Incidence, predictive factors and oncological outcomes of incidental prostate cancer after endoscopic enucleation of the prostate: a systematic review and meta-analysis.

INTRODUCTION: This systematic review aims at reporting the incidence, predictive factors, and the oncological outcomes of incidental prostate cancer (IPCa) in men who underwent endoscopic enucleation of prostate (EEP). METHODS: A literature search was performed using the following Medical Subject Heading (MeSH) terms and keywords: "Prostatic Neoplasms", "Prostate Cancer", "Transurethral Resection of Prostate", "Prostate resection", "Prostate enucleation". Meta-analysis was performed if there were two or more studies reporting the same outcome under the same definition. In case of insufficient data, results were presented in a narrative manner. RESULTS: Sixty-one studies were included in qualitative synthesis and 55 were included in meta-analysis. The pooled IPCa rate was 0.08 (95% CI 0.073-0.088). Increasing age, higher preoperative serum prostate-specific antigen (PSA) level, higher preoperative PSA density (PSAD), smaller prostate volume, higher postoperative PSA velocity and lower enucleated prostate weight, were reported to have significant correlation with IPCa. In BPH patients, the mean pre-operative and post-operative PSA levels were 5.58 ± 1.48 ng/dL and 1.06 ± 0.27 ng/dL, respectively. In patients with IPCa, the mean pre-operative and post-operative PSA levels were 7.72 ± 2.90 ng/dL and 2.77 ± 1.66 ng/dL, respectively. The mean percentage PSA reduction was 82.0% ± 1.8% for BPH patients and 68.2% ± 12.1% for IPCa patients. IPCa was most commonly managed by active surveillance (68.7%). CONCLUSIONS: The pooled incidence of IPCa after EEP was 8%. An absolute post-operative PSA level of < 2.0 and a percentage PSA reduction of > 70% should be expected in BPH patients after EEP.

IDH mutant lower grade (WHO Grades II/III) astrocytomas can be stratified for risk by CDKN2A, CDK4 and PDGFRA copy number alterations.

In the 2016, WHO classification of tumors of the central nervous system, isocitrate dehydrogenase (IDH) mutation is a main classifier for lower grade astrocytomas and IDH-mutated astrocytomas is now regarded as a single group with longer survival. However, the molecular and clinical heterogeneity among IDH mutant lower grade (WHO Grades II/III) astrocytomas have only rarely been investigated. In this study, we recruited 160 IDH mutant lower grade (WHO Grades II/III) astrocytomas, and examined PDGFRA amplification, CDKN2A deletion and CDK4 amplification by FISH analysis, TERT promoter mutation by Sanger sequencing and ATRX loss and p53 expression by immunohistochemistry. We identified PDGFRA amplification, CDKN2A homozygous deletion and CDK4 amplification in 18.8%, 15.0% and 18.1% of our cohort respectively, and these alterations occurred in a mutually exclusive fashion. PDGFRA amplification was associated with shorter PFS (P = 0.0003) and OS (P < 0.0001). In tumors without PDGFRA amplification, CDKN2A homozygous deletion or CDK4 amplification was associated with a shorter OS (P = 0.035). Tumors were divided into three risk groups based on the presence of molecular alterations: high risk (PDGFRA amplification), intermediate risk (CDKN2A deletion or CDK4 amplification) and low risk (neither CDKN2A deletion and CDK4 amplification nor PDGFRA amplification). These three risk groups were significantly different in overall survival with mean survivals of 40.5, 62.9 and 71.5 months. The high-risk group also demonstrated a shorter PFS compared to intermediate- (P = 0.036) and low-risk (P < 0.0001) groups. One limitation of this study is the relatively short follow-up period, a common confounding factor for studies on low-grade tumors. Our data illustrate that IDH mutant lower grade astrocytomas is not a homogeneous group and should be molecularly stratified for risk.