Rate of Gleason 7 or higher prostate cancer on repeat biopsy after a diagnosis of atypical small acinar proliferation

Abstract

BACKGROUND Limited information is known about the clinical significance of cancers diagnosed upon repeat biopsy for the indication of atypical small acinar proliferation (ASAP). With increasing concern regarding overdiagnosis and overtreatment of prostate cancer, and the reported rise in infectious complications related to prostate biopsy, we examined the outcomes of patients rebiopsied for a diagnosis of ASAP. METHODS Clinical, pathologic and outcomes data of patients diagnosed with ASAP on prostate biopsy at our institutions between 2000 and 2010 were abstracted through chart review. Statistical analyses included Fisher’s exact and the two-sample Wilcoxon rank sum tests. Logistic regression evaluated risk factors for the probability of cancer following a diagnosis of ASAP. RESULTS A total of 349 patients met the inclusion criteria with median follow-up of 4.4 years. Median age was 65.3 years with a median PSA of 5.3 ng ml−1. Of men diagnosed with ASAP, 250/349 (71.6%) had a repeat biopsy within 1 year with 94/246 (38.2%) demonstrating prostate cancer; only 26/245 (10.6%) had ≥Gleason 7 disease. Of men diagnosed with ASAP, 284/349 (81.4%) underwent biopsy at some time during follow-up. Prostate cancer was diagnosed in 132/279 (47.3%) of these men, 48/278 (17.3%) with ≥Gleason 7 disease. Multivariate analyses suggested that older age, no previous biopsy and PSA density were predictive of cancer on repeat biopsy within 1 year from ASAP. Univariate analysis revealed PSA density was associated with the presence of ≥Gleason 7 disease at 1 year and any time after a diagnosis of ASAP. CONCLUSIONS The overall rate of intermediate- and high-grade prostate cancer found on repeat biopsy for ASAP is low. Further investigation into ways to further risk stratify these men may be warranted. However, until such tests become available, repeat biopsy of men diagnosed with ASAP remains prudent.

Atypical small acinar proliferation at index prostate biopsy: rethinking the re-biopsy paradigm

“…Consistent with these findings, Tosoian, et al 18 demonstrated 5% of patients with ASAP were diagnosed with Gleason ≥7 disease using magnetic resonance imaging/TRUS fusion-guided for repeat biopsy. Furthermore, another study found 38% of repeat biopsies within 1 year of ASAP diagnosis were upgraded to prostate cancer, but only 11% had clinically significant prostate cancer 8 . Conversely, some studies indicate ASAP has a much higher progression rate to clinically significant prostate cancer.…”

“…First, our study is limited by its retrospective design and small number of patients with ASAP diagnosis. Although sample size is small and not random, our sample mirrors prior index populations in other series 8,9 . Our study showed comparable rates of ASAP diagnosis on initial biopsy from larger retrospective studies and multi-institutional databases (4.5% vs 3.8–5.3%) 5,21,29,30 .…”

“…ASAP occurs at a rate of up to 5% on prostate biopsies, and it is known from prior studies that 30–50% of patients with an initial diagnosis of ASAP have progression to prostate cancer on repeat biopsy 6,7 . Previous studies have risk-stratified prostate cancer into clinically significant versus indolent disease on repeat biopsy following the diagnosis of ASAP 8,9 . However, existing data on its implication with regard to disease risk are conflicting.…”

Integrin Β6 – A Potential Marker for the Early Malignant Transformation in Prostate Cancer

“…Genetic pathway in-between PIA, HGPIN, and PCa also has been demonstrated . Unlike HGPIN, LGPIN is believed do not contribute to PCa and is no longer reported as finding [29][30][31][32][33][34]. However, the likely outcome of isolated LGPIN lesions in prostate biopsies remains unclear.…”

“…In a study performed with younger men, PIN changes were seen even in their 20's and 30's. Most foci were LGPIN, with increasing frequency of HGPIN with advancing age [32][33][34]. Another analysis demonstrated 30% risk of PCa on repeat sextant biopsy in the LGPIN cohort [31].…”