Prostate Cancer In First-degree Relatives Research Articles

Prostate cancer incidence and survival in relation to prostate cancer as second cancer in relatives.

ObjectivesTo investigate if the risk of prostate cancer (PC) differs based on the order of primary PC diagnosed in first‐degree relatives (FDRs) given possibly different risk factors for PC as first primary cancer (PCa‐1) and second primary cancer (PCa‐2).Subjects and MethodsIn this Swedish nationwide cohort, PC diagnosis was followed for among 149,985 men with one FDR affected by PCa‐1, 10,972 with one FDR affected by PCa‐2 and 2,896,561 without any FDRs affected by cancer in a maximum of 57 years. PC patients were further followed for death due to PC since diagnosis. Relative risk (RR) of PC was estimated with Poisson regression and hazard ratio (HR) with Cox proportional hazard model.ResultsCompared to men without any FDRs affected by cancer, the RRs of PC in men with one FDR affected by PCa‐1 and PCa‐2 were 2.12 (95% confidence interval [CI]: 2.07–2.17) and 1.69 (1.54–1.85), respectively. The risk in men with one FDR affected by PCa‐2 was significantly lower than those with one FDR affected by PCa‐1 after additionally adjusting for family relationship (father‐son and brothers) and age at diagnosis of PC in FDR (RR PCa‐2 vs PCa‐1, 0.85, 95% CI, 0.78–0.94). PC patients with a family history of PCa‐2 were more likely to be detected at late‐stage and less likely to be diagnosed by screening, compared to those with a family history of PCa‐1. Patients whose PC was diagnosed after the diagnosis of PCa‐1 in FDRs had a better survival than those without a family history of cancer (HR, 0.88, 95% CI, 0.80–0.97), but no such association was observed among patients with a family history of PCa‐2.ConclusionOur study indicates a discrepancy between PC risks associated with a family history of PCa‐1 and PC‐2 and the reason behind it may be multifactorial.

Germline DNA damage repair gene mutations in pancreatic cancer patients with personal/family histories of pancreas/breast/ovarian/prostate cancer in a Japanese population.

AimCancer patients with personal/family histories of pancreatic/breast/ovarian/prostate cancer are associated with a higher likelihood of harboring DNA damage repair (DDR)‐related germline mutations. Here, we aimed to obtain a better understanding of DDR‐related germline mutations in Japanese pancreatic ductal adenocarcinoma (PDAC) patients with personal and/or family histories of BRCA‐related cancers of the pancreas, breast, ovary, and prostate.MethodsWe performed next‐generation sequencing (NGS) and evaluated germline mutations in nine DDR‐related genes (BRCA1, BRCA2, ATM, PALB2, CHEK2, MLH1, MSH2, MSH6, and PMS2) in PDAC patients with personal and/or family histories.ResultsOf 196 patients with PDAC, 39 (19.9%) fulfilled the criteria for at least one family history of pancreatic/breast/ovarian/prostate cancer in first‐degree relatives (sibling–sibling or parent‐child) or the personal history of these malignancies. Targeted NGS revealed that four (10.2%) of 39 patients with personal/family histories harbored deleterious germline mutations—two in BRCA2, one in ATM, and one in MLH1. Both the BRCA2 variants showed frameshift mutations due to short insertion/deletions. In the 39 patients undergoing NGS, a similar distribution of the clinicopathological characteristics was observed between those with deleterious mutations/variants of unknown significance (VUSs) and with benign/wild types. Patients with deleterious germline mutations/VUSs in DDR‐related genes showed a significantly more favorable prognosis than those with benign mutations/wild‐type genes (hazard ratio: 0.160, P = .040).ConclusionsA significant fraction of PDAC patients with personal/family histories of BRCA‐related cancers harbored deleterious germline mutations in DDR‐related genes. DDR‐related germline gene mutations might be a favorable prognostic factor in patients with pancreatic cancer.

First-degree family history of prostate cancer is associated the risk of breast cancer and ovarian cancer.

The evidence for associations between family history of prostate cancer and the risk of breast cancer and ovarian cancer is inconclusive. The first systematic review and meta-analysis of studies was conducted to assess the risk of breast cancer and ovarian cancer associated with a family history of prostate cancer.A literature search was conducted using MEDLINE, Embase and Web of science databases up to January 31, 2019. Data were screened and extracted independently by 2 reviewers. The pooled risk ratio (RR) and its 95% confidence interval (CI) were calculated using random-effects models. The GRADE approach was used to assess the quality of evidence.Nine observational studies including 8,011,625 individuals were included in the meta-analysis. The meta-analysis showed that family history of prostate cancer in first-degree relatives was associated with an increased risk of breast cancer (RR 1.12, 95%CI 1.09 to 1.14) with moderate quality evidence, subgroup analysis showed consistent results. Compared with no family history of prostate cancer, history of prostate cancer in first-degree relatives was associated with a slight risk of ovarian cancer (1.10, 95%CI 1.01 to 1.20) with moderate quality evidence. Family history of prostate cancer among sibling was associated with a 17% increased risk of ovarian cancer (95% CI 1.03 to 1.34), however, no significant association was found between family history of prostate cancer among parent and risk of ovarian cancer (RR 1.19, 95% CI 0.84 to 1.70).This review demonstrates that women with a family history of prostate cancer in first-degree relatives was associated with an increased risk of breast cancer and ovarian cancer. These findings may aid in screening, earlier detection and treatment of women with a family history of prostate cancer in first-degree relatives.

Intraductal carcinoma of the prostate in an Irish prostate cancer patient cohort-an aggressive pathology and a strong familial link.

BackgroundThe prevalence of intraductal carcinoma of the prostate (IDC-P) is poorly studied in the Irish population. This study investigated the incidence and clinicopathologic characteristics of IDC-P in an Irish prostate cancer (PCa) patient cohort. The study also discusses the rationale for genetic counseling and screening in Irish patients with familial risk factors for IDC-P.Materials and methodsThis study investigated patients diagnosed with IDC-P on prostate biopsy from 2012 to 2016. Primary outcome measurements were incidence, management, and clinical outcomes after follow-up in patients with IDC-P. The secondary outcome measurement was to identify a familial link for IDC-P.ResultsA total of 1,143 patients were diagnosed with PCa on needle biopsy, of which 30 (2.3%) had concomitant IDC-P. Mean age and prostate-specific antigen at diagnosis were 68.6 ± 10.5 years (range 53–85 years) and 9.15 ± 8.65 ng/mL (range 2.1–166 ng/mL), respectively. In total, 17 of 30 patients (57%) were diagnosed with concomitant high-grade (i.e., ≥Gleason score 8) PCa. Eight patients (27%) were treated with radical prostatectomy; of which five had biochemical recurrence (BCR) after 10.55 ± 25.9 months. Eleven patients (37%) received radical radiotherapy; of which one had BCR after 36 months. Eleven patients (37%) presented with advanced PCa and were managed with androgen deprivation therapy ± chemotherapy. A family history for PCa in first-degree relatives was found in eight patients (27%).ConclusionsIDC-P is associated with more aggressive clinicopathologic features and an increased risk of BCR after treatment. In Ireland, clinical guidelines and a genetic screening pathway are required to provide early detection and appropriate multimodal management of patients with IDC-P.

Family History of Breast or Prostate Cancer and Prostate Cancer Risk.

Breast and prostate cancer co-occur in families, and women with a family history of prostate cancer are at increased breast cancer risk. Prostate cancer is among the most heritable cancers, but few studies have investigated its association with familial breast cancer. The objective of this study is to investigate the extent to which familial breast or prostate cancer in first-degree relatives increases prostate cancer risk. A prospective study of 37,002 U.S. men in the Health Professionals Follow-up Study. During the 16-year follow-up to 2012, 4,208 total and 344 lethal cases were diagnosed. Using cause-specific hazards regression, we estimated the multivariable HRs and 95% confidence intervals (CI) for associations between familial breast or prostate cancer and total and lethal prostate cancer. Those with familial breast cancer had a 21% greater risk of prostate cancer overall (95% CI, 1.10-1.34), and a 34% greater risk of lethal disease (HR 1.34; 95% CI, 0.96-1.89). Family history of prostate cancer alone was associated with a 68% increased risk of total disease (95% CI, 1.53-1.83) and a 72% increased risk of lethal disease (95% CI, 1.25-2.38). Men with a family history of both cancers were also at elevated risk. Our study found that men with a family history of breast or prostate cancer had elevated prostate cancer risks, including risk of lethal disease. These findings have translational relevance for cancer risk prediction in men.

Abdominal obesity and prostate cancer risk: epidemiological evidence from the EPICAP study

Introduction Obesity is associated with an increased risk of several cancers, such as breast or colorectal cancers. However, the relationship between obesity and prostate cancer (PCa) remains controversial. Indeed, inconsistent results have been reported between body mass index (BMI) and PCa risk, while some associations have been reported with other anthropometric indicators, such as waist circumference (WC) or waist-hip ratio (WHR), which would better illustrate the concept of body fat distribution. Therefore, we assessed a possible association between anthropometric indicators and PCa risk based on data from the EPICAP study. Methods EPICAP in a French population-based case-control study that enrolled 819 incident cases of PCa diagnosed in 2012 and 2013, aged less than 75 years old and residing in the department of Herault, France. Controls were 879 age-matched (± 5 y) individuals living in the same geographic area. Face-to-face interviews, using a standardized computerized questionnaire, gathered information about sociodemographic characteristics, personal medical history, lifestyle factors, physical activity, residential and occupational history. Anthropometric indicators have also been collected through the questionnaire (self-report of height at 18 years old and weight every decades) or anthropometric measures at time of interview (height, weight, waist and hip circumferences). Logistic regression models were used to assess odds ratios (ORs) for the associations between anthropometric indicators (BMI, WC and WHR) and PCa risk. Analyses were systematically adjusted for age (5-year period), family history of prostate cancer in first-degree relatives and race (Caucasians, others). Analyses were also adjusted for other potential confounding factors such as educational level or physical activity. Separate analyses were conducted by prostate cancer aggressiveness according to the Gleason score (low or intermediate score ≤ 7 [including 3 + 4], high score ≥ 7 [including 4 + 3]). Seeking for relevant interaction between BMI and WC or WHR, we performed stratified analyses according to BMI overweight cut-point (25 kg/m2) defined by the World Health Organization. Results Overall, 47.8% of men were overweight and 23.4% were obese, similarly distributed between cases and controls (OR 0.98, 95% CI 0.78–1.23, OR 0.91 95% CI 0.67–1.23, respectively). We observed a slight, but not significant increased risk of PCa for men with a WC above 94 cm (OR 1.20, 95% CI 0.95–1.51) and an increased risk of PCa for men with a WHR greater or equal to 0.95 (OR 1.27, 95% CI 1.01–1.60), with more pronounced associations after adjustment for BMI (OR 1.48, 95% CI 1.11–1.97, OR 1.39, 95% CI 1.09–1.79, respectively). In addition, analyses stratified on BMI showed that men with a BMI 94 cm or WHR ≥ 0.95 (OR 1.63, 95% CI 1.05–2.52, OR 1.76, 95% CI 1.18–2.63, respectively). Nevertheless, interactions were not significant for WC (P = 0.23) and close to significance for WHR (P = 0.07). Associations regarding central obesity indicators, adjusted for BMI, were more pronounced in men with aggressive prostate cancer, either for WC > 94 cm (OR 2.30, 95% CI 1.38–3.83) or WHR ≥ 0.95 (OR 1.51, 95% CI 0.98–2.32). Conclusions Our results suggest that BMI itself is not associated with prostate cancer, while central obesity is associated with an increased risk of prostate cancer, especially aggressive prostate cancer.

Family history of breast cancer increases the risk of prostate cancer: results from the EPICAP study.

IntroductionFamilial aggregation is now well established with an increased risk of prostate cancer in patients with a family history of prostate cancer in first degree relatives. The aim of this paper was to investigate the role of family history of cancer in first degree relatives in prostate cancer risk.ResultsAs expected, a family history of prostate cancer in first-degree relatives was more frequent in cases than in controls (OR 3.10, 95% CI 2.32–4.15). A family history of early BCa (before age 50) in first-degree relatives was more frequent in cases than in controls (OR 1.79, 95% CI 1.09–2.94) with higher risk of aggressive PCa. The association was more pronounced for BCa in daughters (OR 15.26 95% CI 1.95–120).ConclusionsIn summary, a family history of BCa in first degree relatives before age 50 may increases the risk of PCa with higher Gleason score. This finding could suggest a specific prostate surveillance and/or genetic counselling for men who present such familial history.MethodsEPIdemiological study of Prostate CAncer (EPICAP) is a population-based case-control study specifically designed to investigate the role of environmental and genetic factors in prostate cancer. Detailed information on family history of cancer in first degree relatives (parents, brothers and sisters, children) was collected as well as the age of occurrence and the localization of each cancer. Overall, 819 cases and 879 controls have been included.

Abstract 2543: A family affair: Prostate cancer risk and family history of breast or prostate cancer

Abstract Background - There is suggestive evidence of familial clustering of breast and prostate cancer in first-degree relatives; women with a family history of prostate cancer are at increased risk of breast cancer. Few studies have investigated joint family history of breast and prostate cancer and prostate cancer risk, and no study to date has examined lethal prostate cancer. Methods - We studied 42,672 from the Health Professionals Follow-up Study between 1996 to 2012. During follow-up, 4,258 prostate cancer cases were diagnosed, of whom 380 were lethal disease. Men self-reported family history of breast and prostate cancer, including in siblings or parents. Using cause-specific hazards regression, we estimated hazard ratios (HR) and 95% confidence intervals (CI) of the association between family history and prostate cancer risk and progression. Results - About 8% of men had a family history of prostate cancer, 8.7% had a family history of breast cancer, and 1.4% of men had a family history of both breast and prostate cancer. A family history of prostate cancer was significantly associated with an increased risk of prostate cancer (HR: 1.69; 95% CI: 1.54-1.85). Increased risk was higher for men with a father diagnosed with prostate cancer (HR: 1.64 95% CI: 1.49-1.80) than for men with a diagnosis in a brother(s) (HR: 1.51 95% CI: 1.27-1.80). A positive family history of breast cancer was associated with a small, but significant 22% increased risk (HR: 1.22; 95% CI: 1.11-1.35). Familial breast cancer in a sister (HR: 1.22 95% CI: 1.06-1.41) increased risk more than familial breast cancer in a mother (HR: 1.12; 95% CI: 0.99-1.25). Men with a family history of both prostate and breast cancer had a 52% (HR: 1.52; 95%CI: 1.23-1.88) increased risk of prostate cancer compared to men with no family history of either cancer. Risk of lethal prostate cancer was also significantly increased for men with a positive family history of prostate cancer (HR: 1.64; 95% CI: 1.20-2.24), as well as for men with a family history of breast cancer (HR: 1.47; 95% CI: 1.07-2.01). Conclusions - These results support the findings of familial aggregation of breast and prostate cancer, and for the first time suggest an association between familial breast cancer and lethal prostate cancer. Data from this prospective study have translational relevance for family counseling of cancer patients. Citation Format: Lauren E. Barber, Travis A. Gerke, Sarah C. Markt, Giovanni Parmigiani, Lorelei A. Mucci. A family affair: Prostate cancer risk and family history of breast or prostate cancer. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 2543.

Clinico-Pathological Characterization of Hereditary, Familial and Sporadic Prostate Cancer

Aim: To characterize familial prostate cancer including hereditary prostate cancer and assess the disease-free survival following radical prostatectomy. Methods: A self-administered written questionnaire was forwarded to 709 prostatectomized patients from the Aarhus Prostate Cancer Study containing questions about cases of prostate cancer (PC), age at diagnosis, vital status, and age at death for all first-degree relatives. Patients were then divided into groups according to their family history: hereditary prostate cancer (HPC), familial prostate cancer (FPC), and sporadic prostate cancer (SPC) groups. The information from a subset of both FPC (n = 17) and SPC (n = 17) groups were validated in the Danish Cancer Register and the Civil Registration System. Between groups, we described the association of age, prostatespecific antigen (PSA), postoperative Gleason score and T Stage. A Kaplan-Meier curve demonstrated postoperative disease-free survival in each group. Results: The response rate was 81% (574/709). About 21% of the patients were categorized in the FPC group, of which 7% were identified as having HPC. The median follow-up time was 63 months for HPC, 65 months for FPC and 88 months for SPC. Overall, there was no significant difference between groups in clinical features and disease-free survival except that patients with HPC were significantly associated with younger age than sporadic cases (p = 0.02). The proportion of self-reported PC diagnoses confirmed in the cancer register was 27.8%. The index persons with SPC reported no PC in first-degree relatives and none was found the cancer register. Conclusion: Overall, we found no difference in clinical characteristics and survival, following radical prostatectomy except that patients with HPC were younger at diagnosis. These results are in line with previously reported data.

The 4q27 locus and prostate cancer risk

BackgroundChronic inflammation is considered to be implicated in the development of prostate cancer. In this study we are the first to investigate a potential association between variants in an autoimmune related region on chromosome 4q27 and prostate cancer risk. This region harbors two cytokine genes IL-2 and the recently described IL-21.MethodsWe genotyped six variants previously associated with autoimmune disease (namely rs13151961, rs13119723, rs17388568, rs3136534, rs6822844 and rs6840978) and one functional IL-2 promoter variant (rs2069762) for possible association with prostate cancer risk using the Australian Risk Factors for Prostate Cancer case-control Study.ResultsOverall, our results do not support an association between the seven variants at position 4q27 and prostate cancer risk. Per allele odds ratios (ORs) were not significantly different from 1 (all P-values = 0.06). However, we found suggestive evidence for a significant association between the presence of the rs13119723 variant (located in a protein of unknown function) and men with a family history of prostate cancer in first-degree relatives (P-value for interaction 0.02). The per allele OR associated with this variant was significantly higher than 1 (2.37; 95% C.I. = 1.01-5.57).ConclusionsWe suggest that genetic variation within the chromosome 4q27 locus might be associated with prostate cancer susceptibility in men with a family history of the disease. Furthermore, our study alludes to a potential role of unknown protein KIAA1109 in conferring this risk.

Association between family history of cancers and risk of prostate cancer

Introduction Family history of prostate cancer is an established risk factor for prostate cancer. However, the relationship between family history of cancers other than prostate cancer and prostate cancer risk is inconclusive. This study sought to examine the association between family history of cancers and prostate cancer. Methods A case–control study was conducted in which cases and controls were randomly selected from a large urology clinic in Central Virginia. Cases were 600 histologically confirmed prostate cancer patients who were diagnosed between January 2000 and December 2005, and controls were 686 patients who visited the clinic during the same period and were diagnosed with urological illnesses other than cancers and prostate-related problems. Data on family history of cancers, lifestyle and demographic factors were collected through mail survey utilizing the method suggested by Dillman. Unconditional logistic regression analysis was used to estimate the odds ratios (OR) and the corresponding 95% confidence intervals (CI) after adjustment for potential confounding factors including body mass index (BMI), alcohol intake, physical activity, smoking, diet, history of vasectomy and sexually transmitted disease (STD), age, race, marital history, education, and income. Multiple comparisons adjustments were made using the Bonferroni adjustment. Results Men with a family history of any cancer in first-degree relatives including parents (OR = 2.42, 95% CI = 1.53–3.84) and parents only (OR = 1.90, 95% CI = 1.23– 2.94) were at increased risk of developing prostate cancer. Significant increased risk was also observed with family history of prostate cancer in first-degree relatives (OR = 2.68, 95% CI = 1.53–4.69) and parents only (OR = 3.26, 95% CI = 1.71–6.24). Even after adjustments for multiple comparisons, the significance persisted both in first-degree relatives (OR = 2.68, 95% CI = 1.16–6.21) and parents alone (OR = 3.26, 95% CI = 1.24– 8.63). Conclusion This study demonstrated an increased prostate cancer risk for men with a family history of any cancer or prostate cancer in first-degree relatives and parents alone. Health care providers need to be aware of the potential risk of family history of cancers on prostate 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.

Site-specific familial aggregation of prostate cancer.

Over the last decade, epidemiologic evidence has accumulated in favor of a significant but heterogeneous hereditary component in prostate cancer (PC) susceptibility. In order to map and clone PC susceptibility genes, stratification of PC families into genetically homogeneous groups appears to be a key issue. Subset definition based on age at diagnosis, presumed mode of inheritance, number of affecteds per family and coaggregation of PC with other cancers has already proven successful in some studies. Previously, the finding of the coaggregation of malignancies of the central nervous system within PC families helped to link a prostate-brain cancer susceptibility gene (CAPB) to chromosome 1p36. In this study, we evaluate the risk of PC and malignancies at other sites among first-degree relatives of a large population-based group of Dutch PC patients. A population-based family case-control study was initiated that included Caucasian PC patients newly diagnosed between July 1996 and December 1999. Information on 12,575 first-degree relatives of 704 PC patients and 1,371 controls was collected through postal questionnaires and telephone interviews. All reported PC in first-degree relatives was verified through medical records. In our population, PC has a strong familial component that is reflected by a 2.9-fold increased risk (95% CI = 2.2-3.9) of PC for first-degree relatives of PC patients. This familial risk was somewhat higher among brothers (hazard ratio = 3.9; 95% CI = 2.4-6.4) compared to fathers (hazard ratio = 2.5; 95% CI = 1.7-3.6). Cancers at other sites did not coaggregate with PC. Our data suggest that familial PC, at least in this Western European population, is site-specific, not part of an inherited cancer syndrome.

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 [PR] = 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.

Prostate cancer risk in U.S. blacks and whites with a family history of cancer.

Prostate cancer occurs more frequently in U.S. blacks than whites. A population-based case-control study which investigated the association with family history of cancer was carried out among 981 men (479 black, 502 white) with pathologically confirmed prostate cancer, diagnosed between August 1, 1986, and April 30, 1989, and 1,315 controls (594 black, 721 white). Study subjects, aged 40-79, resided in Atlanta, Detroit, and 10 counties in New Jersey, geographic areas covered by population-based cancer registries. Prostate cancer risk was significantly elevated among those who reported a history of prostate cancer in first-degree relatives (O.R. = 3.2; 95% C.I.: 2.0-5.0), with blacks and whites having similarly elevated risks. These risks were unchanged by statistical adjustment for job-related socio-economic status, education, income, and marital status. Overall, the ORs associated with history of prostate cancer in fathers and brothers were 2.5 (95% C.I.: 1.5-4.2) and 5.3 (95% C.I.: 2.3-12.5), respectively. Risks associated with a family history of prostate cancer were consistently elevated among younger and older subjects. Only small non-significant excesses of prostate cancer risk were associated with a family history of breast, colorectal, or other cancers. While familial occurrence is a key risk factor for prostate cancer and likely to be genetically based, the similar familial risks among blacks and whites suggest that the ethnic disparity in incidence is influenced by environmental factors.