Studies have examined factors related to BMD in older white, but not black, men. We measured BMD in older white and black men and examined factors related to racial differences in BMD. Black men had significantly higher adjusted BMD at all sites. These results may explain, in part, the lower incidence of fractures in older black men.Introduction: Several studies have examined factors associated with bone mineral density (BMD)in older men. None, however, have had sufficient numbers of black men to allow for meaningful comparisons by race. Materials and Methods: A total of 503 white and 191 black men aged 65 and older(75.1 Ϯ 5.8 and 72.2 Ϯ 5.7 years, respectively) were recruited from the Baltimore metropolitan area. All men completed a battery of self-administered questionnaires, underwent a standardized examination, and had BMD measured at the femoral neck, lumbar spine, and total body. Data were analyzed using multiple variable linear regression models, adjusted for potential confounding variables; two-way interactions with main effects were included in models where appropriate. Conclusions:Older black men have significantly higher BMD than older white men, even after adjustment for factors associated with BMD. These differences, especially at the femoral neck, may explain the reduced incidence of hip fracture in black compared with white men.

Previously, an analysis of 14 extended, high-risk Utah pedigrees localized in the chromosome 22q linkage region to 3.2 Mb at 22q12.3-13.1 (flanked on each side by three recombinants) contained 31 annotated genes. In this large, multi-centered, collaborative study, we performed statistical recombinant mapping in 54 pedigrees selected to be informative for recombinant mapping from nine member groups of the International Consortium for Prostate Cancer Genetics (ICPCG). These 54 pedigrees included the 14 extended pedigrees from Utah and 40 pedigrees from eight other ICPCG member groups. The additional 40 pedigrees were selected from a total pool of 1213 such that each pedigree was required to contain both at least four prostate cancer (PRCA) cases and exhibit evidence for linkage to the chromosome 22q region. The recombinant events in these 40 independent pedigrees confirmed the previously proposed region. Further, when all 54 pedigrees were considered, the three-recombinant consensus region was narrowed down by more than a megabase to 2.2 Mb at chromosome 22q12.3 flanked by D22S281 and D22S683. This narrower region eliminated 20 annotated genes from that previously proposed, leaving only 11 genes. This region at 22q12.3 is the most consistently identified and smallest linkage region for PRCA. This collaborative study by the ICPCG illustrates the value of consortium efforts and the continued utility of linkage analysis using informative pedigrees to localize genes for complex diseases.

Purpose To investigate the differences in outcomes among patients with muscle-invasive bladder cancer on 2 NRG Oncology Radiation Therapy Oncology Group protocols who achieved complete response and near-complete response after induction chemoradiation and then completed bladder-preserving therapy with chemoradiation therapy (chemo-RT) to full dose (60-64 Gy). Patients and Methods A pooled analysis was performed on 119 eligible patients with muscle-invasive bladder cancer enrolled on 2 NRG Oncology Radiation Therapy Oncology Group trials, who were classified as having a complete (T0) or near-complete (Ta or Tis) response after induction chemo-RT and completed consolidation with a total RT dose of at least 60 Gy. Bladder recurrence, salvage cystectomy rates, and disease-specific survival were estimated by the cumulative incidence method and bladder-intact and overall survivals by the Kaplan-Meier method. Results Among the 119 eligible patients, 101 (85%) achieved T0, and 18 (15%) achieved Ta or Tis after induction chemo-RT and proceeded to consolidation. After a median follow-up of 5.9 years, 36 of 101 T0 patients (36%) versus 5 of 18 Ta or Tis patients (28%) experienced bladder recurrence (P=.52). Thirteen patients among complete responders eventually required late salvage cystectomy for tumor recurrence, compared with 1 patient among near-complete responders (P=.63). Disease-specific, bladder-intact, and overall survivals were not significantly different between T0 and Ta/Tis cases. Conclusions The bladder recurrence and salvage cystectomy rates of the complete and the near-complete responders were similar. Therefore it is reasonable to recommend that patients with Ta or Tis after induction chemo-RT continue with bladder-sparing therapy with consolidation chemo-RT to full dose (60-64 Gy).

Genome-wide linkage studies have been used to localize rare and highly penetrant prostate cancer (PRCA) susceptibility genes. Linkage studies performed in different ethnic backgrounds and populations have been somewhat disparate, resulting in multiple, often irreproducible signals because of genetic heterogeneity and high sporadic background of the disease. Our first genome-wide linkage study and subsequent fine-mapping study of Finnish hereditary prostate cancer (HPC) families gave evidence of linkage to one region. Here, we conducted subsequent scans with microsatellites and SNPs in a total of 69 Finnish HPC families. GENEHUNTER-PLUS was used for parametric and nonparametric analyses. Our microsatellite genomewide linkage study provided evidence of linkage to 17q12-q23, with a heterogeneity LOD (HLOD) score of 3.14 in a total of 54 of the 69 families. Genome-wide SNP analysis of 59 of the 69 families gave a highest HLOD score of 3.40 at 2q37.3 under a dominant high penetrance model. Analyzing all 69 families by combining microsatellite and SNP maps also yielded HLOD scores of > 3.3 in two regions (2q37.3 and 17q12-q21.3). These significant linkage peaks on chromosome 2 and 17 confirm previous linkage evidence of a locus on 17q from other populations and provide a basis for continued research into genetic factors involved in PRCA. Fine-mapping analysis of these regions is ongoing and candidate genes at linked loci are currently under analysis.Prostate cancer (PRCA) is the most common cancer among men in industrialized countries, including Finland where a total of 4,189 cases were diagnosed in 2007.1 PRCA is also the second most common cause of cancer death in Finland, surpassed only by lung cancer.PRCA is a heterogeneous disease, where definitive risk factors include age, ethnic origin and family history, all of which point to genetic factors. Although environmental factors may play a role in the development of PRCA, there remains the suggestion of a significant role for genetic components in PRCA epidemiology (reviewed in Schaid).2 In fact, the 40% heritability component in PRCA risk is the highest reported for a common malignancy. Despite the evidence for genetic involvement, localization of high penetrant PRCA susceptibility loci has proven challenging. To date, three susceptibility genes, HPC2/ELAC2, HPC1/RNASEL and MSR1 together with multiple other risk loci, such as HPCX1, have been identified through genetic linkage analysis in high-risk hereditary prostate cancer (HPC) families.2 However, the results from the three