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Updated: Jun 14, 2025

Development and Maintenance of a Preclinical Patient Derived Tumor Xenograft Model for the Investigation of Novel Anti-Cancer Therapies
Published on: September 30, 2016
Advances in BRAF mutated colorectal cancer-could deoxycholic acid be the culprit?
Binle Tian1, Xin Xia2, Qi Li1
1Cancer Center, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200080, China; Shanghai Key Laboratory of Pancreatic Disease, Institute of Pancreatic Disease, Shanghai Jiao Tong University School of Medicine, Shanghai 200080, China.
Abstract:
BRAF mutated colorectal cancer (CRC) often demonstrates distinct molecular profiles characterized by a high methylator phenotype with two different microsatellite statuses (MSI and MSS) and corresponding methylation spectra. Prognostic disparities between these two different BRAF mutated CRC arise from divergent carcinogenic pathways, with BRAF-mutated MSS CRC exhibiting particularly unfavorable clinical outcomes. The underlying mechanism of these phenomena stems from epigenetic heterogeneity in methylation landscapes. Emerging evidences linking cholelithiasis and deoxycholic acid (DCA) to BRAF-mutated CRC pathogenesis warrant systematic investigation into their potential mechanistic relationships. Elucidating these connections could unravel novel pathogenetic pathways and inform targeted strategies for risk mitigation, molecular diagnostics, and therapeutic intervention of BRAF-mutated CRC.
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