Predicting clinically significant prostate cancer in elderly patients: A nomogram approach with shear wave elastography.

PURPOSE: This study was to construct a nomogram utilizing shear wave elastography and assess its efficacy in detecting clinically significant prostate cancer (csPCa). METHODS: 290 elderly people with suspected PCa who received prostate biopsy and shear wave elastography (SWE) imaging were respectively registered from April 2022 to December 2023. The elderly participants were stratified into two groups: those with csPCa and those without csPCa, which encompassed cases of clinically insignificant prostate cancer (cisPCa) and non-prostate cancer tissue, as determined by pathology findings. The LASSO algorithm, known as the least absolute shrinkage and selection operator, was utilized to identify features. Logistic regression analysis was utilized to establish models. Receiver operating characteristic (ROC) and calibration curves were utilized to evaluate the discriminatory ability of the nomogram. Bootstrap (1000 bootstrap iterations) was employed for internal validation and comparison with two models. A decision curve and a clinical impact curve were employed to assess the clinical usefulness. RESULTS: Our nomogram, which contained Emean, ΔEmean, prostate volume, prostate-specific antigen density (PSAD), and transrectal ultrasound (TRUS), showed better discrimination (AUC = 0.89; 95% CI: 0.83-0.94), compared to the clinical model without SWE parameters (p = 0.0007). Its accuracy, sensitivity and specificity were 0.83, 0.89 and 0.78, respectively. Based on the analysis of decision curve, the thresholds ranged from 5% to 90%. According to our nomogram, biopsying patients at a 20% probability threshold resulted in a 25% reduction in biopsies without missing any csPCa. The clinical impact curve demonstrated that the nomogram's predicted outcome is closer to the observed outcome when the probability threshold reaches 20% or greater. CONCLUSION: Our nomogram demonstrates efficacy in identifying elderly individuals with clinically significant prostate cancer, thereby facilitating informed clinical decision-making based on diagnostic outcomes and potential clinical benefits.

p38gamma overexpression promotes renal cell carcinoma cell growth, proliferation and migration.

Recent studies have proposed that p38gamma (p38γ) might be critically involved in tumorigenesis and cancer progression. Its expression and potential functions in human renal cell carcinoma (RCC) are studied here. We show that p38γ mRNA and protein levels are upregulated in human RCC tissues, as compared to its levels in the surrounding normal renal tissues. p38γ upregulation was also detected in established (786-O line) and primary human RCC cells. Functional studies in 786-O cells and primary human RCC cells demonstrated that p38γ silencing (by targeted shRNAs) or CRISPR/Cas9-mediated p38γ knockout (KO) potently inhibited cell growth, viability, proliferation and migration. Furthermore, p38γ shRNA or KO in RCC cells decreased retinoblastoma (Rb) phosphorylation and downregulated cyclin E1/A expression. Additionally, significant apoptosis activation was detected in p38γ-silenced and p38γ-KO RCC cells. Contrarily, ectopic overexpression of p38γ facilitated cell growth, viability, proliferation and migration in RCC cells. Taken together, we show that p38γ overexpression promotes RCC cell growth, proliferation and migration. p38γ could be a novel therapeutic target for human RCC.