[Epidermal growth factor receptor gene mutations and clinicopathologic correlation in 309 patients with non-small cell lung cancer].

OBJECTIVE: To investigate the epidermal growth factor receptor (EGFR) gene mutation profile and related clinicopathological features in Chinese patients with non-small cell lung carcinoma (NSCLC). METHODS: Optimized oligonucleotide probe method was applied to detect EGFR mutations involving exons 18 - 21 using formalin fixed paraffin embedded tissue specimens of 309 NSCLC patients. The relationship between EGFR mutations and clinicopathological features were analyzed. RESULTS: The overall EGFR mutation rate was 34% (105/309) in this study cohort. Mutation rates in male and female were 30.4% (56/184) and 39.2% (49/125), respectively. The mutation rate was higher in patients less than 60 years of age, non-smokers and adenocarcinoma subtype than in their counterparts (P<0.05), with the percentage of 40.5% (87/215), 40.2% (51/127), 38.8% (78/201), respectively. The EGFR mutation types included exon 18 G719X mutation (5.7%, 6/105), exon 19 deletion (39.0%, 41/105) and exon 21 L858R mutation (55.2%, 58/105). In large cell undifferentiated carcinomas and squamous cell carcinomas, EGFR mutation rates were 22.2% (58/105) and 3/14, respectively. The overall mutation rate of exon 18 was low, but the proportion of its mutation was higher in squamous and adenosquamous carcinomas than in adenocarcinomas. CONCLUSIONS: There is a higher EGFR mutation rate in female, age of less than 60 years, non-smoker and adenocarcinoma among Chinese patients with NSCLC. Optimized oligonucleotide probe method is a sensitive and convenient method for the detection of EGFR mutations.

Chinese herbal medicines for mild cognitive impairment: A protocol for meta-analysis and trial sequential analysis.

BACKGROUND: Mild cognitive impairment (MCI), as a common neurodegenerative aging disease representing an intermediate stage between normal cognitive functioning and dementia, poses an excessive burden on health care. The clinical benefit of Chinese herbal medicines (CHMs) for MCI remains inconclusive. This study is aimed at evaluating the efficacy and acceptability of CHMs through meta-analysis and trial sequential analysis (TSA). METHODS: We applied extensive strategies on preliminary literature screening to identify relevant randomized controlled trials which meticulously compare any of CHMs interventions with placebo groups as monotherapy for MCI. The primary outcome of this study is the change of global cognitive function, and the secondary outcomes include assessments of activities of daily living, mood, and adverse events. Data synthesis, risk of bias assessment, sensitivity and subgroup analyses, and TSA will be conducted with application of Review Manager, Stata, and TSA software. The quality of the evidence will be evaluated using the Grading of Recommendations Assessment, Development and Evaluation instrument. INPLASY registration number: INPLASY202190006 (https://inplasy.com/inplasy-2021-9-0006/). RESULTS: This study will confirm the clinical efficacy and safety of CHMs when used in the treatment of patients with MCI. CONCLUSION: This study will provide reliable evidence and references for the selection of CHMs in therapy and future clinical research of MCI.

Liver fibrosis and hepatic stellate cells: Etiology, pathological hallmarks and therapeutic targets.

Liver fibrosis is a reversible wound-healing process aimed at maintaining organ integrity, and presents as the critical pre-stage of liver cirrhosis, which will eventually progress to hepatocellular carcinoma in the absence of liver transplantation. Fibrosis generally results from chronic hepatic injury caused by various factors, mainly viral infection, schistosomiasis, and alcoholism; however, the exact pathological mechanisms are still unknown. Although numerous drugs have been shown to have antifibrotic activity in vitro and in animal models, none of these drugs have been shown to be efficacious in the clinic. Importantly, hepatic stellate cells (HSCs) play a key role in the initiation, progression, and regression of liver fibrosis by secreting fibrogenic factors that encourage portal fibrocytes, fibroblasts, and bone marrow-derived myofibroblasts to produce collagen and thereby propagate fibrosis. These cells are subject to intricate cross-talk with adjacent cells, resulting in scarring and subsequent liver damage. Thus, an understanding of the molecular mechanisms of liver fibrosis and their relationships with HSCs is essential for the discovery of new therapeutic targets. This comprehensive review outlines the role of HSCs in liver fibrosis and details novel strategies to suppress HSC activity, thereby providing new insights into potential treatments for liver fibrosis.