
PubMed1996

Indices of exposure to fetal and sperm antigens in relation to the occurrence of breast cancer.

We used data from a population-based case-control study to evaluate Janerich's hypothesis that reduced risk of breast cancer in women with multiple marriages may be attributable to an immune response to fetal or sperm antigens. Risk of breast cancer in women with multiple marriages was reduced relative to that in women who had been married only once; however, there was no indication that such risk was reduced among women whose full-term pregnancies were fathered by different men, relative to women whose pregnancies were each fathered by the same man. Increasing lifetime number of male sexual partners was associated with a trend of decreasing risk of breast cancer. Our results indicate that, if there are effects of exposure to fetal or male antigens on risk of female breast cancer, their impact may be heterogeneous.

Antigens↗
PubMed1996

Occurrence of breast cancer in relation to recreational exercise in women age 50-64 years.

To investigate the relation between recreational physical activity and breast cancer, we conducted an analysis of a population-based case-control study of women age 50-64 years in western Washington State. The study included 537 patients with breast cancer diagnosed during 1988-1990 and 492 randomly selected population control women. Detailed information on recreational exercise habits and other risk factors for breast cancer was ascertained by structured in-person interviews. A similar proportion of cases and controls reported exercise in the 2 years before the referent date (about 50%), or during ages 12-21 years (about 40%). Compared with women who reported no exercise, there was a slightly decreased risk of breast cancer in women who exercised more than 1.5 hours per week in the 2 years before diagnosis (cases) or referent date (controls) [odds ratio (OR) = 0.7; 95% confidence interval (CI) = 0.4-1.1], or who engaged in at least some high-intensity exercise (OR = 0.7;95% CI = 0.4-1.1), but there was no clear decline in risk at the highest categories of duration or intensity. There was no association between any intensity exercise at ages 12-21 years and risk of breast cancer. These results indicate a weak negative association between physical activity and risk of breast cancer in middle-aged women.

Breast Neoplasms↗
PubMed1996

Breast enlargement and reduction: results from a breast cancer case-control study.

In a population-based case-control study of breast cancer that included 2174 cases and 2009 population controls under 55 years of age, prior breast implants were reported by 36 cases versus 44 controls. After adjustment for the matching factors as well as variables associated with both breast cancer risk and breast enlargement (race, family history of breast cancer, body size, screening history), the relative risk of breast cancer associated with a prior implant was 0.6 (95% CI 0.4-1.0). The reduced risk persisted with increasing interval since surgery, arguing against selection bias as an explanation. Further, although a deficit of in situ tumors was seen among women with implants (RR = 0.2), the risk associated with implants remained reduced for both localized and distant tumors (RR = 0.8 for both stages). In a smaller group of women who had prior breast reduction surgery (10 cases, 13 controls), a reduced risk of breast cancer also was observed (RR = 0.7, 95% CI 0.3-1.6). The results of this study must be interpreted cautiously because of the small number of women involved and reliance on patient reports of prior operations. In not showing any elevation in breast cancer risk following a breast implant, our results confirm several record linkage studies but contradict some clinical studies that suggest an adverse effect. Additional investigations are needed in relation to specific types of breast implants, including the polyurethane-coated implants, which have been linked to high cancer rates in laboratory animals.

Adult↗
PubMed1996

Maternal smoking during pregnancy and the risk of congenital urinary tract anomalies.

To study maternal smoking during pregnancy and the risk of congenital urinary tract anomalies, we interviewed mothers of 118 affected infants born to residents of western Washington State during 1990 and 1991 and mothers of 369 control infants randomly selected from those without birth defects delivered during those years in five hospitals in King County, Washington. Maternal smoking was associated with an increased risk of congenital urinary tract anomalies in offspring (adjusted odds ratio [OR] = 2.3; 95% confidence interval [CI] = 1.2, 4.5). This risk was higher among light smokers (1-1000 cigarettes during the pregnancy) (OR = 3.7; 95% CI = 1.7, 8.6) than among heavy smokers (OR = 1.4; 95% CI = 0.6, 3.3). Our results corroborate previous findings and support the hypothesis of a causal relation.

Adult↗
PubMed1996

Vaginal douching and reduced fertility.

OBJECTIVES: This study investigated douching and reduced fertility. METHODS: The monthly probability of conception for douchers and nondouchers was compared in a sample of 840 married, parous women in King County, Washington. Data on the number of months required to conceive were analyzed. RESULTS: In comparison with nondouchers, women who douched were 30% less likely to become pregnant each month they attempted pregnancy. This relationship remained after adjustment for covariates, and it could not be explained by women douching for medical reasons. The reduction was not related to the type of douching preparation used. Young women who douched had significantly greater reductions in monthly fertility than older women (50% reduction for women 18 to 24 years old, 29% reduction for women 25 to 29 years old, and 6% reduction for women 30 to 39 years old). CONCLUSIONS: Douching was associated with reduced fertility. Further research is needed to determine whether the relationship is casual and, if so, to what extent it is mediated by pelvic infection. In the meantime, women should be informed that douching may have adverse effects.

Adolescent↗
PubMed1996

In situ and invasive cervical carcinoma in a cohort of infertile women.

OBJECTIVE: To assess the risk of cervical neoplasia associated with the use of ovulation-inducing agents such as clomiphene citrate (CC) DESIGN: Case-cohort study. SETTING: Infertility clinics in Seattle, Washington. PATIENTS: A cohort of 3,837 women evaluated for infertility at some time during 1974-1985. MAIN OUTCOME MEASURE: Computer linkage with a population-based tumor registry was used to identify women diagnosed with cervical cancer before January 1, 1992. Data regarding infertility testing and treatment were abstracted from medical records for women who developed cancer and a randomly selected subcohort. RESULTS: Thirty-six women in the cohort developed in situ or invasive cervical cancer in comparison with an expected number of 67.8 cases (standardized incidence ratio = 0.5, 95% confidence interval [CI] 0.4 to 0.7). Infertile women with fallopian tube abnormalities were at an increased risk of cervical cancer relative to women whose infertility was believed to be due to other causes. The risk among women who had taken CC was reduced relative to infertile women who had not used this drug (relative risk = 0.4, 95% CI 0.2 to 0.8). This association was present both in women with and without tubal abnormalities. However, the size of the reduction in risk was not influenced by duration of use. CONCLUSIONS: The hypothesis that use of antiestrogenic agents, such as CC, can lead to a reduced risk of cervical neoplasia warrants testing in other studies.

Adult↗
PubMed1996

The relationship of human papillomavirus-related cervical tumors to cigarette smoking, oral contraceptive use, and prior herpes simplex virus type 2 infection.

It has now been established that infection with human papillomavirus (HPV) is necessary for the development of most cervical cancers. HPV is not sufficient for the development of cancer. Other exposures or host factors are necessary for cancer to occur. As part of an ongoing, population-based case-control study of invasive cervical cancer, we investigated the role of cigarette smoking, oral contraceptive (OC) use, and herpes simplex virus type 2 (HSV-2) as potential cofactors with HPV in the development of cervical cancer. Residents of three counties in western Washington State who were diagnosed with invasive squamous cell cervical cancer (n = 314) from January 1986 through December 1992 were interviewed about their sexual, reproductive, contraceptive, and cigarette smoking histories. Similar information was obtained from control women identified through random digit dialing (n = 672). The sera from 206 cases and 522 controls were tested for both HPV 16 capsid antibodies and HSV-2 antibodies. PCR was used to test paraffin-embedded tumor tissues for the presence of HPV DNA types 6, 16, 18, 31, 33, 35, and 39. Women with cervical cancer were more likely to be current smokers at diagnosis than population controls [relative risk (RR), 2.5; 95% confidence interval (CI), 1.8-3.4]. The risk associated with smoking was present to a similar extent among women positive and negative for HPV as measured by HPV 16 capsid antibodies and HPV DNA in the tumor tissue (cases). OC use was only important if first use was at an early age, particularly ages < or = 17 years (RR, 2.3; 95% CI, 1.4-3.8). There was only a slight risk for cervical cancer associated with antibodies to HSV-2 (RR, 1.2; 95% CI, 0.9-1.7). However, when we stratified by markers of HPV exposure, we found a significant increase in risk associated with HSV-2 among women negative for HPV 16 antibodies (RR, 2.0; 95% CI, 1.3-3.0), which was strengthened when we confined our analysis to cases whose tumors were HPV DNA negative (RR, 3.6; 95% CI, 1.6-8.0). There was no indication that cigarette smoking, OC use, or HSV-2 infection influence the ability of HPV infection to cause invasive cervical cancer. OC use may only be important in the etiology of invasive squamous cell cervical tumors if the use occurs at a critical time in the development of a woman's reproductive tract, at ages < or = 17 years. The majority of risk associated with HSV-2 was confined to HPV-negative tumors, indicating a possible separate pathway to disease that may account for 5-10% of invasive cervical cancers.

Adolescent↗
PubMed1996

Measurement of urinary estrogen metabolites using a monoclonal enzyme-linked immunoassay kit: assay performance and feasibility for epidemiological studies.

We evaluated an enzyme-linked immunoassay kit (Estramet 2/16) for the measurement of 2-hydroxyestrone (2-OH E1) and 16-alpha hydroxyestrone (16 alpha-OH E1), major metabolites of estradiol. Urine samples from 14 healthy premenopausal women on days 1, 8, 15, and 22 of their menstrual cycle were assayed along with standards, kit controls, and in-house controls. The intra-assay percentage CVs of 2-OH E1, 16 alpha-OH E1, and the 2-OH E1: 16 alpha-OH E1 ratio were 6.8, 7.4, and 1.8, respectively; the interassay percentage CVs were 15.3, 30.7, and 23.3, respectively. The assay linearity was between 0 and 40 ng/ml. The mean 2-OH E1:16 alpha-OH E1 ratio was relatively constant throughout the day, but it increased by around 50% between the follicular and luteal portions of the menstrual cycle. Individual reagent kits within each lot for 16 alpha-OH E1 were stable for 2 weeks. There was considerable lot-to-lot variation over a 5-month period. In lots used during the last 2 months of the study, values of 2-OH E1 from in-house controls increased by 30-50%, and those of 16 alpha-OH E1 by 50-100%, relative to values obtained initially on the same samples. Depending on the lot, the ratio of the two metabolites ranged from 2 to 5.5. These data suggest that the assay is useful for studies where samples can be assayed with the same kit lot over a period of not more than 2 weeks, but that it is not now suitable for studies that extend over a long enough period of time so that multiple kit lots are required.

Adolescent↗
PubMed1996

Glutathione S-transferase M1 genotypes and the risk of anal cancer: a population-based case-control study.

Some studies have reported an association of the GSTM1-null genotype with the risk of smoking-related cancers, such as lung, bladder, and colon cancer. Because the risk of anal cancer is strongly associated with a history of cigarette smoking, we examined whether the GSTM1-null genotype is a susceptibility marker for anal cancer. We obtained peripheral blood specimens from residents of western Washington who were diagnosed with squamous or transitional cell tumor of the anus between April 1991 and June 1994. Eligible for inclusion were persons 18-74 years of age, with either invasive or in situ lesions. Specimens were also obtained from controls identified via random-digit dialing of western Washington households. We determined GSTM1 genotypes of 71 cases and 360 controls by PCR using primer pair 5'-AACTCCCTGAAAAGCTAAAGC-3' and 5'-GTTGGGCTCAAATATACGGTGG-3'. The frequency of the GSTM1-null genotype in controls was approximately 57%; this differed little in relation to age, sex and smoking status. The incidence of anal cancer appeared to be reduced in persons with the GSTM1-null genotype; only 39.4% of cases had this genotype (age-adjusted odds ratio = 0.5, 95% confidence interval = 0.3-0.9). This inverse association was restricted to persons who had ever smoked cigarettes and was present in both women and men (and in the latter, in both those who had and did not have a male sexual partner). Our data strongly suggest that persons with the GSTM1-null genotype are not at increased risk of anal cancer, and may well be at a decreased risk.

Adolescent↗
PubMed1995

Population-based study of tamoxifen therapy and subsequent ovarian, endometrial, and breast cancers.

BACKGROUND: The success of tamoxifen in reducing the occurrence of contralateral breast cancer among breast cancer patients in clinical trials has prompted the study of its use in the primary prevention of breast cancer. Long-term risks associated with tamoxifen therapy, however, are still being evaluated, particularly with respect to subsequent cancer occurrence at sites other than the breast. PURPOSE: This population-based, nested case-control study investigated the risks of second primary cancers of the ovary, endometrium, and contralateral breast among women receiving tamoxifen for breast cancer in conventional medical practice. METHODS: A cohort of women diagnosed with breast cancer during 1978 through 1990 was identified from a population-based cancer registry. Case subjects included all women in the cohort who subsequently developed second primary ovarian (n = 39), endometrial (n = 42), or contralateral breast (n = 234) cancer prior to 1992. Control subjects were a random sample of the cohort who did not develop a second primary malignancy; they were matched to the case subjects on age, disease stage, and year of initial breast cancer diagnosis (approximately two control subjects per case subject). Information on tamoxifen use as well as on potential risk factors for the second primary cancers was obtained through medical record abstractions and physician questionnaires. RESULTS: The percentage of women who had received tamoxifen was 18% and 20%, respectively, among ovarian cancer case subjects and control subjects; 26% and 31%, respectively, among endometrial cancer case subjects and control subjects; and 10% and 18%, respectively, among contralateral breast cancer case subjects and control subjects. The mean duration of tamoxifen use was less than 2 years for all groups. The relative risks for ovarian and endometrial cancers in women who took tamoxifen were relatively low but were consistent with no association (for ovarian cancer, matched odds ratio [mOR] = 0.6 and 95% confidence interval [CI] = 0.2-1.8; for endometrial cancer, mOR = 0.6 and 95% CI = 0.2-1.9). Tamoxifen therapy was associated with a decreased risk of contralateral breast cancer (mOR = 0.5; 95% CI = 0.3-0.9), especially if the drug had been taken for more than 1 year (mOR = 0.4; 95% CI = 0.2-0.9) or if the women were postmenopausal at initial breast cancer diagnosis (mOR = 0.4; 95% CI = 0.2-0.8). CONCLUSIONS AND IMPLICATIONS: These data suggest that short durations of tamoxifen therapy are not associated with an increased risk of endometrial or ovarian cancer but are associated with a reduction in contralateral breast cancer risk. It would not be appropriate, however, to generalize these results to women who receive tamoxifen for longer periods.

Adult↗
PubMed1995

Combined estrogen and progestin hormone replacement therapy in relation to risk of breast cancer in middle-aged women.

OBJECTIVE: To determine the risk of breast cancer in relation to the use of combined estrogen and progestin hormone replacement therapy (HRT). DESIGN: A population-based case-control study. SETTING: The general female population of King County in western Washington State. PARTICIPANTS: Middle-aged (50 to 64 years) women, including 537 patients with incident primary breast cancer diagnosed between January 1, 1988, and June 30, 1990, who were ascertained through the Seattle-Puget Sound Surveillance, Epidemiology, and End Results cancer registry and 492 randomly selected control women without a history of breast cancer. MAIN OUTCOME MEASURE: Breast cancer risk in relation to use of menopausal hormones. RESULTS: Menopausal hormones of some type had been used by 57.6% of breast cancer cases and 61.0% of comparison women. The women who had ever taken combined estrogen-progestin HRT, representing 21.5% of cases and 21.3% of controls, were not at increased risk of breast cancer (relative odds [RO] = 0.9; 95% confidence interval [CI], 0.7 to 1.3). Compared with nonusers of menopausal hormones, those who used estrogen-progestin HRT for 8 or more years had, if anything, a reduced risk of breast cancer (RO = 0.4; 95% CI, 0.2 to 1.0). CONCLUSIONS: On the whole, the use of estrogen with progestin HRT does not appear to be associated with an increased risk of breast cancer in middle-aged women. Nonetheless, since the use of combined estrogen-progestin HRT has only recently become prevalent, future investigations must assess whether breast cancer incidence is altered many years after estrogen-progestin HRT has been initiated, particularly among long-term users.

Breast Neoplasms↗
PubMed1995

Oral contraceptives and breast cancer risk among younger women.

BACKGROUND: Several studies have suggested a link between oral contraceptive use and breast cancer in younger women, but it is possible that chance or bias, including selective screening of contraceptive users, contributed to the putative association. PURPOSE: Given that oral contraceptives were first marketed in the United States in the early 1960s, we conducted a population-based case-control study to examine the relationship between use of oral contraceptives and breast cancer among women in a recently assembled cohort, focusing on women younger than 45 years of age who had the opportunity for exposure throughout their entire reproductive years. METHODS: Breast cancer patients and healthy control subjects were identified, the latter group by random-digit dialing, in Atlanta, Ga., Seattle/Puget Sound, Wash., and central New Jersey. In Seattle and New Jersey, the study was confined to women 20 through 44 years of age; in Atlanta the age range was extended through 54 years. Patients included women with in situ or invasive breast cancer newly diagnosed during the period of May 1, 1990, through December 31, 1992. In-person interviews were completed by 2203 (86.4%) of 2551 eligible patients and 2009 (78.1%) of 2571 eligible control subjects. Analyses focused on women younger than 45 years of age (1648 patients and 1505 control subjects) to maximize opportunities for extended exposure. Logistic regression analyses were used to obtain maximum likelihood estimates of relative risks (RRs) and their 95% confidence intervals (CIs). RESULTS: Among women younger than 45 years, oral contraceptive use for 6 months or longer was associated with an RR for breast cancer of 1.3 (95% CI = 1.1-1.5). Risks were enhanced for breast cancers occurring prior to age 35 years (RR = 1.7; 95% CI = 1.2-2.6), with the RR rising to 2.2 (95% CI = 1.2-4.1) for users of 10 or more years. The RR for breast cancer for those whose oral contraceptive use began early (before age 18 years) and continued long-term (> 10 years) was even higher (RR = 3.1; 95% CI = 1.4-6.7). The RRs observed for those who used oral contraceptives within 5 years of cancer diagnosis were higher than for those who had not, with the effect most marked for women younger than age 35 years (RR = 2.0; 95% CI = 1.3-3.1). Oral contraceptive associations were also strongest for cancers diagnosed at advanced stages. Evaluation of screening histories and methods of diagnosis failed to support the speculation that associations could be due to selective screening. Among women 45 years of age and older, no associations of risk with use of oral contraceptives were noted. CONCLUSIONS: The relationship between oral contraceptives and breast cancer in young women appears to have a biologic basis rather than to be an artifact or the result of bias.

Adult↗