Risk Of Early-onset Breast Cancer Research Articles

Insulin-like growth factor-1 genotype predicts breast volume after pregnancy and hormonal contraception and is associated with circulating insulin-like growth factor-1 levels: implications for risk of early-onset breast cancer in young women from hereditary breast cancer families

BRCA1/2 mutations predispose to early-onset breast cancer, especially after oral contraceptive (OC) use and pregnancy. However, the majority of breast cancers might be due to more prevalent low penetrance genes that may also modify the risk in BRCA1/2 mutation carriers. The absence of the IGF1 19-CA repeat allele has been associated with high insulin-like growth factor-1 (IGF-1) levels during OC use in nulliparous women of four different ethnic groups. High IGF-1 levels are linked to an increased risk of early-onset breast cancer and to larger breast volumes in the general population. It has also been hypothesized that women whose breast size increases while exposed to OCs may be at increased risk of future breast cancer. We explored the effect of the IGF1 genotype, specifically the absence of the common 19-CA repeat allele in the promoter region of the IGF1 gene, in combination with oral contraceptive (OC) use or parity on breast volume and IGF-1 levels. Two hundred fifty-eight healthy women, </=40 years old, from hereditary breast cancer families participated in this prospective study. Twenty-three women were known BRCA1 mutation carriers, 7 women were known BRCA2 mutation carriers, 54 women were noncarriers from BRCA1/2 families, 111 women belonged to breast cancer families where no BRCA1 or BRCA2 mutations were detected, and 63 women were untested from high-risk breast cancer families. All women completed a questionnaire including information on reproductive factors and OC use. We measured height, weight, breast volumes, and plasma IGF-1 levels once during menstrual cycle days 5-10 and once again during menstrual cycle days 18-23. The IGF1 genotype was successfully analyzed with polymerase chain reaction and fragment analyses in 254 women. Thirteen percent had no IGF1 19-CA repeat allele. The absence of the 19-CA repeat allele was more common among women with known BRCA1 mutations compared to other women (26% versus 12%; P= 0.05). See updated and revised Table 1 from original publication. IGF-1 levels were similar among parous and nulliparous women not using OCs, which is in contrast to results from women in the general population, where parous women have lower IGF-1 levels than nulliparous women. Furthermore, OC use did not affect IGF-1 levels in parous women in our study. BRCA mutation status did not affect age-adjusted IGF-1 levels in either cycle phase among nonusers. Most of the nulliparous OC users had lower IGF-1 levels than nonusers. However, there was an interaction between IGF1 genotype and OC use on IGF-1 levels in nulliparous women (P= 0.026). Compared with nonusers, IGF-1 levels were highly suppressed in OC users with a 19-CA repeat allele (P < 0.001), but not among women lacking the 19-CA repeat allele (P= 0.81). We also observed an interaction between parity and IGF1 genotype on breast volume (P= 0.01). Absence of the 19-CA repeat allele was associated with larger breast volumes in parous versus nulliparous women and OC users, while parous women and OC users with the 19-CA repeat allele had smaller breast volumes than nulliparous women and nonusers adjusted for body weight. During follow-up, six incident breast cancers cases occurred, four in known BRCA1 mutation carriers and two in untested women. Incident breast cancers were associated with absence of the 19-CA repeat allele (log-rank; P= 0.002). Our results suggest that absence of the IGF1 19-CA repeat allele modifies IGF-1 levels, breast volume, and possibly early-onset breast cancer risk after hormone exposure in young, high-risk women. These results warrant confirmation in a larger prospective cohort of high-risk women. If confirmed, the IGF1 genotype could be incorporated as an additional marker to improve risk estimates for early-onset breast cancer during genetic counseling of women from high-risk breast cancer families.

Testosterone levels in relation to oral contraceptive use and the androgen receptor CAG and GGC length polymorphisms in healthy young women

The combined effect from the androgen receptor (AR) CAG and GGC length polymorphisms on testosterone levels has not been studied in young women. Testosterone levels were measured in blood drawn on both menstrual cycle days 5-10 and 18-23 in 258 healthy women, aged < or =40 years, from high-risk breast cancer families. CAG and GGC length polymorphisms were analysed by PCR and fragment analyses. All women completed a questionnaire including information on oral contraceptive (OC) use and reproductive factors. OC users had lower median testosterone levels than non-users during cycle days 5-10 and 18-23 (P < or = 0.005 for both). The BRCA mutation status was associated neither with testosterone levels nor with CAG or GGC length polymorphism. The CAG length polymorphism was not associated with testosterone levels. The cumulative number of long GGC alleles (> or =17 repeats) was significantly associated with lower testosterone levels in OC users during cycle days 5-10 (P(trend) =0.014), but not during cycle days 18-23 or in non-users. The interaction between the GGC length polymorphism and OC status was highly significant during cycle days 5-10 (P = 0.002) and near-significant during days 18-23 (P = 0.07). Incident breast cancer was more common in women with two short GGC alleles (log-rank P = 0.003). The GGC repeat length was the only significant genetic factor modifying the testosterone levels in current OC users from high-risk families. Homozygosity for the short GGC allele may be linked to the increased risk of early-onset breast cancer after OC exposure in high-risk women.

Oral Contraceptive Use and Risk of Early-Onset Breast Cancer in Carriers and Noncarriers of BRCA1 and BRCA2 Mutations

Oral Contraceptive Use and Risk of Early-Onset Breast Cancer in Carriers and Noncarriers of BRCA1 and BRCA2 Mutations

Impact of teenage oral contraceptive use in a population-based series of early-onset breast cancer cases who have undergone BRCA mutation testing

Oral contraceptive (OC) use in young women has been associated with an increased risk of breast cancer. This matched case-control study aims to elucidate the combined effects of OC use and genetic factors in a population-based series of BRCA1/2 mutation-tested early-onset breast cancers. A first invasive breast cancer was diagnosed in 259 women aged ⩽40 years between 1990 and 1995 in the South Swedish Health Care Region. A total of 245 women were included in this study. Information on family history of cancer, reproductive factors, smoking and OC use was obtained from questionnaires or patient charts. Three age-matched controls per case were chosen from a prospective South Swedish cohort. Ever OC use and current OC use were not associated with breast cancer. Cases were more likely to have used OCs before age 20 years (adjusted odds ratio (OR) 2.10 (95% CI 1.32–3.33)) and before their first child (adjusted OR 1.63 (95% CI 1.02–2.62)). When stratified by age, the effect of early OC use was limited to women diagnosed prior to age 36 years (OR 1.53 (1.17–1.99) per year of OC use prior to age 20 years). The risks were similar for low-dose and high-dose OCs. The probability of being a BRCA1/2 mutation carrier was three times higher among cases who started OC use prior to age 20 years compared with cases who started at age 20 years or older or who had never used OCs. However, the duration of OC use was similar among cases with and without BRCA1/2 mutations. No association was seen with a first-degree family history of breast cancer. Each year of OC use prior to age 20 years conferred a significantly increased risk for early-onset breast cancer, while there was no risk associated with use after age 20 years.

DNA damage among thyroid cancer and multiple cancer cases, controls, and long-lived individuals

Variation in the detection, signaling, and repair of DNA damage contributes to human cancer risk. To assess capacity to modulate endogenous DNA damage among radiologic technologists who had been diagnosed with breast cancer and another malignancy (breast-other, n = 42), early-onset breast cancer (early-onset, age ≤35; n = 38), thyroid cancer ( n = 68), long-lived cancer-free individuals (hyper-normals, n = 20) and cancer-free controls ( n = 49) we quantified DNA damage (single strand breaks and abasic sites) in untreated lymphoblastoid cell lines using the alkaline comet assay. Komet™ software provided comet tail length, % DNA in tail (tail DNA), comet distributed moment (CDM), and Olive tail moment (OTM) summarized as the geometric mean of 100 cells. Category cut-points (median and 75th percentile) were determined from the distribution among controls. Tail length (for ≥75% versus below the median, age-adjusted) was most consistently associated with the highest odds ratios in the breast-other, early-onset, and thyroid cancer groups (with risk increased 10-, 5- or 19-fold, respectively, with wide confidence intervals) and decreased risk among the hyper-normal group. For the other three comet measures, risk of breast-other was elevated approximately three-fold. Risk of early-onset breast cancer was mixed and risk of thyroid cancer ranged from null to a two-fold increase. The hyper-normal group showed decreased odds ratios for tail DNA and OTM, but not CDM. DNA damage, as estimated by all comet measures, was relatively unaffected by survival time, reproductive factors, and prior radiation treatment. We detected a continuum of endogenous DNA damage that was highest among cancer cases, less in controls, and suggestively lowest in hyper-normal individuals. Measuring this DNA damage phenotype may contribute to the identification of susceptible sub-groups. Our observations require replication in a prospective study with a large number of pre-diagnostic samples.

Oral contraceptive use and the risk of early-onset breast cancer in carriers and noncarriers ofBRCA1andBRCA2mutations

Oral contraceptive use and the risk of early-onset breast cancer in carriers and noncarriers of<i>BRCA1</i>and<i>BRCA2</i>mutations

Oral contraceptive use and the risk of early-onset breast cancer in carriers and noncarriers of BRCA1 and BRCA2 mutations

Oral contraceptive use and the risk of early-onset breast cancer in carriers and noncarriers of BRCA1 and BRCA2 mutations

Reproductive Issues for Women With BRCA Mutations

Women carrying BRCA1 and BRCA2 mutations face difficult and confusing reproductive decisions that fall into three categories: issues relating to risk-reducing surgeries, issues relating to use of oral contraceptives/tubal ligation, and issues relating to pregnancy and breastfeeding. Risk-reducing surgeries may confer survival benefits, but they also affect quality of life. Oral contraceptives potentially protect mutation carriers against ovarian cancer but increase the risk of early-onset breast cancer, and evidence for the efficacy of tubal ligation in reducing ovarian cancer risk in BRCA mutation carriers is contradictory. Women with BRCA mutations may increase their risk of breast cancer by becoming pregnant before age 40 years, but breastfeeding may decrease risk of breast cancer in women with BRCA mutations, regardless of age. BRCA mutation carriers desiring to become pregnant must deal with a variety of psychosocial issues, some with significant ethical implications, with minimal guidance from research.

Insulin-like growth factor-1 (IGF1) genotype predicts breast volume after pregnancy and hormonal contraception and is associated with circulating IGF-1 levels: implications for risk of early-onset breast cancer in young women from hereditary breast cancer families

BRCA1/2 mutations predispose to early-onset breast cancer, especially after oral contraceptive (OC) use and pregnancy. However, the majority of breast cancers might be due to more prevalent low-penetrance genes, which may also modify the risk in BRCA mutation carriers. The absence of the IGF1 19-repeat allele has been associated with high insulin-like growth factor-1 (IGF-1) levels during OC use. High IGF-1 levels are linked to early-onset breast cancer and larger breast volumes in the general population. The goal of this study was to elucidate the relationships between IGF1 genotype, early-onset breast cancer, breast volume, circulating IGF-1 levels and OC use in a prospective cohort of 258 healthy women ⩽40 years old from high-risk breast cancer families. All women completed a questionnaire including information on reproductive factors and OC use. We measured the height, weight, breast volumes and plasma IGF-1 levels. IGF-1 levels were similar among parous and nulliparous women not using OCs. In all, 13% had no IGF1 19-repeat allele. There was an interaction between IGF1 genotype and OC use on IGF-1 levels (P=0.026) in nulliparous women and another interaction between IGF1 genotype and parity on breast volume (P=0.01). Absence of the 19-repeat allele was associated with high IGF-1 levels in nulliparous OC users and with larger breast volumes in parous women and OC users. Incident breast cancers were also more common in women without the 19-repeat allele (log rank P=0.002). Our results suggest that lack of the IGF1 19-repeat allele modifies IGF-1 levels, breast volume and possibly early-onset breast cancer risk after hormone exposure in young high-risk women.

Oral Contraceptive Use and Risk of Early-Onset Breast Cancer in Carriers and Noncarriers of BRCA1 and BRCA2 Mutations

Recent oral contraceptive use has been associated with a small increase in breast cancer risk and a substantial decrease in ovarian cancer risk. The effects on risks for women with germ line mutations in BRCA1 or BRCA2 are unclear. Subjects were population-based samples of Caucasian women that comprised 1,156 incident cases of invasive breast cancer diagnosed before age 40 (including 47 BRCA1 and 36 BRCA2 mutation carriers) and 815 controls from the San Francisco Bay area, California, Ontario, Canada, and Melbourne and Sydney, Australia. Relative risks by carrier status were estimated using unconditional logistic regression, comparing oral contraceptive use in case groups defined by mutation status with that in controls. After adjustment for potential confounders, oral contraceptive use for at least 12 months was associated with decreased breast cancer risk for BRCA1 mutation carriers [odds ratio (OR), 0.22; 95% confidence interval (CI), 0.10-0.49; P < 0.001], but not for BRCA2 mutation carriers (OR, 1.02; 95% CI, 0.34-3.09) or noncarriers (OR, 0.93; 95% CI, 0.69-1.24). First use during or before 1975 was associated with increased risk for noncarriers (OR, 1.52 per year of use before 1976; 95% CI, 1.22-1.91; P < 0.001). There was no evidence that use of current low-dose oral contraceptive formulations increases risk of early-onset breast cancer for mutation carriers, and there may be a reduced risk for BRCA1 mutation carriers. Because current formulations of oral contraceptives may reduce, or at least not exacerbate, ovarian cancer risk for mutation carriers, they should not be contraindicated for a woman with a germ line mutation in BRCA1 or BRCA2.

A feasibility study of tamoxifen chemoprevention in Hodgkin's disease (HD) survivors

8551 Background: Female survivors of chest radiation (RT) for HD have an increased risk of breast cancer (BC) that develops at a relatively young age, often prior to menopause. Tamoxifen has not been studied in the prevention of radiogenic BC. In order to design a randomized BC prevention trial of tamoxifen for this cohort, we conducted a single-arm study, assessing enrollment, adherence, and toxicity. Methods: Eligible women were diagnosed with HD age ≤30, ≥5 years from mantle/chest RT, completed childbearing and had no history of thrombosis or second malignancy. Women were invited by letter to participate in this one-year study of tamoxifen, annual mammogram, breast exams at 6 and 12 months and other monitoring, (with the option of continuing tamoxifen for 5 years). In addition, patients could be referred by their MD. Results: Of 272 women identified, 67 were lost to follow-up and 14 were ineligible for medical reasons. Of the remaining 191 women, 164 (86%) declined. Reasons were “fear of side effects” (27%); “not completed childbearing”(18%); “too busy” (9%); “do not want to take medication” (8%); “MD advised against” (4%) and other (34%). Twenty-nine women (median age 41, range 34–55; median time since HD 19 years, range 6–36) enrolled on the study and began therapy. Median time of tamoxifen exposure is 18 months (range 2–24 months). Nine women (31%) discontinued tamoxifen prior to completing a full year of treatment. Reasons were side effects (4), other medical problems (2), BC (1), and other (2). There were no unusual or serious side effects. Conclusions: Despite their increased BC risk and tamoxifen's efficacy in other populations, female HD survivors were not eager to take tamoxifen. Because the risk of early onset BC is substantial in HD survivors, other prevention strategies, including novel agents should be considered. No significant financial relationships to disclose.

Birth weight and risk of early-onset breast cancer (Denmark).

To investigate if birth weight is associated with early-onset breast cancer. The mechanism behind an association with high birth weight could be the link between fetal growth and estrogens in utero. We conducted a population-based case-control study in Denmark including 881 women with breast cancer diagnosed before the age of 40 years and 3,423 age-matched controls. Information concerning birth weight and other birth-related variables was obtained from midwife reports. The risk of early-onset breast cancer was increased 1.25 times (95% CI 1.00-2.51) for birth weights above 4,000 g and 1.59 times (95% CI 1.00-1.55) for birth weights below 2,500 g in comparison with birthweights of 3,000-3,499 g. The finding that high birth weight is associated with breast cancer is compatible with the hypothesis that level of estrogen during pregnancy is related to breast cancer in early adult life. The finding that low birth weight is also associated with breast cancer may indicate that other characteristics of the fetal environment may be important for breast cancer in early adult life.

Oral contraceptives and the risk of breast cancer in BRCA1 and BRCA2 mutation carriers.

Oral contraceptive use has been associated with an increase in the risk of breast cancer in young women. We examined whether this association is seen in women at high risk of breast cancer because they carry a mutation in one of two breast cancer susceptibility genes, BRCA1 and BRCA2. We performed a matched case-control study on 1311 pairs of women with known deleterious BRCA1 and/or BRCA2 mutations recruited from 52 centers in 11 countries. Women who had been diagnosed with breast cancer were matched to control subjects by year of birth, country of residence, mutation (BRCA1 or BRCA2), and history of ovarian cancer. All study subjects completed a questionnaire about oral contraceptive use. Odds ratios (ORs) and 95% confidence intervals (CIs) were derived by conditional logistic regression. All statistical tests were two-sided. Among BRCA2 mutation carriers, ever use of oral contraceptives was not associated with an increased risk of breast cancer (OR = 0.94, 95% CI = 0.72 to 1.24). For BRCA1 mutation carriers, ever use of oral contraceptives was associated with a modestly increased risk of breast cancer (OR = 1.20, 95% CI = 1.02 to 1.40). However, compared with BRCA1 mutation carriers who never used oral contraceptives, those who used oral contraceptives for at least 5 years had an increased risk of breast cancer (OR = 1.33, 95% CI = 1.11 to 1.60), as did those who used oral contraceptives before age 30 (OR = 1.29, 95% CI = 1.09 to 1.52), those who were diagnosed with breast cancer before age 40 (OR = 1.38, 95% CI = 1.11 to 1.72), and those who first used oral contraceptives before 1975 (OR = 1.42, 95% CI = 1.17 to 1.75). Among BRCA1 mutation carriers, women who first used oral contraceptives before 1975, who used them before age 30, or who used them for 5 or more years may have an increased risk of early-onset breast cancer. Oral contraceptives do not appear to be associated with risk of breast cancer in BRCA2 carriers, but data for BRCA2 carriers are limited.

Genetic Factors Related to Racial Variation in Plasma Levels of Insulin-Like Growth Factor-1: Implications for Premenopausal Breast Cancer Risk

The oral contraceptive pill is associated with a modest increase in the risk of early-onset breast cancer in the general population, but it is possible that the risk is higher in certain subgroups of women. The relative risk of breast cancer associated with oral contraceptive use has been reported to be higher for African-American women than for white women. African-American women also have a higher incidence of premenopausal breast cancer than white women. Circulating levels of insulin-like growth factor-1 (IGF-I) vary between ethnic groups and are positively associated with the risk of premenopausal breast cancer. In general, the plasma level of IGF-I is lower in women who take oral contraceptives than in women who do not. In an attempt to explain the observed ethnic difference in IGF-I levels with oral contraceptive use, we sought to identify polymorphic variants of genes that are associated with IGF-I levels and estrogen metabolism. We measured IGF-I and IGFBP-3 plasma levels in 503 nulligravid women between the ages of 17 and 35. All women filled out a questionnaire that included information about ethnic background and oral contraceptive use. Samples of DNA were used to genotype the women for known polymorphic variants in the IGF1, AIB1, and CYP3A4 genes. Black women had significantly higher mean IGF-I levels than white women (330 ng/ml versus 284 ng/ml; P = 0.001, adjusted for age and oral contraceptive use). IGF-I levels were significantly suppressed by oral contraceptives in white women (301 ng/ml versus 267 ng/ml; P = 0.0003), but not in black women. Among oral contraceptive users, the IGF-I level was positively associated with the absence of the IGF1 19-repeat allele (338 ng/ml versus 265 ng/ml; P = 0.00007), with the presence of the CYP3A4 variant allele (320 ng/ml versus 269 ng/ml; P = 0.01), and with the presence of the AIB1 26-repeat allele (291 ng/ml versus 271; P = 0.08). After adjusting for genotypes, ethnic group was no longer a significant predictor of the IGF-I level. IGF-I levels are higher among black than white women. Polymorphic variants in the CYP3A4, IGF1, and AIB1 genes are associated with increases in the plasma levels of IGF-I among oral contraceptive users and the variant alleles are much more common in black women than in white women. The high incidence of premenopausal breast cancer among black women may be mediated through genetic modifiers of circulating levels of IGF-I.

After BRCA1 and BRCA2—What Next? Multifactorial Segregation Analyses of Three-Generation, Population-Based Australian Families Affected by Female Breast Cancer

Mutations in BRCA1 and BRCA2 that cause a dominantly inherited high risk of female breast cancer seem to explain only a small proportion of the aggregation of the disease. To study the possible additional genetic components, we conducted single-locus and two-locus segregation analyses, with and without a polygenic background, using three-generation families ascertained through 858 women with breast cancer diagnosed at age <40 years, ascertained through population cancer registries in Melbourne and Sydney, Australia. Extensive testing for deleterious mutations in BRCA1 and BRCA2, to date, has identified 34 carriers. Our analysis suggested that, after other possible unmeasured familial factors are adjusted for and the known BRCA1 and BRCA2 mutation carriers are excluded, there appears to be a residual dominantly inherited risk of female breast cancer in addition to that derived from mutations in BRCA1 and BRCA2. This study also suggests that there is a substantial recessively inherited risk of early-onset breast cancer. According to the best-fitting model, after excluding known carriers of mutations in BRCA1 and BRCA2, about 1/250 (95% confidence interval [CI] 1/500 to 1/125) women have a recessive risk of 86% (95% CI 69%-100%) by age 50 years and of almost 100% by age 60 years. Possible reasons that our study has implicated a novel strong recessive effect include our inclusion of data on lineal aunts and grandmothers, study of families ascertained through women with early-onset breast cancer, allowance for multiple familial factors in the analysis, and removal of families for whom the cause (i.e., BRCA1 or BRCA2) is known. Our findings may have implications for attempts to identify new breast cancer-susceptibility genes.

Smoking during pregnancy and breast cancer risk in very young women (United States).

To evaluate the association of smoking during a woman's first pregnancy, a period of pronounced growth and differentiation of mammary tissue, and her subsequent breast cancer risk. In this matched case-control study, we used linked birth certificate and tumor registry data from the New York State Health Department. Cases were 319 women aged 26-45 who were diagnosed with breast cancer in New York State between 1989 and 1995 and who completed a first pregnancy in New York State after 1987 at least one year prior to diagnosis of cancer. Controls were 768 primiparous women matched to cases on county of residence and delivery date. Information on prenatal smoking and other factors characterizing the woman's first pregnancy was obtained from the pregnancy record of each subject, and the association of these factors to breast cancer risk was assessed using conditional logistic regression. Smoking during pregnancy was associated with increased risk for breast cancer (crude OR = 2.7, 95% confidence interval (CI): 1.1-6.3). Adjustment for maternal age, subject age, race, and education strengthened this association (OR = 4.8, CI 1.6-14.6). These findings suggest that cigarette smoking during a woman's first pregnancy may increase her risk for early-onset breast cancer.

HRAS1 rare minisatellite alleles and breast cancer in Australian women under age forty years.

A recent meta-analysis of 23 studies supported the empirically derived hypothesis that women who lack one of the four common minisatellite alleles at the HRAS1 locus are at increased risk of breast cancer. These studies relied on visual sizing of alleles on electrophoretic gels and may have underreported rare alleles. We determined whether this hypothesis applied to early-onset breast cancer by using a new method to size minisatellite alleles. We conducted a population-based, case-control-family study of 249 Australian women under 40 years old at diagnosis of a first primary breast cancer and 234 randomly selected women, frequency matched for age. We sized HRAS1 minisatellite alleles with an Applied Biosystems model 373 automated DNA sequencer and GENESCAN(TM) software. All P values are two-sided. We found no association of rare alleles with breast cancer, before or after adjustment for risk factors and irrespective of how their effects were modeled (crude odds ratio = 1.04; 95% confidence interval [CI] = 0.071-1.53; P =.8). The rare allele frequency was 0. 173 (95% CI = 0.149-0.197), three times the pooled estimate of 0.058 (95% CI = 0.050-0.066) from previous studies (P<.001), and was similar for case subjects, 0.177 (95% CI = 0.143-0.221), and control subjects, 0.169 (95% CI = 0.135-0.203) (P =.7). There was no support for an association between rare HRAS1 alleles and the risk of early-onset breast cancer, despite 80% power to detect effects of the magnitude of those associations (1.7-fold) previously suggested. The question of whether cancer risk is associated with rare minisatellite HRAS1 alleles needs to be revisited with the use of new methods that have a greater ability to distinguish rare alleles from similarly sized common alleles.

Risk of breast cancer in offspring of male breast-cancer patients

There is a link between the BRCA2 mutation and the increased risk of early-onset breast cancer in families.1 This gene is clearly associated with male breast cancer2,3 and mutation in the BRCA2 gene was shown in 40% of male breast-cancer cases in Iceland.2 We therefore expected breast cancer risk to be high in daughters of male breastcancer patients.

Diet during adolescence and risk of breast cancer among young women.

A variety of breast cancer risk factors pertain to a woman's adolescence and may be related to nutritional influences. We assessed risk of early-onset breast cancer related to diet during adolescence in a case-control study. Study participants were accrued from the following three geographical regions covered by cancer registries: Atlanta, GA; Seattle/Puget Sound, WA; and central New Jersey. Case patients (n = 1647) were newly diagnosed with breast cancer, and control subjects (n = 1501) were identified by random-digit-dialing techniques. In an interview, each subject was asked to recall the frequency of consumption and portion size of 29 key food items at ages 12-13 years. Mothers of a subset of respondents completed questionnaires, and food groups were recalculated after removal of foods with poor agreement between mother and daughter. Logistic regression analyses were used to calculate odds ratios and 95% confidence intervals. When high versus low quartiles of consumption were compared, there was a suggestion of a reduced risk associated with high consumption of fruits and vegetables, although this finding was not statistically significant. Slight increases (of borderline statistical significance) in risk of breast cancer were found for intake of chicken or high-fat meat. Intake of animal fat, high-fat foods, high-fat snacks and desserts, or dairy products during adolescence had no apparent influence on breast cancer risk. Removal of foods suspected to be poorly recalled by the daughters did not change any of the risk estimates. These data do not provide evidence for a strong influence of dietary intakes during adolescence on risk of early-onset breast cancer.

Age-related differences in breast cancer stage at diagnosis between black and white patients in an urban community hospital.

Breast cancer mortality is significantly higher among black patients compared to white patients. Black women are reportedly at increased risk for early-onset breast cancer. Our goal was to evaluate stage distribution relative to age among black and white breast cancer patients in an institution with a relatively high minority patient population. We evaluated 425 patients diagnosed with breast cancer between 1990 and 1994: 56% white, 34% black, the remainder were other ethnicities. Patients were stratified by age: under 50 years versus 50 and older. Socioeconomic status was estimated by utilization of medical care in the private-practice setting versus the public clinic. Significantly more black patients were younger at diagnosis compared to white patients (32% vs. 20%; p = 0.008). There was a significantly more advanced stage distribution among the younger black patients, but not among the older black patients. Most of the black and white patients received private-practice care. These age-related differences in breast cancer stage distribution between black and white patients (which appeared independent of socioeconomic status) indicate that more aggressive screening and public education programs directed toward younger black women is warranted, and they lend support to the possibility of ethnicity-related variation in primary tumor biology.