Testicular, other genital, and breast cancers in first-degree relatives of testicular cancer patients and controls.

Previous studies showed an increased prevalence of testicular cancer among fathers and brothers of testicular cancer patients. We examined whether testicular, other genital, and breast cancers aggregate in parents and siblings of testicular cancer patients in a population-based case-control study, including males, ages 15 to 69 years at diagnosis, with primary malignant tumors of the testes or extragonadal germ cell tumors. Controls were ascertained through the mandatory registries of residents and frequency matched to the cases by age and region of residence. In a face-to-face interview, 269 cases and 797 controls provided health-related information on parents and siblings. We calculated odds ratios (OR) and corresponding 95% confidence intervals (95% CI) based on the generalized estimating equations technique, adjusting for the matching variables and relatives' age. Three (1.1%) fathers and eight (3.2%) brothers of cases were affected with testicular cancer compared with four (0.5%) fathers and two (0.2%) brothers of controls. The OR (95% CI) of familial testicular cancer was 6.6 (2.35-18.77). Only nonseminoma patients had fathers with testicular cancer, whereas the affected brothers were all related to seminoma patients. Overall, we found an increased risk for genital other than testicular cancers (OR 2.5, 95% CI 1.43-4.43). For breast cancer, we detected an increased risk in sisters (OR 9.5, 95% CI 2.01-45.16, adjusted for age of study participant and age of sister) but not in mothers. Our findings support the hypothesis that testicular and other genital cancers have a common familial component that may be due to genetic and shared exogenous factors such as estrogen exposure during fetal development.     

Risk of cancer in first‐ and second‐degree relatives of testicular germ cell tumor cases and controls

Risk factors for testicular germ cell tumors (TGCT) have not been well identified; however, data suggest that risks of cancer in family members of men with TGCT is elevated. Using family history data from 738 cases and 904 controls enrolled in the U.S. Servicemen's Testicular Tumor Environmental and Endocrine Determinants (STEED) Study from 2002 to 2005, the risk of cancer in first‐ and second‐degree family members of these men was examined. Relative risks (RRs) and 95% confidence intervals (CIs) were estimated using Cox proportional hazards models, adjusting for reference age of case or control, race/ethnicity of case or control, sex of family member and lineage (maternal vs. paternal). An increased risk of all cancer among first‐degree relatives of cases compared to controls was observed (RR = 1.17, 95% CI: 1.01–1.35). There were suggestions of differences in risk when stratifying all relatives by lineage. For maternal relatives, there was a statistically significant increased risk of all cancer (RR = 1.16, 95% CI: 1.04–1.30), digestive tract (RR = 1.52, 95% CI: 1.15–2.00) and male genital organ cancer (RR = 1.70, 95% CI: 1.15–2.51); there was also a suggestion of increased risks of hematopoetic cancers, cancers in the female genital organs and nonmelanoma skin cancer. For paternal relatives, there was a statistically significant association only with decreased risk of lung cancer (RR = 0.69, 95% CI: 0.51–0.94). Thus, this study suggests that there may be aggregation of cancer among families of men diagnosed with TGCT. Published 2008 Wiley‐Liss, Inc.     

CDKN2a mutation‐negative melanoma families have increased risk exclusively for skin cancers but not for other malignancies

Germline CDKN2A mutations are found in 5–20% of melanoma families. Numerous studies have shown that carriers of CDKN2A mutations have increased risks of non‐melanoma cancers, but so far there have been no studies investigating cancer risks in CDKN2A wild type (wt) melanoma families. In this prospective cohort study, index melanoma cases (n = 224) and their first‐degree relatives (n = 944) were identified from 154 confirmed CDKN2A wt melanoma families. Cancer diagnoses in family members and matched controls were obtained from the Swedish Cancer Registry. Relative risks (RR), odds ratios (OR) and two‐sided 95% confidence intervals (95% CI) were calculated. In index cases and first‐degree relatives, the prospective RR for melanoma was 56.9 (95% CI 31.4–102.1) and 7.0 (95% CI 4.2–11.4), respectively, and for squamous cell skin cancers 9.1 (95% CI 6.0–13.7) and 3.4 (95% CI 2.2–5.2), respectively. In neither group, elevated risks were seen for non‐skin cancers. In a subgroup analysis, CDKN2A wt melanoma families with young (<40 years) melanoma cases were found to have increased risk of non‐skin cancers (RR 1.5, 95% CI 1.0–1.5). Further, MC1R gene variants were increased in familial melanoma cases compared to controls (OR 2.4, 95% CI 1.6–3.4). Our findings suggest that in the majority of CDKN2A wt melanoma families, a segregation of variants in low‐risk melanoma genes such as MC1R causes increased skin cancer susceptibility, rather than mutations in high‐risk cancer predisposing genes, such mutations are more probable to be found in melanoma families with young melanoma cases. This study further supports an implication of CDKN2A mutation screening as a clinical test that determines counseling and follows up routines of melanoma families.     

Familial testicular cancer in a single-centre population

Familial occurrence of testicular cancer suggests a genetic predisposition to the disease. A genetic susceptibility may also be reflected by the occurrence of bilateral testicular neoplasms and the high rates of urogenital developmental anomalies in families prone to testicular cancer. In this study, the proportion of familial testicular cancer cases was analyzed retrospectively in a single-centre population of 693 testicular cancer patients treated between 1977 and 1997 and the relative risk (RR) for first-degree relatives of patients was estimated. In addition, the existence of bilateral testicular neoplasms and urogenital developmental anomalies in familial testicular cancer patients was evaluated. 24 of the 693 patients (3.5%) had a first-degree relative with testicular cancer. These 24 cases belonged to 17 families; in 7 of these 17 families both affected first-degree family members were part of the study population of 693 patients. Consequently, the 693 studied patients belonged to a total of 686 families. Thus, the actual proportion of familial testicular cancer was 2.5% (17 of 686 families). The familial cases consisted of 11 brother pairs, including 2 pairs of identical twins and 1 pair which also had two affected cousins, and 6 father-son pairs (in total 36 cases, 12 treated elsewhere). Estimates of the RR to first-degree relatives showed a 9- to 13-fold increased RR to brothers (P < 0.001) and a 2-fold increased RR to fathers (P = non-significant (n.s)) of testicular cancer patients. Among the 36 patients with familial testicular cancer, 2 (5.6%) had bilateral testicular cancer, 4 (11.1%) had undescended testis, 3 (8.3%) had inguinal hernia, and 1 (2.8%) showed renal hypoplasia. The present data on familial occurrence of testicular cancer may lend support to a role of genetic factors in the aetiology of testicular cancer.     

Prospective study of body mass index,physical activity and thyroid cancer

Increased body size and physical inactivity are positively related to risk of several cancers, but only few epidemiologic studies have investigated body‐mass index (BMI) and physical activity in relation to thyroid cancer. We examined the relations of BMI and physical activity to thyroid cancer in a prospective cohort of 484,326 United States men and women, followed from 1995/1996 to 2003. During 3,490,300 person‐years of follow‐up, we documented 352 newly incident cases of thyroid cancer. The multivariate relative risks (RR) of thyroid cancer for BMI values of 18.5–24.9 (reference), 25.0–29.9 and ≥30 kg m^?2 were 1.0, 1.27 and 1.39 [95% confidence interval (CI) = 1.05–1.85]. Adiposity predicted papillary thyroid cancers (RR comparing extreme BMI categories = 1.47; 95% CI = 1.03–2.10) and, based on small numbers, suggestively predicted follicular thyroid cancers (RR = 1.49; 95% CI = 0.79–2.82) and anaplastic thyroid cancers (RR = 5.80; 95% CI = 0.99–34.19). No relation with BMI was noted for medullary thyroid cancers (RR = 0.97; 95% CI = 0.27–3.43). The positive relation of BMI to total thyroid cancer was evident for men but not for women. However, the test of interaction (p = 0.463) indicated no statistically significant gender difference. Physical activity was unassociated with thyroid cancer. The RRs of total thyroid cancer for low (reference), intermediate, and high level of physical activity were 1.0, 1.01 and 1.01 (95% CI = 0.76–1.34, p for trend = 0.931), respectively. Our results support an adverse effect of adiposity on risk for developing total and papillary, and possibly follicular thyroid cancers. Based on only 15 cases, adiposity was unrelated to medullary thyroid cancers. Physical activity was unrelated to total thyroid cancer.     

Second malignancies following pure seminoma

PURPOSE: Second malignancies in patients with pure testicular seminoma were studied in order to look for adverse late effects of treatment and to study the significance of second malignancies during follow-up. PATIENTS, METHODS: In a multicentric investigation, 839 consecutive patients with pure testicular seminoma were observed for a median follow-up of 3.9 years. Thirty-seven patients had been excluded from the study because they already had had either a contralateral testicular germ cell tumor or another malignancy. 758 patients received radiotherapy, 76 underwent chemotherapy, 5 had surveillance only. The expected rate of second cancers was calculated according to the data of the cancer registry of Saarland, Germany. RESULTS: Twenty-two second cancers (13 contralateral testicular tumors, 9 extratesticular malignancies) were recorded. The overall risk of having a second cancer was RR = 4.8 (95% CI 3. 0-7.3). The risk of having a subsequent testicular tumor is RR = 44. 8 (95% Cl 23.9-76.7). 1.1% of the patients developed a nontesticular second tumor. The risk of having a nontesticular second cancer is RR = 2.1 (95% CI 1.0-4.0). A significantly increased risk was observed for renal cell cancer as well (RR = 12.5; 95% Cl: 1.5-45.1). Increased RR without reaching statistical significance were found for rectal cancer (RR = 5.0; 95% Cl: 0.1-27.9) and non-Hodgkin lymphoma (RR = 6.7; 95% CI 0.2-37.1). None of the second cancers were directly located within the radiation field; 5 neoplasms arose at the border of the radiation field. CONCLUSIONS: This study confirmed the increased risk of having a second testicular germ cell cancer. There is also a small but definitely increased overall risk of having a nontesticular second cancer. Treatment-unrelated factors - possibly genetic predisposition - must be considered for a substantial number of these second tumors, since in the present study the follow-up was rather short and most of the second cancers were located outside of the radiation fields. In particular, the association of renal cancer with testicular cancer appears to be a more than chance occurrence. Second cancer is a real hazard following treatment of testicular cancers and should always be considered during follow-up.     

Risk of cancer in a large cohort of U.S. veterans with diabetes

Prior studies of cancer risk among diabetic men have reported inconsistent findings. The aim of this study was to assess the risk of cancer among a large cohort (n = 4,501,578) of black and white U.S. veterans admitted to Veterans Affairs hospitals. The cancer risk among men with diabetes (n = 594,815) was compared to the risk among men without diabetes (n = 3,906,763). Poisson regression was used to estimate adjusted relative risks (RRs) and 95% confidence intervals (CIs). Overall, men with diabetes had a significantly lower risk of cancer (RR = 0.93, 95%CI = 0.93–0.94). Men with diabetes, however, had increased risks of cancers of the liver (RR = 1.95, 95%CI = 1.82–2.09), pancreas (RR = 1.50, 95%CI = 1.42–1.59), biliary tract (RR = 1.41, 95%CI = 1.22–1.62), colon (RR = 1.20, 95%CI = 1.16–1.25), rectum (RR = 1.12, 95%CI = 1.07–1.18), and kidney (RR = 1.09, 95%CI = 1.03–1.16), as well as leukemia (RR = 1.14, 95%CI = 1.08–1.21) and melanoma (RR = 1.13, 95%CI = 1.03–1.24). In contrast, men with diabetes had decreased risks of cancers of the prostate (RR = 0.89, 95%CI = 0.87–0.91), brain (RR = 0.91, 95% CI = 0.82–0.99), buccal cavity (RR = 0.85, 95%CI = 0.82–0.89), lung (RR = 0.79, 95%CI = 0.77–0.80), esophagus (RR = 0.77, 95%CI = 0.72–0.82), and larynx (RR = 0.76, 95%CI = 0.71–0.80). These findings indicate that black and white men with diabetes are at significantly lower risk of total cancer and of two of the most common cancers among U.S. males; lung and prostate cancers. These decreased risks were offset, however, by increased risks of cancer at several sites. Hyperinsulinemia may explain the increased risks of the digestive cancers, while lower testosterone levels, in the case of prostate cancer, and higher BMI, in the case of lung cancer, may explain the decreased risks of those tumors.     

Aspirin and cancer risk: a quantitative review to 2011

BackgroundAspirin has been associated to a reduced risk of colorectal and possibly of a few other common cancers.MethodsTo provide an up-to-date quantification of this association, we conducted a meta-analysis of all observational studies on aspirin and 12 selected cancer sites published up to September 2011.ResultsRegular aspirin is associated with a statistically significant reduced risk of colorectal cancer [summary relative risk (RR) from random effects models = 0.73, 95% confidence interval (CI) 0.67–0.79], and of other digestive tract cancers (RR = 0.61, 95% CI = 0.50–0.76, for squamous cell esophageal cancer; RR = 0.64, 95% CI = 0.52–0.78, for esophageal and gastric cardia adenocarcinoma; and RR = 0.67, 95% CI = 0.54–0.83, for gastric cancer), with somewhat stronger reductions in risk in case–control than in cohort studies. Modest inverse associations were also observed for breast (RR = 0.90, 95% CI = 0.85–0.95) and prostate cancer (RR = 0.90, 95% CI = 0.85–0.96), while lung cancer was significantly reduced in case–control studies (0.73, 95% CI = 0.55–0.98) but not in cohort ones (RR = 0.98, 95% CI = 0.92–1.05). No meaningful overall associations were observed for cancers of the pancreas, endometrium, ovary, bladder, and kidney.ConclusionsObservational studies indicate a beneficial role of aspirin on colorectal and other digestive tract cancers; modest risk reductions were also observed for breast and prostate cancer. Results are, however, heterogeneous across studies and dose–risk and duration–risk relationships are still unclear.     

Familial testicular cancer in Norway and southern Sweden.

Information about occurrence of testicular cancer (TC) in relatives of TC patients has been collected using questionnaires from 797 out of 922 consecutive Norwegian and 178 out of 237 Swedish patients with TC seen at the Norwegian Radium Hospital and the University Hospital Lund in Sweden during 1981-91. Fifty-one Norwegian and five Swedish patients had a relative with confirmed TC. Thus, 51/922 (5.5%) of the Norwegian and 5/237 (2.1%) of the Swedish patients treated during the time interval investigated were considered to have familial TC. Thirty-two of the patients had an affected first-degree relative. Expected numbers of cancers in the relatives were computed from data in the Norwegian and Swedish Cancer Registries. Standardised incidence ratios (SIRs) were taken as observed numbers of TC/expected numbers of TC in the relatives. The SIR for brothers was 10.2 (95% confidence interval 6.22-15.77). SIR for fathers was 4.3 (1.6-9.3) and for sons 5.7 (0.7-23.2). The point estimate for the risk to brothers in the Norwegian part of the sample to develop TC by the age of 60 was 4.1% (95% CI 1.7-6.6%). This study indicates that genetic factors may be of greater importance in TC than previously assumed. Patients with familial testicular cancer had bilateral tumours more often than sporadic cases (9.8% bilaterality in familial vs 2.8% in sporadic cases, P=0.02). For patients with seminoma age of onset was lower in familial than in sporadic cases (32.9 vs 37.6 years, P=0.06). In father-son pairs, there was a statistically significant earlier age of diagnosis in the generation of sons (28.8 years vs 44.9 years, P=0.04). The prevalence of undescended testis (UDT) did not seem to be higher in familial than in sporadic TC (8.2% in familial TC and 13.3% in sporadic cases). This may indicate that different factors are of importance for the development of familial TC and UDT.     

Birth order and risk of testicular cancer

To explore the etiology of testicular cancer, cases of testicular cancer were identified among members of a cobort of Danish boys born between 1941 and 1957 (inclusive), who had attended schools in Copenhagen and Gentofte and whose school health records were contained in an archive under the supervision of the Danish Cancer Registry. One hundred and eighty-three cases of testicular cancer diagnosed before 31 December 1984 were identified; 366 controls, matched to cases by sex and age, were selected from the same cohort. Information on potential risk factors and confounders was obtained from two sources: school health records and midwife protocols, both of which were recorded prior to the diagnosis of testicular cancer in cases. Relative risks (RR) approximated by the odds ratios were calculated and, in logistic regression analyses, adjustments were done for known or suspected confounders. A decreasing risk of testicular cancer with increasing birth order was observed (P=0.020). Compared with being firstborn, being number four or more in birth order was associated with a significantly decreased RR for all testicular cancers (RR=0.3,95 percent confidence interval [CI]=0.3–0.8) and testicular seminoma (RR=0.1, CI=0.02–0.9). No association was observed between high social class and the risk of testicular cancer (RR=1.4, CI=0.8–2.3); neither was age at which the study subjects had mumps or measles related to risk of testicular cancer. No cases of mumps orchitis were observed before or during school years. A slightly increased RR for testicular cancer among boys from small families could be explained by the association between family size and birth order. The observed association between rank in birth order and the risk of testicular cancer was attributed to the reported differences in maternal estrogen levels in first cf second pregnancy, and supports the hypothesis of a tumor-initializing effect of high levels of estrogen early in a pregnancy on the developing testicular tissues.Dr Jensen, formerly Director of the Danish Cancer Registry and member of the CCC Editorial Board, died last year.     

Use of acetochlor and cancer incidence in the Agricultural Health Study

Since its registration in 1994 acetochlor has become a commonly used herbicide in the US, yet no epidemiologic study has evaluated its carcinogenicity in humans. We evaluated the use of acetochlor and cancer incidence among licensed pesticide applicators in the Agricultural Health Study. In telephone interviews administered during 1999–2005, participants provided information on acetochlor use, use of other pesticides and additional potential confounders. We used Poisson regression to estimate relative risks (RR) and 95% confidence intervals (95% CI) for cancers that occurred from the time of interview through 2011 in Iowa and 2010 in North Carolina. Among 33,484 men, there were 4,026 applicators who used acetochlor and 3,234 incident cancers, with 304 acetochlor‐exposed cases. Increased risk of lung cancer was observed among acetochlor users (RR = 1.74; 95% CI: 1.07–2.84) compared to nonusers, and among individuals who reported using acetochlor/atrazine product mixtures (RR = 2.33; 95% CI: 1.30–4.17), compared to nonusers of acetochlor. Colorectal cancer risk was significantly elevated among the highest category of acetochlor users (RR = 1.75; 95% CI: 1.08–2.83) compared to never users. Additionally, borderline significantly increased risk of melanoma (RR = 1.61; 95% CI: 0.98–2.66) and pancreatic cancer (RR = 2.36; 95% CI: 0.98–5.65) were observed among acetochlor users. The associations between acetochlor use and lung cancer, colorectal cancer, melanoma and pancreatic cancer are suggestive, however the lack of exposure‐response trends, small number of exposed cases and relatively short time between acetochlor use and cancer development prohibit definitive conclusions.     

Family history of cancer is a risk factor for squamous cell carcinoma of the head and neck in Brazil: A case-control study

To determine the role of familial factors in head and neck cancer, we analysed data from a hospital-based case-control study of squamous cell carcinoma of the head and neck in Brazil. There were 754 cases of squamous cell carcinoma of the head and neck (SCCHN) and 1,507 age- and gender-matched hospital-based controls with non-malignant diseases. Subjects provided information on the occurrence of cancer in first-degree relatives, as well as about other risk factors, including tobacco and alcohol consumption. Relative risks (RRs) were estimated for developing mouth, pharynx and larynx cancer when cancers in relatives were observed. RRs were adjusted for age, sex, city of admission and alcohol and tobacco consumption. The RR for developing SCCHN if a first-degree relative had cancer at any site was significantly elevated at 1.97. The RR was 3.65 (95% Cl: 1.97–6.76) if the relative had head and neck cancer. Significantly elevated risks for developing head and neck cancer were associated with siblings with head and neck cancer (RR = 8.57) and, to a lesser extent, with fathers with head and neck cancer (RR = 2.49). There was no significantly increased risk associated with mothers with head and neck cancer, but these tumours were rare among mothers. Our data show that familial, possibly genetic, factors are important in the aetiology of head and neck cancer. © 1995 Wiley-Liss, Inc.     

Cancer in first-degree relatives and risk of testicular cancer in Denmark

Familial aggregation of testicular cancer has been reported consistently, but it is less clear if there is any association between risk of testicular cancer and other cancers in the family. We conducted a population-based case-control study to examine the relationship between risk of testicular cancer and 22 different cancers in first-degree relatives. We included 3,297 cases of testicular cancer notified to the Danish Cancer Registry between 1991 and 2003. A total of 6,594 matched controls were selected from the Danish Civil Registration System, which also provided the identity of 40,104 first-degree relatives of case and controls. Familial cancer was identified by linkage to the Danish Cancer Registry, and we used conditional logistic regression to analyze whether cancer among first-degree relatives was associated with higher risk of testicular cancer. Rate ratio for testicular cancer was 4.63 (95% CI: 2.41-8.87) when a father, 8.30 (95% CI: 3.81-18.10) when a brother and 5.23 (95% CI: 1.35-20.26) when a son had testicular cancer compared to no familial testicular cancer. Results were similar when analyses were stratified by histologic subtypes of testicular cancer. Familial non-Hodgkin lymphoma and esophageal cancer were associated with testicular cancer; however, these may be chance findings. The familial aggregation of testicular and possibly other cancers may be explained by shared genes and/or shared environmental factors, but the mutual importance of each of these is difficult to determine.     

Cancer in patients with ulcerative colitis

A cohort of 5,546 ulcerative colitis patients was identified from the Danish Hospital Discharge Register for 1977–1989. Patients not included in the cohort comprised those with proctitis, those treated in outpatient clinics and those for whom follow-up was less than 1 year. The cohort was linked to the Danish Cancer Registry in order to assess the risks for colorectal and other cancers. The linkage revealed a significant increase in the number of colorectal cancers over that in the general population (RR = 1.8; n = 42; 95% CI = 1.3–2.4) with consistent relative risks during early and late follow-up. The relative risk was considerably higher among younger (20–39 years: RR = 22; n = 8; 95% CI = 9.7–44) than older patients (≥60 years: RR = 1.3; n = 25; 95% CI = 0.8–1.9), but the risk difference between patients and the general population was approximately constant across all ages. In addition, we observed a significant increase in the relative risk of hepatobiliary cancers (RR = 2.3; n = 9; 95% = 1.0–4.3) and a slight but significant increase in the relative risk of non-melanoma skin cancer (RR = 1.4; n = 37; 95% CI = 1.0–1.9). In summary, our population-based study confirms the increased risk of colorectal cancer among patients with ulcerative colitis and provides new leads suggesting that hepatobiliary cancer and non-melanoma skin cancer should be considered as possible sites for future patient monitoring. © 1995 Wiley-Liss, Inc.     

Relation of body mass index to cancer risk in 362,552 Swedish men

Background Obesity has been linked with increased risk for cancers of the colon, kidney, breast, endometrium and gallbladder. For other cancer sites, the relationship with obesity is less well quantified, and the effect of weight change on cancer risk is unclear. Methods We examined the health records of 362,552 Swedish men who underwent at least one physical examination from 1971 to 1992, and were followed until death or the end of 1999. Incident cancer cases were identified by linkage to the Swedish cancer registry. Poisson regression models were used to estimate relative risks of cancer for both body-mass index (BMI) at baseline exam and, in a subgroup of 107,815 men, change in BMI after six years of follow-up, adjusting for age and smoking status. Results Compared to men of normal weight, obese men had a significantly increased risk of all cancers combined (RR = 1.1; 95% CI = 1.0–1.2). The risks were most pronounced for esophageal adenocarcinoma (RR = 2.7; 95% CI = 1.3–5.6), renal cell carcinoma (RR = 1.8; 95% CI = 1.4–2.4), malignant melanoma (RR = 1.4; 95% CI = 1.1–1.7), and cancers of the colon (RR = 1.7; 95% CI = 1.5–2.0), rectum (RR = 1.4; 95% CI = 1.1–1.7), and liver (RR = 3.6; 95% CI = 2.6–5.0). Risk of esophageal squamous cell carcinoma was elevated for underweight men whose BMI was less than 18.5 (RR = 3.1; 95% CI = 1.1–8.3). An excess risk for cancers of the pancreas and connective tissue was observed only among nonsmokers. Compared to men whose weight remained stable, men with more than a 15% increase in BMI after six years of follow-up had an elevated risk of pancreas and renal cell cancers. Conclusions Obesity and weight gain increase the risk for several forms of cancer in men, and underscore the need for further study into carcinogenic mechanisms and preventive interventions.     

Breast Cancer Following Multiple Chest Fluoroscopies Among Tuberculosis Patients a Case-Control Study in Denmark

A case-control study of breast cancer among tuberculosis (TB) patients in Denmark (1937-1954) was conducted to provide additional information on the radiation risk associated with low-dose chest fluoroscopy exposures. Records of 46013 TB patients were linked to the Danish Cancer Registry and 125 subsequent female breast cancers identified. Medical records were located for 89 (71%) of these women who developed breast cancer and on 390 controls, who were individually matched to cases on age and calendar year of TB diagnosis, and survival. Common risk factors for breast cancer such as nulliparity (relative risk (RR)=2.5) and high relative weight (RR=2.6) were also identified in this population of TB patients. However no risk was evident with exposure to any type of fluoroscopy (RR=0.6; 95% CI=0.2-1.4), or to fluoroscopies performed to monitor lung collapse therapy (RR=0.8; 95% CI=0.5-1.4). Although based on only 7 breast cancers, there was a suggestion of an increased risk among women who received greater than 1 Gy to their breasts (RR=1.6; 95% CI=0.4-6.3). Because of the infrequent use of fluoroscopy in our study, the breast doses were too low, 0.27 Gy on average, to expect to detect a significant elevation in breast cancer risk overall. The findings do suggest, however, that current estimates of breast cancer risk following radiation are not greater than presently accepted, and that a relative excess of 40 per cent can be excluded with reasonable confidence following breast doses on the order of 0.3 Gy.     

Prospective study of breast cancer in relation to coffee,tea and caffeine in Sweden

Studies of coffee and tea consumption and caffeine intake as risk factors for breast cancer are inconclusive. We assessed coffee and tea consumption, caffeine intake, and possible confounding factors among 42,099 women from the Swedish Women's Lifestyle and Health study, the participants of which were aged 30–49 years at enrollment in 1991–1992. Complete follow‐up for breast cancer incidence was performed through 2012 via linkage to national registries. Poisson regression models were used to estimate relative risks (RRs) and 95% confidence intervals (CIs) for breast cancer. During follow‐up 1,395 breast cancers were diagnosed. The RR was 0.97 (95% CI 0.94–0.99) for a 1‐unit increase in cups of coffee/day, 1.14 (95% CI 1.05–1.24) for a 1‐unit increase in cups of tea/day, and 0.97 (95% CI 0.95–1.00) for a 100 mg/day increase in caffeine intake. Although the RR for no consumption (RR = 0.86, 95% CI 0.69–1.08), a group with a relatively small number of women, was not statistically significant, women with higher consumption had a decreased breast cancer risk (3–4 cups/day: RR = 0.87, 95% CI 0.76–1.00; ≥5 cups/day: RR = 0.81, 95% CI 0.70–0.94) compared to women consuming 1–2 cups of coffee/day. Compared to no consumption, women consuming >1 cups tea/day showed an increased breast cancer risk (RR = 1.19, 95% CI 1.00–1.42). Similar patterns of estimates were observed for breast cancer risk overall, during pre‐ and postmenopausal years, and for ER+ or PR+ breast cancer, but not for ER? and PR? breast cancer. Our findings suggest that coffee consumption and caffeine intake is negatively associated with the risk of overall and ER+/PR? breast cancer, and tea consumption is positively associated with the risk of overall and ER+/PR+ breast cancer.     

Continuing increased risk of oral/esophageal cancer after allogeneic hematopoietic stem cell transplantation in adults in association with chronic graft-versus-host disease

BackgroundThe number of long-term survivors after hematopoietic stem cell transplantation (HSCT) showed steady increase in the past two decades. Second malignancies after HSCT are a devastating late complication. We analyzed the incidence of, risk compared with that in the general population, and risk factors for secondary solid cancers.Patients and methodsPatients were 17 545 adult recipients of a first allogeneic stem cell transplantation between 1990 and 2007 in Japan. Risks of developing secondary solid tumors were compared with general population by using standard incidence ratios (SIRs).ResultsTwo-hundred sixty-nine secondary solid cancers were identified. The cumulative incidence was 0.7% [95% confidence interval (CI), 0.6%–0.9%] at 5 years and 1.7% (95% CI, 1.4%–1.9%) at 10 years after transplant. The risk was significantly higher than that in the general population (SIR = 1.8, 95% CI, 1.5–2.0). Risk was higher for oral cancer (SIR = 15.7, 95% CI, 12.1–20.1), esophageal cancer (SIR = 8.5, 95% CI, 6.1–11.5), colon cancer (SIR = 1.9, 95% CI, 1.2–2.7), skin cancer (SIR = 7.2, 95% CI, 3.9–12.4), and brain/nervous system cancer (SIR = 4.1, 95% CI, 1.6–8.4). The risk of developing oral, esophageal, or skin cancer was higher at all times after 1-year post-transplant. Extensive-type chronic graft-versus-host disease (GVHD) was a significant risk factor for the development of all solid tumors (RR = 1.8, P < 0.001), as well as for oral (RR = 2.9, P < 0.001) and esophageal (RR = 5.3, P < 0.001) cancers. Limited-type chronic GVHD was an independent risk factor for skin cancers (RR = 5.8, P = 0.016).ConclusionRecipients of allogeneic HSCT had a significantly higher ∼2-fold risk of developing secondary solid cancers than the general population. Lifelong screening for high-risk organ sites, especially oral or esophageal cancers, is important for recipients with active, or a history of, chronic GVHD.     

Age-specific familial risks in common cancers of the offspring

Quantitative data on familial cancer risks are important for clinical, psychological and scientific reasons. The available estimates carry many uncertainties due to sample size and possible bias in data collection and often refer to first-degree relatives of unspecified age and sex. We calculated sex- and age-specific familial hazard ratios (FHRs) of cancer in offspring aged 15–53 years of cancer probands at 16 male and 17 female cancer sites, based on registered nation-wide data, free from bias. The familial risks in offspring were high, >5 for thyroid (FHR 10.7 in all offspring, CI 95% 6.9–16.6), and testicular cancer (FHR 5.4, CI 95% 2.6–11.3), or intermediate, FHR 2–5, for colon, rectal, lung, breast, cervical, uterine, ovarian, skin (melanoma and squamous cell) and other endocrine gland cancers. FHRs <2.0 were observed for stomach, renal and nervous system cancers, lymphomas and leukemias. Some sex differences were observed: FHRs for male breast (only 2 cases) and thyroid cancers were over 2 times higher than the respective female ones. When parents were diagnosed before age 50 years, offspring were at an increased risk of familial breast, renal, skin (melanoma), nervous system, thyroid and non-thyroid endocrine gland cancers, particularly affecting young (<40 years) individuals. The parental diagnostic age also affected offspring's risk of colon, rectal, uterine and ovarian cancers, but young individuals were not at a particular risk. No effect of age was noted for cervical cancer and lymphoma.Int. J. Cancer 78:172–175, 1998.© 1998 Wiley-Liss, Inc.     

Fatherhood status and prostate cancer risk

BACKGROUND: Whether fatherhood status affects prostate cancer risk remains controversial. Recently, it was proposed that childless men are at lower prostate cancer risk than men with children and that men with sons may be at lower risk than men with daughters only. METHODS: National population-based register data were used to address these associations between fatherhood status and prostate cancer risk. The cohort comprised all men born in Denmark between 1935 and 1988, among whom 3400 developed prostate cancer during a total of 51.6 million person-years of follow-up between 1968 and 2003. RESULTS: Childless men were found to be at a 16% reduced risk of prostate cancer compared with fathers (rate ratio [RR] of 0.84; 95% confidence interval [95% CI], 0.73-0.95). The sex of the offspring did not affect prostate cancer risk (fathers with sons vs fathers without sons: RR of 0.99; 95% CI, 0.90-1.08). Among fathers, a significant trend was observed of gradually reduced prostate cancer risk with increasing number of children (P = .009), a pattern applying to both sons (P = .01) and daughters (P = .04). CONCLUSIONS: Our national cohort study corroborates the view that men without children constitute a group that is at a moderately reduced risk of prostate cancer. Among men with children, there appears to be a linear decline in prostate cancer risk with increasing number of children that is independent of the sex of the offspring.