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Background: Prostate cancer is a common cancer in males, frequently leading to mortality. Multiple genetic factors play roles in prostate cancer pathogenesis. Demonstration of pathological pathways and customised treatment options have been possible with next-generation sequencing. Aim: In this study, we aimed to evaluate the relationships of the changes in the prostate cancer pathways genes with the pathological, immunohistochemical and the clinical parameters. Study Design: Retrospective cross-sectional study. Materials and Methods: Among the prostate needle biopsy materials investigated in Adnan Menderes University Faculty of Medicine, Department of Pathology, thirty-one cases, who had been analysed using the next-generation sequencing system, were included in this study. Results: As a result of statistical analysis, a significant relationship was found between the pathogenic mutation detected in androgen receptor and Breast Cancer Gene 2 genes and tumour volume. In all cases with a pathogenic mutation in the androgen receptor gene, a pathogenic mutation in the Protein Tyrosine Phosphatase and Tensin Homolog gene was also observed and a significant relationship was found between them. Castration resistance was observed in cases with high tumour volume, and a statistically significant difference was found. A statistically significant relationship was found between tumour volume and Ki-67 expression. In addition, a significant relationship was observed between the castration resistance and Ki-67, c-erbB2 expressions. A statistically significant relationship was found between Ki-67 and c-erbB2. Conclusion: Regarding prognosis prediction and treatment, identifying the molecular changes in genes playing roles in prostate cancer with next-generation sequencing is very important.

Background & aimsPrognostic factors of metastatic rectal cancer are not well known. We aim to determine prognostic factors affecting survival for metastatic rectal cancer patients and also to investigate the effect of tumor localization on overall survival.MethodsMetastatic rectal cancer patients who received treatment in 5 different centers between 2012 and 2022 were included. Prognostic factors for survival were evaluated using univariate and multivariate analysis. The statistical methods included Pearson’s chi-square test, Fisher exact test, Log-rank test, and Cox regression model.ResultsA total of 283 patients with metastatic rectal cancer were included in the study. The median OS was not significantly different among the three groups (upper rectum 30.1 months, middle rectum 28.3 months, and low rectum cancer 24.8 months; log-rank p = 0.25). In univariate analysis, Grade 3, ECOG performance status 2, the presence of multiple metastatic sites, the presence of KRAS mutation, the presence of liver metastases, the presence of nonregional lymph node metastases, and the presence of bone metastases were significant predictors of poor survival. In multivariate analysis, Grade 3, ECOG performance status 2, and the presence of multiple metastatic sites were determined as indicators of worse prognosis.ConclusionOur findings, primary tumor location did not affect survival in metastatic rectal cancer. The most important factors affecting survival were multiple metastatic sites, tumor grade, and ECOG performance status.

Abstract Background There is no standard treatment recommended at category 1 level in international guidelines for subsequent therapy after cyclin-dependent kinase 4/6 inhibitor (CDK4/6) based therapy. We aimed to evaluate which subsequent treatment oncologists prefer in patients with disease progression under CDKi. In addition, we aimed to show the effectiveness of systemic treatments after CDKi and whether there is a survival difference between hormonal treatments (monotherapy vs. mTOR-based). Methods A total of 609 patients from 53 centers were included in the study. Progression-free-survivals (PFS) of subsequent treatments (chemotherapy (CT, n:434) or endocrine therapy (ET, n:175)) after CDKi were calculated. Patients were evaluated in three groups as those who received CDKi in first-line (group A, n:202), second-line (group B, n: 153) and ≥ 3rd-line (group C, n: 254). PFS was compared according to the use of ET and CT. In addition, ET was compared as monotherapy versus everolimus-based combination therapy. Results The median duration of CDKi in the ET arms of Group A, B, and C was 17.0, 11.0, and 8.5 months in respectively; it was 9.0, 7.0, and 5.0 months in the CT arm. Median PFS after CDKi was 9.5 (5.0–14.0) months in the ET arm of group A, and 5.3 (3.9–6.8) months in the CT arm (p = 0.073). It was 6.7 (5.8–7.7) months in the ET arm of group B, and 5.7 (4.6–6.7) months in the CT arm (p = 0.311). It was 5.3 (2.5–8.0) months in the ET arm of group C and 4.0 (3.5–4.6) months in the CT arm (p = 0.434). Patients who received ET after CDKi were compared as those who received everolimus-based combination therapy versus those who received monotherapy ET: the median PFS in group A, B, and C was 11.0 vs. 5.9 (p = 0.047), 6.7 vs. 5.0 (p = 0.164), 6.7 vs. 3.9 (p = 0.763) months. Conclusion Physicians preferred CT rather than ET in patients with early progression under CDKi. It has been shown that subsequent ET after CDKi can be as effective as CT. It was also observed that better PFS could be achieved with the subsequent everolimus-based treatments after first-line CDKi compared to monotherapy ET.