Tian Binle, Xia Xin, Li Qi, Qin Jian
Cancer 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.
Department of Hematology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200080, China; Department of Hematology, Tongji Hospital, Tongji University School of Medicine, Shanghai 200065, China.
Biochim Biophys Acta Rev Cancer. 2025 Jul;1880(3):189347. doi: 10.1016/j.bbcan.2025.189347. Epub 2025 May 6.
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.
BRAF 突变型结直肠癌（CRC）通常表现出独特的分子特征，其特征为具有两种不同微卫星状态（MSI 和 MSS）的高甲基化表型以及相应的甲基化谱。这两种不同的 BRAF 突变型 CRC 之间的预后差异源于不同的致癌途径，其中 BRAF 突变的 MSS CRC 表现出特别不利的临床结果。这些现象的潜在机制源于甲基化图谱中的表观遗传异质性。将胆石症和脱氧胆酸（DCA）与 BRAF 突变型 CRC 发病机制联系起来的新证据，有必要对它们潜在的机制关系进行系统研究。阐明这些联系可能揭示新的致病途径，并为 BRAF 突变型 CRC 的风险降低、分子诊断和治疗干预提供有针对性的策略。
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