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Treatment options for patients with advanced gastric cancer (AGC) are limited. One approach to improving survival in patients with AGC is to optimize the available agents via sequential therapy. However, clinical trial reports of first-line chemotherapy indicate that elderly patients and patients with massive ascites are less likely to receive subsequent lines of therapy. In addition, clinical trials of second- and third-line chemotherapy generally exclude these two patient populations because they are likely to have poor performance status and additional issues that are difficult to manage. Good patient management is likely to be key to the successful use of sequential therapy in these two patient populations by minimizing adverse effects to allow patients to derive benefit from the additional treatment. This narrative review summarizes the available information on AGC treatment and patient management in elderly patients and patients with massive ascites. The available data suggest that elderly patients benefit from chemotherapy; however, monitoring toxicity is essential to avoid chemotherapy-related toxicities. Important aspects of patient management for elderly patients include symptom monitoring, nutritional support, and fall prevention. The available data for patients with massive ascites show limited success for a range of treatment approaches, including systemic chemotherapy. The management of ascites is also challenging, with no clear guidance on the preferred strategies. To address these gaps in knowledge, future clinical trials should incorporate more inclusive eligibility criteria to enroll populations of patients with AGC that are more reflective of the real-world population with respect to age, complications, and overall health status.OBJECTIVE Osteosarcoma is one of the most common malignant bone tumors which mainly occurs in children and adolescents. It is characterized by high malignancy and high metastasis rate, resulting in high mortality and disability. Accumulating studies have validated that long noncoding RNAs (lncRNAs) exerted vital roles in multiple cancer progression by regulating the expression of specific genes. This work aimed to explore the potential molecular mechanism of EWS in osteosarcoma. RESULTS In this study, we discovered that both EWS and Sox2 were highly expressed in osteosarcoma tissue samples. In addition, the expression of EWS was positively associated with Sox2 level. We conducted a series of functional assays and observed that Sox2 overexpression could significantly overturned the enhancement of cell proliferation and the decline of cell apoptosis induced by EWS knockdown in osteosarcoma. Moreover, we found a key upstream regulatory gene of Sox2 miR-199a-5p. CONCLUSIONS Through molecular biology studies and rescue assays, we further demonstrated that EWS promotes tumor growth through the miR-199a-5p/Sox2 signaling axis in osteosarcoma. These findings may provide an important theoretical basis for the clinical diagnosis and treatment of osteosarcoma.OBJECTIVE To investigate the functions of eIF3b in chronic myelogenous leukemia (CML). METHODS The expression of eIF3b was inhibited by transfecting aspecifically designed shRNA into the CML cell lines of TK-6 and K562. The CCK8 assay was conducted to determine cell viability, and flow cytometry was used to examine the change in the cell cycle and cell apoptosis. RNAsequencing was applied to screen the candidate targets of eIF3b to identify the underlying mechanisms of eIF3b.An in vivo tumour xenograft mouse model was established by injecting shRNA transfected cells into the NCG mice. The tumour size and body weight of mice were monitored every other day. The mice were sacrificed 2 weeks after the tumour cell injection. The expression of eIF3b and target genes in the tumour tissues were determined by immunohistochemical staining and Western blotting. RESULTS The group with inhibited expression of eIF3b led to about 50% lower cell viability compared with that of the control group (P  less then  0.05). Flow cytometry suggested that the percentage of increase in apoptotic cells was eight times higher than those in control group for TK-6 and K562 cells (P  less then  0.05). However, the difference between the cell amounts in the S phase for the experiment and control groups was not significant. After RNAsequencing and further validation via qPCR, C3G was screened as the potential target of eIF3b involved in the cell proliferation and apoptosis of CML cell lines. Subsequent in vivo analysis proved that the inhibition of eIF3b suppressed tumour formation and decreased C3G expression, thereby indicating that C3G was the potential target of eIF3b. CONCLUSION eIF3b is correlated with the cell proliferation and cell apoptosis of CML. Moreover, eIF3b regulation most probably occurs via regulating the expression of C3G.OBJECTIVE GSK-3 has been reported to be upregulated in malignant diseases, including lung cancers, thus suggesting it to be a valid target for cancer treatment. The study elucidates the possible mechanism involved in the ability of GSK-3 inhibitors BIO and CHIR 98014 to regulate proteins involved in cell death of H1975 lung cancer cells. RESULTS BIO and CHIR 98014 successfully induced apoptosis at lower concentrations in H1975 cells but not in H460 lung cancer cells. Moreover, increased ROS generation and depolarization of mitochondrial membrane potential were observed in both treatments. EPZ020411 molecular weight Cleavage of caspase-3 was observed in both BIO and CHIR 98014-treated cells after 72 h with monolayer and tumorsphere cell culture models. CONCLUSIONS The use of GSK-3 inhibitors shows promising apoptotic abilities in clinical cancer treatments, particularly for lung cancer cells. This study is the first report to describe the significant apoptotic effects of BIO and CHIR 98014 through multiple mechanisms of H1975 NSCLC that are linked to their proliferative and migratory capacities.BACKGROUND Ventral hernia repair (VHR) is a commonly performed procedure and is especially prevalent in patients who have undergone previous open abdominal surgery up to 28% of patients who have undergone laparotomy will develop a ventral hernia. There is increasing interest in robotic-assisted VHR (RVHR) as a minimally invasive approach to VHR not requiring myofascial release and in RVHR outcomes relative to outcomes associated with laparoscopic VHR (LVHR). We hypothesized real-world evidence from the Americas Hernia Society Quality Collaborative (AHSQC) database will indicate comparable clinical outcomes from RVHR and LVHR approaches not employing myofascial release. METHODS Retrospective, comparative analysis of prospectively collected data describing laparoscopic and robotic-assisted elective ventral hernia repair procedures reported in the multi-institutional AHSQC database. A one-to-one propensity score matching algorithm identified comparable groups of patients to adjust for potential selection bias that could result from surgeon choice of repair approach.

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