Short- and long-term effects of rapamycin on ischemic damage and apoptotic changes in torsion of rat testes.

Rapamycin has antioxidant defense mechanisms and immune suppressive effects. To detect the short- and long-term effects of rapamycin on ischemic damage and apoptotic changes in torsion of rat testes, mature male albino Wistar rats (n = 48) were included in the study as control, sham, early torsion-detorsion (T/D), early rapamycin treatment, early rapamycin control, late T/D, late rapamycin treatment, and late rapamycin control. The right testis was rotated 720° in a clockwise direction during 4 h in operation groups. Rapamycin was administered orally three times: 30 min before detorsion and 24 and 48 h after detorsion. The animals were killed on the third day in early groups and on the tenth day in late groups after detorsion. Statistically significant differences among all groups were detected for SOD and TBARS, mean seminiferous tubule diameter (MSTD) and Cosentino's histologic score (CHS), caspase 3, bax, average number of apoptotic cells per tubule (ANPCT), and percentage of apoptotic tubule (PAT) values. ANPCT values ​​were 10% lower in the rapamycin treatment groups compared with the untreated T/D groups, and the PAT values ​​were also approximately 1.3 times lower. Although short-term usage of rapamycin may reduce to the tubular injury caused by I/R conversely to apoptosis in the testicular tissue after testicular torsion, rapamycin may have the potential to increase the long-term apoptosis with/without testicular torsion and a subsequent regression in fertility.

KRAS, BRAF, PIK3CA mutation frequency of radical prostatectomy samples and review of the literature.

OBJECTIVE: The molecular basis of prostate cancer is highly heterogeneous. Our study aimed to perform the mutation analysis of KRAS, BRAF, PIK3CA, and immunohistochemical (IHC) evaluation of EGFR, HER2, p16, and PTEN to demonstrate new areas for targeted therapies. METHODS: A total of 24 prostatectomy samples diagnosed with adenocarcinoma were analyzed by microarray hybridization. Also, these samples were IHC stained for EGFR, HER2, P16, and PTEN. The cases were divided into two groups based on low and high Gleason scores. All findings were compared with the clinicopathological parameters of the patients. RESULTS: While KRAS mutation was in 3/24 (12.5%) of our cases, BRAF and PIK3CA mutations were not detected. There was no significant difference between the groups in terms of KRAS mutation frequency. HER2 was immunohistochemically negative in all samples. There was no correlation between EGFR, P16 immunopositivity, and clinicopathological features. CONCLUSION: KRAS mutation frequency is similar to those in Asian populations. BRAF and PIK3CA mutation frequencies have been reported in the literature in the range of 0-15% and 0-10.4%, respectively, consistent with our study findings. HER2 immunoexpression is a controversial issue in the literature. EGFR and p16 expressions may not correlate with the stage.