Search

Since December, 2019, Wuhan, China, has experienced an outbreak of coronavirus disease 2019 (COVID-19), caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Epidemiological and clinical characteristics of patients with COVID-19 have been reported but risk factors for mortality and a detailed clinical course of illness, including viral shedding, have not been well described.In this retrospective, multicentre cohort study, we included all adult inpatients (≥18 years old) with laboratory-confirmed COVID-19 from Jinyintan Hospital and Wuhan Pulmonary Hospital (Wuhan, China) who had been discharged or had died by Jan 31, 2020. Demographic, clinical, treatment, and laboratory data, including serial samples for viral RNA detection, were extracted from electronic medical records and compared between survivors and non-survivors. We used univariable and multivariable logistic regression methods to explore the risk factors associated with in-hospital death.191 patients (135 from Jinyintan Hospital and 56 from Wuhan Pulmonary Hospital) were included in this study, of whom 137 were discharged and 54 died in hospital. 91 (48%) patients had a comorbidity, with hypertension being the most common (58 [30%] patients), followed by diabetes (36 [19%] patients) and coronary heart disease (15 [8%] patients). Multivariable regression showed increasing odds of in-hospital death associated with older age (odds ratio 1·10, 95% CI 1·03-1·17, per year increase; p=0·0043), higher Sequential Organ Failure Assessment (SOFA) score (5·65, 2·61-12·23; p0·0001), and d-dimer greater than 1 μg/mL (18·42, 2·64-128·55; p=0·0033) on admission. Median duration of viral shedding was 20·0 days (IQR 17·0-24·0) in survivors, but SARS-CoV-2 was detectable until death in non-survivors. The longest observed duration of viral shedding in survivors was 37 days.The potential risk factors of older age, high SOFA score, and d-dimer greater than 1 μg/mL could help clinicians to identify patients with poor prognosis at an early stage. Prolonged viral shedding provides the rationale for a strategy of isolation of infected patients and optimal antiviral interventions in the future.Chinese Academy of Medical Sciences Innovation Fund for Medical Sciences; National Science Grant for Distinguished Young Scholars; National Key Research and Development Program of China; The Beijing Science and Technology Project; and Major Projects of National Science and Technology on New Drug Creation and Development.

Highlights • Programmed death 1 (PD-1) inhibitors have been proved to be effective in advanced esophageal cancer. • PD-1 inhibitors significantly prolonged the OS when compared with chemotherapy. • There was no significant improvement in terms of PFS and ORR for PD-1 inhibitors when compared with chemotherapy. • PD-1 inhibitors lowered grade 3 - 5 treatment-related adverse effects versus chemotherapy. • A subgroup analysis showed that esophageal squamous cell carcinoma was more effective than adenocarcinoma for PD-1 inhibitors., Background A novel therapy based on programmed death 1 (PD-1) inhibitors has been proved to be effective in advanced esophageal cancer. This article is a meta-analysis that aims to compare the efficacy and safety of anti-PD-1 therapy with chemotherapy in esophageal cancer. Patients and methods Data were collected from eligible studies searched from PubMed, Web of Science, Cochrane Library, and Embase. Pooled hazard ratio (HR) for overall survival (OS), progression-free survival (PFS), and objective response rate (ORR) was estimated to assess the efficacy of PD-1 inhibitors versus chemotherapy. The subgroup analysis was also performed to evaluate the OS benefits. The OR for the occurrence of treatment-related adverse effects was calculated to assess the safety of anti-PD-1 therapy. Results A total of 4 studies were analyzed. Compared with patients with chemotherapy, patients with anti-PD-1 therapy had a significant improvement in OS (HR = 0.79, 95% CI: 0.71–0.88, and P

Long non‐coding RNAs (lncRNAs) have been illustrated to function as important regulators in carcinogenesis and cancer progression. However, the roles of lncRNA NNT‐AS1 in gastric cancer remain unclear. In the present study, we investigate the biological role of NNT‐AS1 in gastric cancer tumorigenesis. Results revealed that NNT‐AS1 expression level was significantly up‐regulated in GC tissue and cell lines compared with adjacent normal tissue and normal cell lines. The ectopic overexpression of NNT‐AS1 indicated the poor prognosis of GC patients. In vitro experiments validated that NNT‐AS1 knockdown suppressed the proliferation and invasion ability and induced the GC cell cycle progression arrest at G0/G1 phase. In vivo xenograft assay, NNT‐AS1 silencing decreased the tumour growth of GC cells. Bioinformatics online program predicted that miR‐424 targeted the 3′‐UTR of NNT‐AS1. Luciferase reporter assay, RNA‐immunoprecipitation (RIP) and RNA pull‐down assay validated the molecular binding within NNT‐AS1 and miR‐424, therefore jointly forming the RNA‐induced silencing complex (RISC). Moreover, E2F1 was verified to act as the target gene of NNT‐AS1/miR‐424, indicating the NNT‐AS1/miR‐424/E2F1 axis. In conclusion, our study indicates that NNT‐AS1 sponges miR‐424/E2F1 to facilitate GC tumorigenesis and cycle progress, revealing the oncogenic role of NNT‐AS1 for GC.

Gastric cancer remains the second most common cause of cancer-related death worldwide. Because of the poor prognosis of late-stage gastric cancer patients, it is imperative to develop new strategies to improve the survival rate of this disease. Currently, immunotherapy is considered as an innovative approach for cancers such as lung cancer, gastric cancer and breast cancer. In fact, previous works have revealed promising results in this field. With further understanding of immunogenomics of gastric cancer, new immune checkpoint regulators could become more important. In addition, whole-genome sequencing and genome editing provide us with more information on the heterogeneity of gastric cancer, showing helpful tools to identify new predictive biomarkers and to achieve personalized treatment. Further research and better understanding of the functions of immune system will enhance immunotherapy treatment in the future.