BackgroundCamrelizumab and chemotherapy demonstrated durable antitumor activity with a manageable safety profile as first-line treatment in patients with advanced esophageal squamous cell carcinoma (ESCC). This study aimed to evaluate the safety and efficacy of camrelizumab plus neoadjuvant chemotherapy, using pathologically complete response (pCR) as primary endpoint, in the treatment for locally advanced ESCC.MethodsPatients with locally advanced but resectable thoracic ESCC, staged as T1b-4a, N2-3 (≥3 stations), and M0 or M1 lymph node metastasis (confined to the supraclavicular lymph nodes) were enrolled. Eligible patients received intravenous camrelizumab (200 mg, day 1) plus nab-paclitaxel (100 mg/m2, day 1, 8, 15) and carboplatin (area under curve of 5 mg/mL/min, day 1) of each 21-days cycle, for two cycles before surgery. The primary endpoint is pCR rate in the per-protocol population. Safety was assessed in the modified intention-to-treat population that was treated with at least one dose of camrelizumab.ResultsFrom November 20, 2019 to December 22, 2020, 60 patients were enrolled. 55 (91.7%) patients completed the full two-cycle treatment successfully. 51 patients underwent surgery and R0 resection was achieved in 50 (98.0%) patients. pCR (ypT0N0) was identified in 20 (39.2%) patients and 5 (9.8%) patients had complete response of the primary tumor but residual disease in lymph nodes alone (ypT0N+). 58 patients (96.7%) had any-grade treatment-related adverse events (TRAEs), with the most common being leukocytopenia (86.7%). 34 patients (56.7%) had adverse events of grade 3 or worse, and one patient (1.7%) occurred a grade 5 adverse event. There was no in-hospital and postoperative 30-day as well as 90-day mortality.ConclusionsThe robust antitumor activity of camrelizumab and chemotherapy was confirmed and demonstrated without unexpected safety signals. Our findings established camrelizumab and chemotherapy as a promising neoadjuvant treatment for locally advanced ESCC.Trial registration numberChiCTR1900026240.

Background and Objective: Since December 2019, coronavirus disease 2019 (COVID-19) has spread rapidly around the world. Studies found that the incidence of acute kidney injury (AKI) in COVID-19 patients was more than double the incidence of AKI in non-COVID-19 patients. Some findings confirmed that AKI is a strong independent risk factor for mortality in patients with COVID-19 and is associated with a three-fold increase in the odds of in-hospital mortality. However, little information is available about AKI in COVID-19 patients. This study aimed to analyse the risk factors for AKI in adult patients with COVID-19.Methods: A systematic literature search was conducted in PubMed, EMBASE, Web of Science, the Cochrane Library, CNKI, VIP and WanFang Data from 1 December 2019 to 30 January 2021. We extracted data from eligible studies to compare the effects of age, sex, chronic diseases and potential risk factors for AKI on the prognosis of adult patients with COVID-19.Results: In total, 38 studies with 42,779 patients were included in this analysis. The meta-analysis showed that male sex (OR = 1.37), older age (MD = 5.63), smoking (OR = 1.23), obesity (OR = 1.12), hypertension (OR=1.85), diabetes (OR=1.71), pneumopathy (OR = 1.36), cardiovascular disease (OR = 1.98), cancer (OR = 1.26), chronic kidney disease (CKD) (OR = 4.56), mechanical ventilation (OR = 8.61) and the use of vasopressors (OR = 8.33) were significant risk factors for AKI (P < 0.05).Conclusions: AKI is a common and serious complication of COVID-19. Overall, male sex, age, smoking, obesity, hypertension, diabetes, pneumopathy, cardiovascular disease, cancer, CKD, mechanical ventilation and the use of vasopressors were independent risk factors for AKI in adult patients with COVID-19. Clinicians need to be aware of these risk factors to reduce the incidence of AKI.System Review Registration: PROSPERO, identifier [CRD42021282233].

Background Patients with lung adenocarcinoma (LUAD) have high mortality rate and poor prognosis. The LUAD cells display increased aerobic glycolysis, which generates energy required for their survival and proliferation. Deregulation of Wnt/β-catenin signaling pathway induces the metabolism switching and oncogenesis in tumor cells. RING finger protein 115 (RNF115) is an E3 ligase for ubiquitin-mediated degradation. Although the oncogenic functions of RNF115 have been revealed in breast tumor cells, the effect of RNF115 on lung cancer is still not clear. Methods RNF115 expression and its correlation with the features of LUAD patients were analyzed by using public database and our own cohort. The functions of RNF115 in proliferation and energy metabolism in LUAD cells were explored by downregulating or upregulating RNF115 expression. Results We demonstrated that RNF115 was overexpressed in LUAD tissues and its expression was positively correlated with the poor overall survival of LUAD patients. Moreover, RNF115 overexpression inhibited LUAD cell apoptosis and promoted cellular proliferation and metabolism in LUAD cells. On the contrary, RNF115 knockdown displayed reverse effects. Furthermore, the underlying mechanism of the biological function of RNF115 in LUAD was through regulating Wnt/β-catenin pathway via ubiquitination of adenomatous polyposis coli (APC). Conclusion The current study reveals a close association between RNF115 expression and prognostic conditions in LUAD patients and the oncogenic roles of RNF115 in LUAD at the first time. These findings may help establish the foundation for the development of therapeutics strategies and clinical management for lung cancer in future.

Bioinformatic tools were used to analyze GSE6188, GSE13937 and GSE43732 microarrays, and the top 10 upregulated and downregulated genes of each microarray were identified. It was determined that human microRNA (hsa-miR)-1 and hsa-miR-203 were two downregulated genes in common. Subsequently, it was identified that there were 145 and 335 genes in common targeted by hsa-miR-1 and hsa-miR-203, respectively. In order to narrow the number of target genes down further, the target genes were compared with GSE26886 microarray data. There were five upregulated genes in common with hsa-miR-1, i.e., MMD, BICD1, PTPRG, SDC2 and SEMA6D, and there were eight upregulated genes in common with hsa-miR-203, i.e., PXDN, NRCAM, FMNL2, EIF5A2, GLI3, FSL1, GREM1 and AHR. These genes may become promising biomarkers for the diagnosis of esophageal cancer.