Zhikang Chen

Background: Invasive neoplasia (Tis-T1) are increasingly being encountered in the daily routine of endoscopic polypectomy. However, the need for salvage surgery following endoscopic therapy for invasive neoplasia is controversially discussed. Patients and Methods: Patients with endoscopic removal of invasive neoplasia were identified from the national Surveillance Epidemiology and End Results (SEER) Database 2005 to 2015. Survival analysis and Cox proportional hazard regression analysis in cancer-specific mortality and overall survival rate was used, which were stratified by T stage and polyp size. Results: A total of 5805 patients with endoscopic removal of invasive neoplasia were included in the analysis, of whom 1214 (20.9%) underwent endoscopic treatment alone and 4591 (79.1%) underwent endoscopic resection plus surgery. The survival analysis revealed that patients undergoing salvage surgery had a significantly better cancer-specific survival (97.4% vs. 95.8%, p-value = 0.017). In patients with T1 stage, additional salvage surgery led to a significantly higher cancer-specific survival (92.1% vs. 95.0%, p value = 0.047). Conclusion: Salvage surgery following endoscopic polypectomy may improve the oncological survival of patients with invasive neoplasia, especially in patients with T1 stage. Furthermore, the T stage, size, and localization of polyps, as well as the level of CEA, could be identified as significant predictors for lymphonodal and distant metastases.

Although castration-resistant prostate cancer (CRPC) as a whole, by its name, refers to the tumors that relapse and/or regrow independently of androgen after androgen deprivation therapy (ADT), untreated tumor, even in early-stage primary prostate cancer (PCa), contains androgen-independent (AI) PCa cells. The transformation of androgen-dependent (AD) PCa to AI PCa under ADT is a forced evolutionary process, in which the small group of AI PCa cells that exist in primary tumors has the unique opportunity to proliferate and expand selectively and dominantly, while some AD PCa cells that have escaped from ADT-induced death acquire the capability to survive in an androgen-depleted environment. The adaptation and reprogramming of both PCa cells and the tumor microenvironment (TME) under ADT make PCa much stronger than primary tumors so that, currently, there are no effective therapeutic methods available for the treatment of CRPC. Many mechanisms have been found to be related to the emergence and maintenance of PCa castration resistance; in this review, we focus on the role of inflammatory signaling in both PCa cells and the TME for the emergence and maintenance of CRPC and summarize the recent advances of therapeutic strategies that target inflammatory signaling for the treatment of CRPC.

Yes‐associated protein (YAP) is a transcriptional coactivator that promotes cell proliferation, stem cell maintenance and tissue homeostasis. The YAP activity is primarily regulated through an inhibitory phosphorylation by the serine/threonine kinases of Hippo pathway. Here, we show that receptor tyrosine kinase (RTK) erythropoietin‐producing hepatocellular receptor A2 (EphA2) interacts with and phosphorylates YAP protein, leading to stabilization, nuclear translocation and activation of YAP in gastric cancer (GC) cells. EphA2 induces chemotherapy‐resistance by increasing YAP stability and nuclear YAP protein. Knockdown of YAP blocks EphA2‐induced tumor growth in GC xenograft mouse models. Importantly, the coactivation of EphA2 and YAP is manifested in clinical human GC, and is related to GC recurrence. Thus, our results establish a novel EphA2‐to‐YAP pathway that drives GC growth, progression and therapy‐resistance, targeting this pathway would be an efficient way for the treatment of GC, particularly chemotherapy‐resistant GC.