Familial risk of colon and rectal cancer in Iceland: Evidence for different etiologic factors?

The aim of this study was to characterize the familial risk of colon and rectal cancer using 2 population-based registries in Iceland, the Icelandic Cancer Registry and a genealogy database. The standardized incidence ratio (SIR) was used to estimate the risk among relatives of colorectal cancer index cases diagnosed in Iceland over a 46-year period (1955-2000). The 2,770 colorectal cancer patients had 23,272 first-degree relatives. Among first-degree relatives, there was an increased risk of both colon (SIR 1.47, 95% confidence interval (CI) 1.34-1.62) and rectal cancer (SIR 1.24, 95% CI 1.04-1.47). An increased risk of colon cancer was observed among siblings of colon cancer patients (SIR 2.03, 95% CI 1.76-2.33), whereas no such increase was observed for parents or offspring. Furthermore, the risk of rectal cancer was only increased among brothers (SIR 2.46 95% CI 1.46-3.89) of rectal cancer patients and not among their sisters (SIR 1.0 95% CI 0.40-2.06). The added risk of colon cancer among first-degree relatives was independent of site of colon cancer in the proband. Our results confirm that family history of colorectal cancer is a risk factor for the disease. However, family history has a different association with colon cancer than with rectal cancer, suggesting that the 2 cancer types may have different etiologic factors. Our results have implications for colon and rectal cancer screening programs.     

Family history of cancer and risk of colorectal cancer in Italy.

Subjects with a family history of colorectal cancer (CRC) are at increased risk of CRC, but quantification of the risk in different populations, the possible differences in risk according to localization of the cancer and the association of family history of other cancers with CRC risk are still open issues. We have therefore analysed data from a multicentric case-control study conducted in six Italian areas between 1992 and 1996 of 1225 incident cases of colon cancer, 728 cases of rectal cancer and 4154 controls admitted for acute conditions to the same network of hospitals as the cases. Unconditional logistic regression models including terms for gender, age, study centre, years of education and number of siblings were used to estimate the odds ratios (ORs) of CRC according to various aspects of history of CRC and other cancers in first-degree relatives. The OR for family history of CRC was 3.2 (95% confidence interval, CI, 2.5-4.1) for colon cancer and 2.2 (95% CI 1.6-3.1) for rectal cancer. Colon cancer was significantly associated with a family history of stomach (OR 1.4), bone (OR 2.1) and kidney (OR 2.3) cancers, while rectal cancer was significantly associated with a family history of lymphomas (OR 2.8). There was a 30% higher risk of colon and rectal cancer in subjects with a family history of any cancer, excluding intestine. The ORs for family history of CRC were 5.2 for colon and 6.3 for rectum when the proband''s age was below 45 years. The ORs were similar when the affected relative was a parent or a sibling and in different strata of age of relative(s). For subjects with two or more first-degree relatives with CRC, the risk was 6.9 for the right colon, 5.8 for the transverse and descending colon, 3.8 for the sigma, 3.2 for the rectosigmoid junction and 1.9 for the rectum. This study confirms that a family history of CRC in first-degree relatives increases the risk of both colon and rectal cancer, the association being stronger at younger ages and for right colon.     

Associations between apoE genotype and colon and rectal cancer

Apolipoprotein E (apoE) plays a major role in the metabolism of bile acids, cholesterol and triglycerides, and has recently been proposed as being involved in the carcinogenic process. Given the potential role of bile acids in colorectal cancer etiology, it is reasonable that colorectal cancer risk might be modified by apoE genotype. We used data collected from a case-control study of colon cancer (n=1556 cases and 1948 controls) and rectal cancer (n=777 cases and 988 controls). The absence of an e3 apoE allele significantly increased the risk of colon cancer (OR=1.37 95% CI 1.00-1.87), particularly among those diagnosed when older than 64 years (OR=1.88 95% CI 1.17-3.04; P interaction between age and apoE genotype equal to 0.05). A significant three-way interaction was detected for family history of colorectal cancer, age at diagnosis and apoE genotype (P = 0.05), in those diagnosed when older, not having an e3 allele and having a significantly increased risk of colon cancer with family history of colorectal cancer (OR=3.93 95% CI 1.23-12.6). This was compared with the risk associated with family history of colorectal cancer among those diagnosed when older, with an e3 allele of 1.61 (95% CI 1.17-2.23) or those diagnosed when younger without an e3 allele (OR=2.40 95% CI 0.56-10.3). Among those diagnosed when older than 64 years, associations of BMI and prudent diet with colon cancer were stronger among individuals without an e3 allele, although the P for interaction was not significant. We did not detect any significant associations between apoE genotype and rectal cancer, survival after diagnosis with colorectal cancer, stage of disease at diagnosis or type of tumor mutation. These findings suggest those apoE genotypes that do not include the e3 allele, the same genotypes that are associated with increased risk of coronary heart disease, may influence development of colon cancer among those who are older at diagnosis.     

Allergy and other selected diseases and risk of colorectal cancer

It has been reported that allergy and other diseases may be related to colorectal cancer risk. The aim of this study was to perform a systematic analysis using information about medical histories specifically to see if there was any relation between allergies or other medical conditions and colorectal cancer risk. A multicentric case-control study was conducted in six Italian areas between 1992 and 1996 on 1225 incident cases of colon cancer, 728 cases of rectal cancer and 4154 controls comparable with cases according to sex and age group, admitted for acute conditions to the same network of hospitals where cases had been identified. Unconditional logistic regression models including terms for sex, age, study centre, years of education, body mass index, physical activity, smoking, history of colorectal cancer in first-degree relatives and energy intake were used to estimate the odds ratios (OR) of colon and rectal cancer according to history of allergy and other selected diseases. The OR for history of allergy was 0.88 (95% confidence interval, CI, 0.67-1.14) for colon and 0.64 (95% CI, 0.44-0.92) for rectal cancer, and the inverse association was stronger when allergy was diagnosed at age 35 years or more, or less than 10 years before the cancer diagnosis. No clear pattern emerged in strata of age and sex. History of other selected diseases, including hypertension and cholelithiasis, was not related to colon or rectal cancer risk, though there was a moderate increase in the risk of colon cancer (OR = 1.18, 95% CI, 0.66-2.14) in patients with a history of intestinal polyps. This study lends support to the hypothesis that allergic individuals may be at a lower risk of developing colorectal cancer.     

Family history of cancer and risk of lung cancer among nonsmoking Chinese women.

The relationship between family cancer history in first-degree relatives and risk of lung cancer was evaluated among a population-based cohort of 71,392 female nonsmokers in Shanghai, China. A total of 179 newly diagnosed lung cancer patients were identified during 441,410 person-years of follow-up. Lung cancer risk was not elevated among those with a family history of lung cancer. However, risk of lung cancer was increased among subjects who had two or more first-degree relatives with any type of cancers {rate ratio [RR], 1.95 [95% confidence intervals (95% CI), 1.08-3.54] for two relatives with any cancers and RR, 3.17 [95% CI, 1.00-10.03] for three or more relatives with any cancer}. Having a family history of colorectal cancer (RR, 2.38; 95% CI, 1.21-4.70) and having siblings with stomach cancer (RR, 2.16; 95% CI, 1.01-4.65) and pancreatic cancer (RR, 4.19; 95% CI, 1.04-16.95) were also found to be associated with lung cancer risk. This cohort study indicated a moderate association of lung cancer risk with a family cancer history in general, but not with a family history of lung cancer specifically. The associations were stronger when a sibling, rather than a parent, was affected. The apparent link between lung cancer risk and a family history of colorectal, stomach, and pancreas cancers may be worth further investigation.     

The correlation between a family history of colorectal cancer and survival of patients with colorectal cancer

The purpose was to analyze survival of patients with colorectal cancer and a positive family history for colorectal cancer in first degree relatives compared with those with no such family history and to determine whether differences in survival could be explained by known clinico-pathological factors. During 2000–2003, 318 consecutive patients with colorectal cancer answered a written questionnaire about their family history for colorectal cancer. During a 6-year follow-up, recurrences and survival were registered. Thirty-one (10%) patients had a first-degree relative with colorectal cancer, moreover two patients fulfilled the criteria of hereditary non-polyposis colorectal cancer and were excluded. Patients with a first-degree relative with colorectal cancer had better survival and lower risk for recurrences compared to those with no relatives with colorectal cancer. In a multivariate analysis including age, gender, stage of disease, tumor differentiation, vascular invasion and family history, patients with first-degree relatives with colorectal cancer had lower risks for death (RR 0.37; 95% CI 0.17–0.78) and death from cancer (RR 0.25; 95% CI 0.08–0.80), compared to those with a no relative with colorectal cancer. The differences were seen in patients with colon cancer but not rectal cancer. Family history for colorectal cancer in a first-degree relative is an individual prognostic factor in patients with colon cancer and could not be explained by known clinico-pathological factors. The value of family history taking in patients with colon cancer is therefore not only to identify families with hereditary colorectal cancer, but also to add information to the prognosis of the patients.     

Cancer in first-degree relatives and risk of glioma in adults.

Relatively few studies have examined glioma risk in relation to history of cancer in first-degree relatives. We sought to describe such risks in a large hospital-based case-control study. Histologically confirmed incident adult glioma cases (n = 489) were identified at three regional referral hospitals between June 1994 and August 1998. Controls (n = 799) admitted to the same hospitals for nonmalignant conditions were frequency-matched on age, sex, race/ethnicity, hospital, and proximity of residence to hospital. Participants received a personal interview, including questions regarding cancer in family members. Odds ratios (ORs) were calculated to estimate the risk of glioma associated with a history of cancer in a first-degree relative using conditional logistic regression and compared with standardized incidence ratios among relatives of cases versus relatives of controls. Among participants reporting a family history of a brain cancer or a brain tumor, risk of glioma was 1.6 [95% confidence interval (CI), 0.5-5.3; n = 5] and 3.0 (95% CI, 0.9-10.8; n = 7), respectively, in comparison with those without such family histories. Participants who had a family history of stomach (OR, 2.2; 95% CI, 1.0-4.6), colon (OR, 1.4; 95% CI, 0.9-2.2), or prostate cancer (OR, 2.1; 95% CI, 1.1-3.8) or Hodgkin disease (OR, 2.4; 95% CI, 0.9-6.3) had an increased glioma risk. OR estimates were similar to the ratios of standardized incidence ratios for cancer in relatives of cases versus controls. Shared environmental or genetic factors in families may influence glioma risk. Our findings suggest that individuals with a family history of specific cancers other than glioma may have an increased glioma risk.     

A case-control study of male colorectal cancer in Aichi Prefecture, Japan: with special reference to occupational activity level, drinking habits and family history

The relationships of occupational activity level, drinking habits and family history of cancer to the risk of male colorectal cancer by subsites were investigated in a case-control study involving 1,716 cases with colon cancer, 1,611 cases with rectal cancer and 16,600 controls with other sites of cancer identified from the Aichi Cancer Registry, Japan 1979-1987. An occupation with a low activity level was associated with an increased risk of colorectal cancer; the age-adjusted relative risk (RR) compared to the high activity level group was 1.92 (95% confidence interval (CI): 1.38-2.67) for proximal colon cancer, 1.52 (95% CI: 1.19-1.94) for distal colon cancer and 1.38 (95% CI: 1.17-1.62) for rectal cancer. Beer drinkers showed an increased risk of colorectal cancer; the age-adjusted RR was 1.49 (95% CI: 1.13-1.95) for proximal colon cancer, 1.65 (95% CI: 1.34-2.04) for distal colon cancer and 1.88 (95% CI: 1.62-2.18) for rectal cancer. The RR for family history of colorectal cancer was 3.40 (95% CI: 2.19-5.29) for proximal colon cancer, 2.54 (95% CI: 1.73-3.75) for distal colon cancer and 1.78 (95% CI: 1.28-2.49) for rectal cancer. Multivariate analysis controlled for age, residence, marital status and smoking in addition to occupational activity level, beer drinking and family history of colorectal cancer did not materially change the RRs. When these three variables were combined, the RR was 15.72 (95% CI: 5.40-45.78) for proximal colon cancer, 10.55 (95% CI: 4.24-26.27) for distal colon cancer and 6.69 (95% CI: 3.12-14.36) for rectal cancer.     

Risk of Other Cancers in Individuals with a Family History of Pancreas Cancer

Background

Inherited predisposition to pancreas cancer accounts for approximately 10% of cases. Familial aggregation may be influenced by shared environmental factors and shared genes. We evaluate whether a family history of pancreas cancer is a risk factor for ten specified cancers in first-degree relatives: bladder, breast, colon, head and neck, lung, lymphoma, melanoma, ovary, pancreas, and prostate.

Methods

Risk factor data and cancer family history were obtained for 1,816 first-degree relatives of pancreas cancer case probands (n?=?247) and 3,157 first-degree relatives of control probands (n?=?420). Unconditional logistic regression models using generalized estimating equations were used to estimate odds ratios (ORs), and 95% confidence intervals of having a first-degree relative a specified cancer.

Results

A family history of pancreas cancer was associated with a doubled risk of lymphoma (OR?=?2.83, 95% CI?=?1.02–7.86) and ovarian cancer (OR?=?2.25, 95% CI?=?0.77–6.60) among relatives after adjustment. Relatives with a family history of early-onset pancreas cancer in a proband had a sevenfold increased risk of lymphoma (OR?=?7.31, 95% CI?=?1.45 to 36.7). Relatives who ever smoked and had a family history of pancreas cancer had a fivefold increased risk of ovarian cancer (OR?=?4.89, 95% CI?=?1.16–20.6).

Conclusion

Family history assessment of cancer risk should include all cancers. Assessment of other known and suspected risk factors in relatives will improve risk evaluation. As screening and surveillance methods are developed, identifying those at highest risk is crucial for a successful screening program.     

Relation of Family History of Cancer and Environmental Factors to the Risk of Colorectal Cancer: A Case-control Study

The relation of a family history of cancer and environmentalfactors to colorectal cancer was investigated in a case-controlstudy conducted from 1992 to 1994 at 10 medical institutionsin Japan using a self-administered questionnaire, and 363 casesof colorectal cancer were compared with 363 controls matchedfor sex and age. A family history of colorectal cancer was positivelyassociated with colon cancer (odds ratio (OR)=2.0, 95% confidenceinterval(Cl)1.03–3.87) and rectal cancer (OR=2.1 Cl 0.94–4.48),but a family history of other cancers did not increase the risk.The proportion of patients with a family history of colorectalcancer within first-degree relatives was 12.4% — appreciablyhigher than figures previously reported in Japan. On the otherhand, the incidence of hereditary non-polyposis colorectal cancerwas 1.4%, and lower than previous estimates. Among dietary factors,a western-style diet significantly increased the risk of bothcolon and rectal cancer (OR = 2.3 Cl 1.30–3.88 and OR=2.1Cl 1.26–3.63, respectively). Consumption of rice was protectiveagainst both colon and rectal cancer(OR=0.5 Cl 0.31–0.82and OR = 0.3 Cl 0.18–0.65, respectively). Animal meat,oily food, fish, vegetables and fruit were shown to affect therisk, but no statistically significant correlation was found.Among other factors, constipation increased the risk of coloncancer (OR= 2.0 Cl 1.02–3.76) and consumption of coffeeraised the risk of rectal cancer (OR =1.7 Cl 1.07–2.82).Our findings suggest that a family history of colorectal canceris an important risk factor for this disease, and does not contradictthe hypothesis that the risk of colorectal cancer in Japan maybe influenced by westernization of lifestyle. However, we wereunable to find conclusive evidence that familial clusteringof this disease is strongly affected by environmental factorsor genetic diseases such as hereditary non-polyposis colorectalcancer.     

Risk of colon cancer associated with a family history of cancer or colorectal polyps: The Diet,Activity, and Reproduction in Colon Cancer Study

The Diet, Activity, and Reproduction in Colon Cancer (DARCC) study is a large, multi-center case-control study of colon cancer. We examined family histories of cancer among first-degree relatives obtained by computer-assisted in-person interviews from the DARCC to study the impact of family histories of several cancers and colorectal polyps on colon cancer risk. We examined familial cancer risks both by treating a family history of polyps or cancer as a covariate in a logistic regression model, and by comparing cancer or polyp incidence among relatives of cases to incidence among relatives of controls in a proportional hazards model. There were few differences between the odds ratios (OR) or confidence intervals (CI) generated from logistic regression models and the hazard rate ratios (HRR) generated from the proportional hazards models. Overall, the OR of colon cancer among subjects with a family history of colorectal cancer was 1.77. There were only minor differences in risk by sex, age and subsite. A family history of colorectal polyps also increased risk by about the same amount as a family history of colorectal cancer. The increased risk associated with a family history of polyps did not appear to decrease with age. Int. J. Cancer 78:157–160, 1998.© 1998 Wiley-Liss, Inc.     

Dietary calcium, vitamin D, VDR genotypes and colorectal cancer

The vitamin D receptor (VDR) may importantly modulate risk of colorectal cancer either independently or in conjunction with calcium and vitamin D intake. We evaluate the association between calcium, vitamin D, dairy products, and VDR polymorphisms in 2 case-control studies of colon and rectal cancer (n = 2,306 cases and 2,749 controls). Dietary intake was evaluated using a detailed diet history questionnaire. Two VDR polymorphisms were evaluated: an intron 8 Bsm 1 polymorphism and a 3' untranslated region poly-A length polymorphism (designated S for short and L for long). The SS genotype reduced risk of colorectal cancer for men (odds ratio [OR] = 0.71; 95% confidence interval [CI] = 0.55-0.92). High levels of calcium intake reduced risk of rectal cancer in women (OR = 0.39; 95% CI = 0.24-0.64) but were not associated with rectal cancer in men (OR = 1.02; 95% CI = 0.66-1.56). Similar reduced rectal cancer risk among women was observed at high levels of vitamin D (OR = 0.52; 95% CI = 0.32-0.85) and low-fat dairy products (OR = 0.61; 95% CI = 0.39-0.94). High levels of sunshine exposure reduced risk of rectal cancer among those diagnosed when <60 years of age (OR = 0.62, 95% CI = 0.42-0.93). Examination of calcium in conjunction with VDR genotype showed that a significant 40% reduction in risk of rectal cancer was observed for the SS or BB VDR genotypes when calcium intake was low (p interaction = 0.01 for calcium interaction). For colon cancer, high levels of dietary intake of calcium, vitamin D, and low-fat dairy products reduced risk of cancer for the SS or BB VDR genotypes, although the p for interaction was not statistically significant. These data support previous observations that high levels of calcium and vitamin D reduce risk of rectal cancer and provide support for a weak protective effect for the SS and BB VDR genotypes. The risk associated with VDR genotype seems to depend upon the level of dietary calcium and vitamin D and tumor site.     

Familial risk of hepatocellular carcinoma among chronic hepatitis B carriers and their relatives

BACKGROUND: Familial predisposition as a risk factor for hepatocellular carcinoma (HCC) in hepatitis B virus (HBV) carriers has not been thoroughly explored. METHODS: The HCC risk associated with having parents and/or siblings with HCC was evaluated by use of a cohort study of 4808 male HBV carriers. A case-control family study was also conducted on data from first-degree relatives of 553 HBV carriers who had newly diagnosed HCC (case subjects) and 4684 HBV carriers without HCC (control subjects). RESULTS: In the cohort study, HBV carriers with a family history of HCC had a multivariate-adjusted rate ratio for HCC of 2.41 (95% confidence interval [CI] = 1.47-3.95) compared with HBV carriers without a family history of HCC. For carriers with two or more affected relatives, the ratio increased to 5.55 (95% CI = 2.02-15.26). Cumulative HCC risk by age 70 years was 235.6 per 1000 (95% CI = 95. 3-375.9 per 1000) for HBV carriers with family history compared with 88.9 per 1000 (95% CI = 67.9-109.9 per 1000) for those without. In the case-control family study, first-degree relatives of case subjects were more likely to have HCC (age-sex-adjusted odds ratio [OR] = 2.57; 95% CI = 2.03-3.25) than first-degree relatives of control subjects. The excess risk of HCC among relatives was particularly evident in siblings (sisters-age-adjusted OR = 4.55 [95% CI = 2.22-9.31]; brothers-age-adjusted OR = 3.73 [95% CI = 2. 64-5.27]), but it was also observed in parents. The cumulative risk of HCC to age 80 years was 83.0 per 1000 among relatives of case subjects and 42.0 per 1000 among relatives of control subjects. Among relatives of case subjects, the cumulative risk of HCC was greater if the case subjects were diagnosed before age 50 years (two-sided P =.047). Liver cirrhosis was 2.29 (95% CI = 1.68-3.11) times more frequent in relatives of case subjects than in relatives of control subjects. CONCLUSIONS: First-degree relatives of patients with HBV-related HCC appear to be at increased risk of HCC and should be considered in the formulation of HCC-screening programs.     

Family history of colorectal adenomatous polyps as a risk factor for colorectal cancer

The aim of this study was to evaluate the risk of common colorectal cancer among first-degree relatives of patients with colorectal adenomatous polyps. In a population screening programme, 59406 subjects underwent an immunochemical faecal occult blood test. In a medical check-up-based cross-sectional study, 6139 subjects had a colonoscopic examination. They were divided into two groups, according to the results of a questionnaire on family history of colorectal adenomatous polyps, and the detection rates for colorectal cancer were compared in the groups positive or negative for a family history of colorectal adenomatous polyps. In the screening programme-based cross-sectional study, the detection rate for colorectal cancer was 0.57% (95% confidence interval (CI): 0.38-0.76) and 0.15% (95% CI: 0.12-0.18) in subjects with and without a family history of colorectal adenomatous polyps, respectively, showing a significant difference in the detection rate for colorectal cancer between the two groups (P<0.05). In the medical check-up-based cross-sectional study, the detection rate for colorectal cancer was 2.31% (95% CI: 1.15-3.47) and 0.53% (95% CI: 0. 34-0.72) in subjects with and without a family history of colorectal adenomatous polyps, respectively, indicating a significant difference between the two groups (P<0.05). These findings indicate that first-degree relatives of patients with colorectal adenomatous polyps have an elevated risk for common colorectal cancer, and that people with a family history of colorectal adenomatous polyps should be considered as a priority group for colorectal cancer screening.     

Risk of bladder cancer associated with family history of cancer: do low-penetrance polymorphisms account for the increase in risk?

The relationship between family history of cancer in first-degree relatives and risk of bladder cancer was examined in the Spanish Bladder Cancer Study. Information on family history of cancer was obtained for 1,158 newly diagnosed bladder cancer cases and 1,244 controls included in 18 hospitals between 1998 and 2001. A total of 464 (40.1%) cases and 436 (35.1%) controls reported a family history of cancer in >/=1 relative [odds ratio (OR), 1.32; 95% confidence interval (95% CI), 1.11-1.59]; the OR was 1.23 (95% CI, 1.01-1.50) among those with only one relative affected and 1.67 (95% CI, 1.23-2.29) among those with >/=2 affected relatives (P(trend) = 0.0004). A greater risk of bladder cancer was observed among those diagnosed at age 相似文献   

Family history of cancer and associated risk of developing neuroendocrine tumors: a case-control study.

BACKGROUND: Carcinoids are rare neuroendocrine tumors (NET). Familial clusterings of NETs are rarely reported, except for a small proportion associated with multiple endocrine neoplasia syndrome type 1. We evaluated the effect of positive family history of NET as well as other cancers on the development of NETs arising at five different locations. METHODS: We conducted a retrospective, hospital-based, case-control study involving 740 patients with histologically confirmed NETs and 924 healthy controls. Information on family history of cancer was collected, and unconditional logistic regression analysis was used to determine adjusted odds ratios (AOR) and 95% confidence intervals (CI). RESULTS: The authors observed a significant relationship between first-degree relatives with cancers and the development of NETs arising at the small intestine, stomach, lung, and pancreas; AORs (95% CI) were 1.6 (1.1-2.4), 2.5 (1.1-6.3), 2.6 (1.5-4.5), and 1.8 (1.1-3.1), respectively. A first-degree family history of esophageal cancer was significantly associated with pancreatic NETs; AOR, 5.6 (95% CI, 1.1-29.6). There was a 70% and 130% increased risk of developing small intestinal NETs among subjects with family histories of colorectal cancer and prostate cancer, respectively. Moreover, individuals with a family history of lung cancer had a 2-fold increase in risk of developing pulmonary NETs. CONCLUSIONS: Having a first-degree relative with any cancer in general, and NET in particular, was a risk factor for NETs. The elevated risk of developing NETs extended to individuals with a family history of other cancers (not NETs) among first-degree relatives. These results suggested that risk of NETs may be partially explained by genetic factors.     

Family history of hemolymphopoietic and other cancers and risk of non-Hodgkin's lymphoma.

We investigated the risk of lymphomas, hemolymphopoietic (HLP) cancers (including lymphomas), and non-HLP cancers in first-degree relatives of non-Hodgkin's lymphoma (NHL) cases in an Italian case-control study on 225 patients (median age, 59 years) with a new diagnosis of NHL and 504 hospital controls (median age, 63 years), admitted for a wide spectrum of acute, nonneoplastic, nonimmune conditions. We estimated odds ratios (OR) adjusted for sex, age, family size, and other potential confounders. We also built the cohort of all first-degree relatives and computed age and sex adjusted hazard ratios (HR) using proportional hazard models. A history of lymphoma in first-degree relatives was reported by 5 NHL cases and 3 controls [OR, 3.2; 95% confidence interval (95% CI), 0.7-14.4] whereas 14 cases and 11 controls reported a family history of HLP cancers (OR, 3.0; 95% CI, 1.2-7.0). The HR of relatives of NHL cases, compared with relatives of controls, was 4.5 (95% CI, 1.1-18.8) for lymphomas, 3.5 (95% CI, 1.5-7.4) for HLP cancers, 1.6 (95% CI, 1.3-2.0) for all cancers, and 1.0 (95% CI, 0.9-1.1) for all causes of deaths. The HRs were higher for relatives of NHL cases diagnosed before the age of 50 years: 7.1 for HLP cancers, 2.0 for all cancers, and 1.6 for all deaths. A family history of cancer of the liver (OR, 2.1; 95% CI, 1.0-4.2), breast (OR, 2.0; 95% CI, 1.0-3.6), and kidney (OR, 4.6; 95% CI, 1.0-20.9) increased NHL risk. The OR was also elevated for all cancer sites (OR, 1.7 95% CI, 1.2-2.4) and the risk increased with the number of affected relatives also when HLP cancers were excluded.     

Risk of malignancy in first-degree relatives of patients with pancreatic carcinoma

BACKGROUND: Approximately 5-10% of pancreatic carcinoma (PC) patients report a family history of the disease. In some families, mutations of tumor suppressor genes have been elucidated, but for most the causative gene remains unidentified. Counseling the families of PC patients regarding their risk of cancer remains problematic because little information is available. METHODS: The authors analyzed family history questionnaires completed by 426 unselected, sequential Mayo Clinic patients with PC. The prevalence of malignancy reported among 3355 of their first-degree relatives was compared with the Surveillance, Epidemiology, and End Results Project (SEER) 9 (2000) registry. Age-adjusted and gender-adjusted standardized incidence ratios (SIRs) were generated. RESULTS: Greater than 130,000 person-years at risk for cancer among the first-degree relatives were analyzed. The risk of PC was found to be increased among the first-degree relatives of patients with PC (SIR of 1.88; 95% confidence interval [95% CI], 1.27-2.68), as was the risk of liver carcinoma (SIR of 2.70; 95% CI, 1.51-4.46). Lymphoma (SIR of 0.28; 95% CI, 0.12-0.55), bladder carcinoma (SIR of 0.55; 95% CI, 0.31-0.89), breast carcinoma (SIR of 0.73; 95% CI, 0.57-0.92), lung carcinoma (SIR of 0.62; 95% CI, 0.47-0.80), and prostate carcinoma (SIR of 0.71; 95% CI, 0.54-0.92) were found to be underrepresented. When the proband was age < 60 years, the risk of PC to first-degree relatives was found to be increased further (SIR of 2.86; 95% CI, 1.15-5.89). In this subgroup, no other malignancies were found to be significantly increased, although the risks of melanoma (SIR of 1.73; 95% CI, 0.70-3.57), ovarian carcinoma (SIR of 2.20; 95% CI, 0.72-5.12), and colon carcinoma (SIR of 1.37; 95% CI, 0.80-2.19) were suggestive. CONCLUSIONS: There was a nearly twofold increased risk of PC in the first-degree relatives of PC probands. This risk was found to increase nearly threefold when patients were diagnosed before age 60 years. At the current time, in the absence of a pedigree suggestive of known familial cancer syndromes, the current study results do not support targeted screening for other malignancies in the first-degree relatives of patients with sporadic PC.     

A Case-Control Study of Male Colorectal Cancer in Aichi Prefecture, Japan: with Special Reference to Occupational Activity Level, Drinking Habits and Family History

The relationships of occupational activity level, drinking habits and family history of cancer to the risk of male colorectal cancer by subsites were investigated in a case-control study involving 1,716 cases with colon cancer, 1,611 cases with rectal cancer and 16,600 controls with other sites of cancer identified from the Aichi Cancer Registry, Japan 1979–1987. An occupation with a low activity level was associated with an increased risk of colorectal cancer; the age-adjusted relative risk (RR) compared to the high activity level group was 1.92 (95% confidence interval (CI): 1.38–2.67) for proximal colon cancer, 1.52 (95% CI: 1.19–1.94) for distal colon cancer and 1.38 (95% CI: 1.17–1.62) for rectal cancer. Beer drinkers showed an increased risk of colorectal cancer; the age-adjusted RR was 1.49 (95% CI: 1.13–1.95) for proximal colon cancer, 1.65 (95% CI: 1.34-2.04) for distal colon cancer and 1.88 (95% CI: 1.62–2.18) for rectal cancer. The RR for family history of colorectal cancer was 3.40 (95% CI: 2.19–5.29) for proximal colon cancer, 2.54 (95% CI: 1.73–3.75) for distal colon cancer and 1.78 (95% CI: 1.28–2.49) for rectal cancer. Multivariate analysis controlled for age, residence, marital status and smoking in addition to occupational activity level, beer drinking and family history of colorectal cancer did not materially change the RRs. When these three variables were combined, the RR was 15.72 (95% CI: 5.40–45.78) for proximal colon cancer, 10.55 (95% CI: 4.24–26.27) for distal colon cancer and 6.69 (95% CI: 3.12–14.36) for rectal cancer.     

Family history and risk of breast cancer in hispanic and non-hispanic women: the New Mexico Women's Health Study

Objectives: Many epidemiologic studies have demonstrated that an increased risk of breast cancer is associated with positive family history of this disease. Little information had been available on the relationship of breast cancer risk with family history in Hispanic women. To investigate the association of family history of breast cancer on the risk of breast cancer, we examined the data from the New Mexico Women's Health Study (NMWHS), a statewide case–control study. Methods: In this study 712 women (332 Hispanics and 380 non-Hispanic whites) with breast cancer and 844 controls (388 Hispanics and 456 non-Hispanic whites) were included. Conditional logistic regression was used to estimate the odds ratio (OR) and 95% confidence interval (95% CI), adjusted for sociodemographic, medical, and reproductive factors. Results: We found an increased risk in women with a history of breast cancer in one or more first-degree or second-degree relatives (OR = 1.5, 95% CI 1.2–1.9), first-degree relatives (OR = 1.3, 95% CI 1.0–1.8) and second-degree relatives (OR = 1.6, 95% CI 1.2–2.2). Hispanic women had higher risk estimates for a positive family history (OR = 1.7, 95% CI 1.1–2.5) than non-Hispanic white women (OR = 1.4, 95% CI 1.0–2.0); however, the differences were not statistically significant. In both ethnic groups a higher risk was observed in premenopausal women compared with postmenopausal women and women diagnosed with breast cancer before age 50years compared with older women. Conclusions: The results indicate that Hispanic women with a family history of breast cancer are at increased risk of breast cancer.