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Chandrayee Ghosh | Editor | SciTechnol | Journal of Clinical & E

Chandrayee Ghosh

Editorial Board Member

Post-doctoral Fellow, Dept. of General Surgery, Stanford University, California, USA

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Biography

I have a broad background in the field of Cancer and Immunology, with specific training and expertise in cancer therapeutics and translational science pertaining to natural compounds and drug repurposing. My current research includes identifying novel functions of FDA approved compounds and their combinations in targeting endocrine cancers and assessing their mechanism of actions. I have worked elaborately in pancreatic ductal adenocarcinoma and have identified the potential interaction KDM3A with DCLK-1 and their role in PDAC tumorigenesis and stemness. In this work I also established that N-oxalylglycine (NOG), α-ketoglutarate mimetic affects KDM3A activity. In another project I focused on identifying the cluster of master transcription factors or Super-Enhancers as novel targets for Pancreatic Adenocarcinoma using Combination of natural Compounds as anticancer agents. My doctoral thesis was on identification and characterization of Toll-like Receptors (TLR-2, 4, 6) in thymic, splenic and lymph node lymphocytes and macrophages of Swiss albino mice and their role in S. aureus infection and lipopolysaccharide administration. In addition, I have successfully published my research works in good peer-reviewed journals.

Research Interest

Postdoctoral training: For my postdoctoral training, I am currently working on the novel combination of PLX4720 and ponatinib showing synergistic anticancer activity in BRAFV600E mutant thyroid cancer cells based on in vitro and in vivo studies. The synergistic mechanism of action results in more effective inhibition of the MAPK pathway with lower pERK and c-JUN levels, and induces caspase-dependent apoptosis. Combination PLX4720 and ponatinib is able to overcome resistance in PLX4720 resistant BRAFV600E mutant cell. In another study I am conducting screening on a wide range of FDA approved drugs on Thyroid cancer to find potential effective candidates in novel therapeutics. In vitro and In vivo validation of the selected candidates are under process. In my previous laboratory at KUMC, I have learned cell culture techniques for studying compounds against pancreatic cancer. I worked on different molecular biology-based projects that involve techniques like ChIP-seq, RNA-seq, Flow cytometry, western blot, Bioinformatics analysis, Immunohistochemistry, microscopy and mouse models (orthotopic surgery, PDX xenograft, KPC model generation). I have been working on pancreatic cancer with the agenda of ascertaining possible therapeutic or preventive strategies that involve the understanding of key signaling pathways in cancer cells and how targeting those with natural or synthetic compounds will contribute to the treatment of cancer patients. In one of the projects I have identified significant H3K27ac marks at the TSS and enhancer region of numerous genes that act as master transcription factors in Pancreatic Cancer (PDAC). The goal was to identify the most prominent enhancer and super-enhancers (SE) regions for PDAC. Differential association of SE cancerous and metastatic cell lines of PDAC has been implicated in comparison to non-cancerous cells. In this study, we found that combination of natural compounds, affects acetylation of some of the major SE related genes and at a higher dose, a complete reduction in acetylation marks was seen in embryonic stem cell transcription factors. In another project, I have identified that green tea extract Epigallocatechin gallate (EGCG) has anti-cancer activity on PDAC and exerts a cytotoxic effect in gemcitabine-resistant cells. I have analyzed that EGCG impairs stemness by modulating Sonic Hedgehog pathway and will be a potent agent for new therapeutic strategies for inhibition of PDAC tumorigenesis by inducing cytotoxicity in gemcitabine-resistant cells.  I was involved in another project where I determined the mechanism by which N-oxalylglycine (NOG), α-ketoglutarate mimetic affects KDM3A activity.

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