Search

We examined associations between two forms of testosterone therapy (TT) and risks of seven cancers among men.SEER-Medicare combines cancer registry data from the Surveillance, Epidemiology, and End Results programme with Medicare claims. Our population-based case-control study included incident cancer cases diagnosed between 1992-2015: prostate (n = 130,713), lung (n = 105,466), colorectal (n = 56,433), bladder (n = 38,873), non-Hodgkin lymphoma (n = 17,854), melanoma (n = 14,241), and oesophageal (n = 9116). We selected 100,000 controls from a 5% random sample of Medicare beneficiaries and used logistic regression to estimate odds ratios (OR) and 95% confidence intervals (CI).TT was associated with lower risk of distant-stage prostate cancer (injection/implantation OR = 0.72, 95% CI: 0.60-0.86; topical OR = 0.50, 95% CI: 0.24-1.03). We also observed inverse associations for distant-stage colorectal cancer (injection/implantation OR = 0.75, 95% CI: 0.62-0.90; topical OR = 0.11, 95% CI: 0.05-0.24). Risks of distant-stage colorectal and prostate cancers decreased with time after initiating TT by injection/implantation. By contrast, TT was positively associated with distant-stage melanoma (injection/implantation OR = 1.70, 95% CI: 1.37-2.11). TT was not associated with bladder cancer, oesophageal cancer, lung cancer or non-Hodgkin lymphoma.TT was inversely associated with distant-stage prostate and colorectal cancers but was positively associated with distant-stage melanoma. These observations may suggest an aetiologic role for TT or the presence of residual confounding.

BackgroundDifferential uptake of prostate-specific antigen testing in the US and UK has been linked to between-country differences for prostate cancer incidence. We examined stage-specificfatalprostate cancer incidence trends in the US and England, by treatment and race/ethnicity.MethodsUsing data from the National Cancer Institute’s Surveillance, Epidemiology, and End Results program and Public Health England’s National Cancer Registration and Analysis Service, we identified prostate cancer patients diagnosed between 1995 and 2005, aged 45–84 years. Fatal prostate cancer was defined as death attributed to the disease within 10 years of diagnosis. We used age–period–cohort models to assess trends in fatal prostate cancer incidence.ResultsFatal prostate cancer incidence declined in the US by −7.5% each year and increased in England by 7.7% annually. These trends were primarily driven by locoregional disease in the US and distant disease in England. Black men in both countries had twofold to threefold higher fatal prostate cancer incidence rates, when compared with their white counterparts; however, receipt of radical prostatectomy lessened this disparity.ConclusionsWe report a significant increasing rate of fatal prostate cancer incidence among English men. The black–white racial disparity appears pervasive but is attenuated among those who received radical prostatectomy in the US.

Background: Chromosome 8q24 has emerged as an important genetic susceptibility region for several cancers, including prostate cancer; however, little is known about the contribution of DNA methylation in this region to risk. Methods: We prospectively evaluated DNA methylation at 8q24 in relation to prostate cancer using pre-diagnostic blood samples from 694 prostate cancer cases (including 172 aggressive cases) and 703 controls in the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial. We used logistic regression to estimate odds ratios and 95% confidence intervals. Results: Although none remained significant after adjustment for multiple testing (q>0.05), of the 50 CpG sites meeting quality control, we identified 8 sites that were nominally associated with prostate cancer (Ptrend

Background: Elevated body mass index (BMI, kg m−2) has been consistently associated with oesophageal adenocarcinoma (EA) and gastric cardia adenocarcinoma (GCA) incidence. However, effects of adiposity over the life course in relation to EA/GCA have not been thoroughly explored. Methods: We pooled two prospective cohort studies: NIH-AARP Diet and Health Study and Prostate, Lung, Colorectal, and Ovarian (PLCO) Cancer Screening Trial, with data on 409 796 individuals (633 EA, 415 GCA). At baseline, participants reported their height and weight at ages 20 and 50 years, and current. Body mass index trajectories were determined using latent class analysis. Hazard ratios (HRs) and 95% confidence intervals (CI) were estimated using proportional hazards regression. Results: Compared with individuals with a BMI

Background: It has been hypothesised that intrauterine exposures are important for subsequent prostate cancer risk. Prior epidemiological studies have used birthweight as a proxy of cumulative intrauterine exposures to test this hypothesis, but results have been inconsistent partly because of limited statistical power. Methods: We investigated birthweight in relation to prostate cancer in the Medical Research Council (MRC) National Survey of Health and Development (NSHD) using Cox proportional hazards models. We then conducted a meta-analysis of birthweight in relation to total and aggressive/lethal prostate cancer risks, combining results from the NSHD analysis with 13 additional studies on this relationship identified from a systematic search in four major scientific literature databases through January 2015. Results: Random-effects models found that per kg increase in birthweight was positively associated with total (OR=1.02, 95% confidence interval (95% CI)=1.00, 1.05; I2=13%) and aggressive/lethal prostate cancer (OR=1.08, 95% CI=0.99, 1.19; I2=40%). Sensitivity analyses restricted to studies with birthweight extracted from medical records demonstrated stronger positive associations with total (OR=1.11, 95% CI=1.03, 1.19; I2=0%) and aggressive/lethal (OR=1.37, 95% CI=1.09, 1.74; I2=0%) prostate cancer. These studies heavily overlapped with those based in Nordic countries. Conclusions: This study provides evidence that heavier birthweight may be associated with modest increased risks of total and aggressive/lethal prostate cancer, which supports the hypothesis that intrauterine exposures may be related to subsequent prostate cancer risks.

Background: Middle-aged obese adults are at substantially elevated risk of oesophageal adenocarcinoma. It is unclear whether this risk originates earlier in life. Methods: We assessed associations between childhood body mass index (BMI) and height—measured annually between ages 7 and 13—with adult oesophageal adenocarcinoma in a cohort from the Copenhagen School Health Records Register. Analyses included 255 053 children born during 1930–1971. Danish Cancer Registry linkage provided outcomes. We calculated hazard ratios (HRs) and 95% confidence intervals (CIs) using Cox proportional hazards regression. Results: During 5.4 million person-years of follow-up, 254 (216 males) incident oesophageal adenocarcinomas occurred. At each examined age, cancer risk increased linearly per unit BMI z-score, although associations were only statistically significant for ages 9–13. The HR for the age of 13 years was 1.31 (95% CI: 1.13, 1.51) per unit BMI z-score. Associations were similar in men and women and across birth cohorts. Childhood height was not related to cancer risk in men but was in women, although these analyses included just 38 female cases. HRs per unit height z-score at the age of 13 years were 1.04 (0.90, 1.19) in males and 1.77 (1.27, 2.47) in females, with similar results observed at the other examined ages. Conclusion: Individuals with higher childhood BMI were at elevated risk of oesophageal adenocarcinoma, even though these cancers occurred many decades later in life. Although the mechanisms require further investigation, our findings provide additional evidence for the long-term health risks of childhood obesity.

Prostate cancer is the second most common cancer among men worldwide and it is most frequent in high-income countries (World Cancer Research Fund/American Institute for Cancer Research, 2007; Globocan, 2012). Despite affecting large numbers of men, the aetiology of the disease is poorly understood. Moreover, none of the well-established risk factors such as age, ethnicity or a family history of prostate cancer are modifiable. Other prostate cancer risk factors that have been identified include adult obesity and dietary components, each of which are potentially modifiable, as well as non-modifiable risk factors such as adult height, genetic polymorphisms and hormonal factors. The contributions of these factors to the aetiology of prostate cancer are, however, unclear (Gronberg, 2003; Hsing and Chokkalingam, 2006). Adult anthropometry has been evaluated in relation to prostate cancer risk in several studies. Two meta-analyses have established that taller men have an increased risk of prostate cancer, however the effect sizes are modest (MacInnis and English, 2006;Zuccolo et al, 2008). Recently we found that tall boys, especially in late childhood, had an elevated risk of developing prostate cancer in adulthood (Cook et al, 2013). Additionally, several studies have found indications that adult obesity increases the risk of prostate cancer. However, the effect of greater adult body mass index (BMI; kg m−2) on prostate cancer risk is relatively weak (ranging in magnitude from a 3 to 6% increased risk per 5 kg m−2; MacInnis and English, 2006; Renehan et al, 2008), although the effects appear to be stronger for aggressive and fatal prostate cancers (MacInnis and English, 2006;Discacciati et al, 2011; Discacciati et al, 2012). As the growth of the prostate organ starts early in life, and the development of prostate cancer likely occurs over a long period before it manifests clinically, it is plausible that this process originates early in life (Freedland and Platz, 2007; Wilson, 2011). Consequently, childhood may represent an essential period where early exposures could affect prostate cancer risk later in life. Excess weight during childhood has various adverse consequences for long-term health (Ahlgren et al, 2004; Baker et al, 2007; Reilly and Kelly, 2011). Only a few studies have, however, investigated if childhood body size is associated with the risk of prostate cancer in adulthood, and their findings are equivocal (Andersson et al, 1995; Ilic et al, 1996; Giovannucci et al, 1997; Hsing et al, 2000; Dal et al, 2004; Jeffreys et al, 2004; Robinson et al, 2005; Barba et al, 2008). The only cohort study using measured heights and weights did not find an effect of childhood BMI, but this study was limited by a low number of prostate cancer cases as well as a wide age range of the included boys (Jeffreys et al, 2004). The remaining studies relied on a mid-life recall of childhood weight (Andersson et al, 1995; Ilic et al, 1996) or body size (Giovannucci et al, 1997; Hsing et al, 2000; Dal et al, 2004; Robinson et al, 2005; Barba et al, 2008), which might have resulted in exposure misclassification bias that usually results in attenuation of effects towards the null. We investigated whether a larger BMI in childhood, independent of and adjusted for height, as well as longitudinal changes in BMI during childhood were associated with an increased risk of prostate cancer in adulthood in a large Danish population-based cohort of men. In addition, to examine whether changes in diagnostic procedures over time and the stage of the cancer affected these associations, we conducted additional analyses exploring the effects of the introduction of prostate-specific antigen (PSA) testing and the Tumour, Node, Metastasis (TNM) stage of the neoplasm.

The US Servicemen's Testicular Tumor Environmental and Endocrine Determinants (STEED) case–control study of testicular germ-cell tumours (TGCTs) enrolled participants and their mothers in 2002–2005. Hours of sports or vigorous childhood physical activity per week were ascertained for three time periods; 1st–5th grades, 6th–8th grades and 9th–12th grades. Son- and mother-reports were analysed separately and included 539 control son–mother pairs and 499 case son–mother pairs. Odds ratios and 95% confidence intervals were produced. The analysis of the sons' responses found no relationship between childhood physical activity and TGCT, while the mothers' analysis found an inverse association, which was solely due to nonseminoma. Future studies should seek to validate responses further using recorded information sources such as school records.

Background: Studies assessing the relationships of anthropometry and testicular germ-cell tumour (TGCT) have reported heterogeneous findings. Methods: We undertook a systematic review and meta-analysis of the associations between adult height, weight, body mass index (BMI), and testicular cancer. Search strategies were conducted in PubMed, EMBASE, Scopus, and Web of Science on 26 May 2009. Studies that met our inclusion criteria were included in meta-analytic models using STATA 11. Results: A total of 3255 references were retrieved, of which 14 met the inclusion criteria. Random effects meta-analysis found adult height (odds ratio (OR) per 5-cm increase 1.13, 95% confidence interval (CI) 1.07–1.19, P

Background: In the United States, the rates and temporal trends of oesophageal cancer overall and for the two predominant histologic types – adenocarcinoma (ADC) and squamous cell carcinoma (SCC) – differ between Blacks and Whites, but little is known with regard to the patterns among Asians/Pacific Islanders or Hispanics. Methods: Using the Surveillance, Epidemiology, and End Results programme data, we analysed oesophageal cancer incidence patterns by race, sex, and histologic type for the period 1977–2005. Results: Total oesophageal cancer incidence has been increasing among Whites only; the rates among all other race groups have declined. Moreover, rates among White men surpassed those among Blacks in 2004. Oesophageal SCC rates have been decreasing among virtually all racial/ethnic groups; rates among Hispanic and Asian/Pacific Islander men have been intermediate to those of Blacks and Whites, with rates among women being lower than those among Blacks or Whites. The ADC rates among Hispanic men may be rising, akin to the historical trends among Whites and Blacks. The sex ratios for these cancers also varied markedly. Conclusions: These observations may provide clues for aetiological research.