Studies of families with breast cancer have indicated that male carriers of BRCA2 mutations are at increased risk of prostate cancer, particularly at an early age. To evaluate the contribution of BRCA2 mutations to early-onset prostate cancer, we screened the complete coding sequence of BRCA2 for germline mutations, in 263 men with diagnoses of prostate cancer who were

Ninety-nine black colorectal cancer patients and 280 matched controls from hospitals and multiphasic health checkup clinics were interviewed about past dietary habits and other traits. The colon cancer cases tended to report less frequent use of foods with at least 0.5% fiber content than did their controls. This relationship, though small, showed a consistent dose-response gradient, appeared in both case-hospital control and case-multiphasic health checkup control comparisons, and could not be accounted for by the effects of other variables. Colon and rectosigmoid junction cancer patients tended to have eaten foods with at least 5% saturated fat somewhat more often than controls. When consumption of these two groups of foods was considered in combination, significantly more colon cancer patients than controls reported a high saturated fat foods-low fibrous foods eating pattern, as opposed to a low saturated fat foods-high fibrous foods diet. Statistically significant excesses of the following traits were also reported by the colorectal cancer patients: prolonged cigar smoking in men, nulliparity in women, and history of colorectal polyps.

We investigated the association between seven polymorphisms in four candidate genes involved in vitamin D and androgen metabolism with early-onset prostate cancer (CaP) risk. The polymorphisms were genotyped in 288 UK males who were diagnosed with CaP at the age of 55 y or younger and up to 700 population-based controls. An additional 50 cases (not selected for age) and 76 controls were also genotyped. Short (p22 repeats) AR (CAG) n repeats were associated with a significantly reduced risk of early onset CaP (OR 0.68, 95% CI 0.50-0.91) compared with men with long (422) repeats. Men homozygous for the leucine variant of SRD5A2 p.89V4L were also found to be at a significantly increased risk of CaP compared with men who were homozygous for the valine allele (OR 1.84, 95% CI 1.15-2.98). No associations were found with the AR (GGC) n , CYP17 Msp A1 I, VDR Taq I, SRD5A2 (TA) n and p.49A4T polymorphisms and CaP risk. These findings suggest that common polymorphisms in the AR and SRD5A2 genes may be associated with early-onset CaP in British men.

It remains unclear whether screening for advanced fibrosis in the community can identify the subgroup of people with nonalcoholic fatty liver disease (NAFLD) at higher risk for development of liver‐related complications. We aimed to determine the prognostic value of baseline noninvasive fibrosis tests for predicting liver‐related outcomes and mortality in patients with NAFLD from type 2 diabetes (T2D) clinics or primary care. Patients (n = 243) who were screened for NAFLD with advanced fibrosis by using NAFLD fibrosis score (NFS), fibrosis 4 score (FIB‐4), enhanced liver fibrosis (ELF) test, and liver stiffness measurements (LSMs) were followed up for clinical outcomes by review of electronic medical records. During a median follow‐up of 50 months, decompensated liver disease or primary liver cancer occurred in 6 of 35 (17.1%) patients with baseline LSM > 13 kPa, 1 of 17 (5.9%) patients with LSM 9.5‐13 kPa, and in no patients with LSM < 9.5 kPa. No patient with low‐risk NFS developed liver decompensation or liver‐related mortality. Following repeat NFSs at the end of follow‐up, all patients with a liver‐related complication were in the high‐risk NFS category. Patients who developed liver‐related complications were also more likely to have baseline high‐risk FIB‐4 scores or ELF test ≥9.8 compared to patients who did not develop liver outcomes. Conclusion: Liver fibrosis risk stratification in non‐hepatology settings can identify the subset of patients at risk of liver‐related complications. Although the rate of development of a decompensation event or hepatocellular carcinoma was low (2.1% per year) in our patients with compensated cirrhosis (LSM > 13 kPa), these events are projected to lead to a substantial increase in NAFLD‐related disease burden over the next decade due to the high prevalence of NAFLD in people with obesity and T2D.

The candidate prostate cancer susceptibility gene HPC2/ELAC2 has two common coding polymorphisms: (Ser?Leu 217) and (Ala?Thr 541). The Thr541 variant in the HPC2/ELAC2 gene has previously been reported to be at an increased frequency in prostate cancer cases. To evaluate this hypothesis we genotyped 432 prostate cancer patients (including 262 patients diagnosed 455 years) and 469 UK, population based control individuals with no family history of cancer. We found no significant difference in the frequencies of Thr541-containing genotypes between cases and controls (OR=1.41, 95% CI 0.79 -2.50). The association remained non-significant when the analysis was restricted to cases divided by age of onset into those diagnosed 455 years (OR=1.50, 95% CI 0.79 -2.85) or to patients diagnosed 455 years (OR=1.27, 95% CI 0.59 -2.74). We conclude that any association between the Thr541 variant and prostate cancer is likely to be weak.