Yu Liu

As a key experimental method to study the pathogenesis of brain tumors, the establishment of standardized operation process for intracranial orthotopic tumor modeling is of great significance. At present, although this technology has become the main method for brain tumor research, it has been reported in the literature that there is significant heterogeneity in the injection sites, and there is a lack of systematic verification, which leads to the repeatability of the experiment being questioned. In view of this technical bottleneck, this study used female C57BL mice as a model to establish a standardized intracranial tumor formation operation system. By systematically analyzing the two anatomical markers of bregma and lambda in mice, we not only clarified the quantitative relationship between body weight and bregma-lambda distance in C57BL mice, but also defined the normal range of bregma-lambda distance. More importantly, we found and verified a new standardized injection site. Based on this finding, this study finally constructed a complete set of intracranial tumor formation technology scheme including positioning method, operation specification and quality control.

Background Esophageal carcinoma (EC) is the eighth most common cancer, which is a major health problem on a global scale. Comprehensive treatments such as surgery, radiotherapy and chemotherapy have demonstrated efficacy in certain patients with early-stage esophageal carcinoma. However, it is crucial to explore improved treatment modalities for individuals with advanced, recurrent and metastatic esophageal carcinoma. Methods The eQTL datasets were obtained from Drug-Gene Interaction Database (DGIdb V.4.2.0) and an interesting review about druggable genes. The two-sample MR was used to identify potential drug targets. Co-localization analysis was applied to evaluate if the genes expression single nucleotide polymorphisms (SNPs) drove and was associated with EC risk. And drug prediction and molecular docking were used to verify the pharmaceutical value of potential clinical drugs. Results The present study found thirty potential drug targets that were remarkably correlated with the risk of developing esophageal carcinoma at least in two eQTL datasets by two-sample MR analysis. Five genes colocalized with esophageal carcinoma were identified through colocalization analysis and the medicinal value of four potential clinical drugs was testified by molecular docking. Conclusions We identified five drug targets by MR analysis and co-localization analysis and four drugs by drug prediction and molecular docking analysis respectively, which provide new insights for treatment of esophageal carcinoma.

Utilizing the newly identified M.MedI-N377K methyltransferase, we developed a novel method of CMD-seq for the stoichiometric detection of 5mC in DNA at single-nucleotide resolution.

The OMA-seq method allows for accurate and quantitative detection of 5hmC at single-nucleotide resolution by leveraging natural deaminases. The use of orthologous enzymes for 5hmC detection enhances the toolkit available for epigenetic study.

KDM5C influence H3K4me3 peaks width via its histone demethylase activity.

Delineating KDM5C and BRD4 localization and illustrating the definitions of transcriptional elements.

Loss of KDM5C sensitize tumor cells to BETi treatment.

BRD4 is a vulnerability of KDM5C deficient tumor cells.