Racial variation in prostate needle biopsy templates directed anterior to the peripheral zone.

OBJECTIVES: African Americans (AA) have been reported to have both increased incidence and increased aggressiveness of prostate cancer (PCa) located anterior to the peripheral zone (APZ). We sought to evaluate the utility of prostate biopsies directed toward the APZ in a predominantly AA cohort. METHODS AND MATERIALS: We reviewed all patients with PCa found on biopsy schema that included needle biopsies directed at both the peripheral zone (PZ) and APZ from 2010 to 2014. Self-identified race was recorded for all patients. To evaluate the reliability of APZ-directed prostate biopsies, we performed pathologic secondary review of 25 radical prostatectomy specimens. A series of the Mann-Whitney U and Chi-square tests were used to compare variables. RESULTS: We identified 398 men, of which 277 (70%) were AA. Compared with non-AA, AA had more National Comprehensive Cancer Network-defined intermediate or high-risk (50% vs. 39%, P = 0.25) PCa. Most patients had PCa limited to the PZ only (n = 190) or in both the PZ and APZ (n = 191). For 17 patients (4%), PCa was limited only to the APZ core(s), 14 (5%) AA vs. 3 (2%) non-AA (P = 0.24). Most of these 17 patients (n = 14, 82%) had Gleason 6 disease. Patients with PCa in both the PZ and APZ had higher serum prostate-specific antigen, prostate-specific antigen density, volume of disease, and increased grade and National Comprehensive Cancer Network category (all P<0.01). Of these patients, there were no differences in race (AA = 135, 71% vs. non-AA = 56, 29%; P = 0.48). In only 21 men (11%), without racial variation, APZ tumor grade was greater than PZ. Radical prostatectomy and APZ-directed biopsies demonstrated a concordance rate of 80% (20/25), false positive rate of 8% (2/25), and false negative rate of 12% (3/25). CONCLUSIONS: APZ-directed prostate biopsies are rarely the sole location of PCa and do not show a clear racial predilection. In those men with PCa identified in both regions, the APZ biopsy did not frequently change treatment recommendations. Biopsies directed at the APZ are not of greater benefit to AA than non-AA.

Lack of mutation-histopathology correlation in a patient with Proteus syndrome.

Proteus syndrome (PS) is characterized by progressive, disproportionate, segmental overgrowth, and tumor susceptibility caused by a somatic mosaic AKT1 activating mutation. Each individual has unique manifestations making this disorder extremely heterogeneous. We correlated three variables in 38 tissue samples from a patient who died with PS: the gross affection status, the microscopic affection status, and the mutation level. The AKT1 mutation was measured using a PCR-based RFLP assay. Thirteen samples were grossly normal; six had detectable mutation (2-29%) although four of these six were histopathologically normal. Of the seven grossly normal samples that had no mutation, only four were histologically normal. The mutation level in the grossly abnormal samples was 3-35% and all but the right and left kidneys, skull, and left knee bone, with mutation levels of 19%, 15%, 26%, and 17%, respectively, had abnormal histopathology. The highest mutation level was in a toe bone sample whereas the lowest levels were in the soft tissue surrounding that toe, and an omental fat nodule. We also show here that PS overgrowth can be caused by cellular proliferation or by extracellular matrix expansion. Additionally, papillary thyroid carcinoma was identified, a tumor not previously associated with PS. We conclude that gross pathology and histopathology correlate poorly with mutation levels in PS, that overgrowth can be mediated by cellular proliferation or extracellular matrix expansion, and that papillary thyroid carcinoma is part of the tumor susceptibility of PS. New methods need to be developed to facilitate genotype-phenotype correlation in mosaic disorders. © 2016 Wiley Periodicals, Inc.