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<p>Gallbladder cancer (GBC) is a highly aggressive malignancy with late presentation, limited therapeutic options, and dismal survival rates. Despite recent advances in molecular profiling, our understanding of GBC remains fragmented, with most studies focusing on isolated genetic or epigenetic events rather than integrating the broader molecular interplay. Frequently altered genes—including TP53, KRAS, ERBB2, and CDKN2A—impact critical signaling cascades such as Ras/MAPK, PI3K/AKT/mTOR, Wnt/β-catenin, and p53, with aberrant ERK pathway activation emerging as a pivotal driver. Epigenetic modifications, dysregulated non-coding RNAs, and immune microenvironmental factors add further layers of complexity but remain underexplored in a unified context. Currently, no comprehensive framework links these alterations into a generalized molecular mechanism that could accelerate biomarker discovery and therapeutic innovation. This review integrates genomic, epigenomic, and immunologic data, complemented by KEGG pathway enrichment analysis, to present a consolidated molecular landscape of GBC. By mapping converging oncogenic hubs and signaling cross-talk, we aim to identify actionable targets—particularly within the ERK axis—that could inform early detection, guide precision therapy, and direct future translational research.</p>

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Molecular convergence in gallbladder cancer: MEK–ERK signalling at the crossroads of oncogenic hubs and pathway cross-talks

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年5月27日

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  • Deeptima Jaiswar,
  • Manjusha Dixit

摘要

Gallbladder cancer (GBC) is a highly aggressive malignancy with late presentation, limited therapeutic options, and dismal survival rates. Despite recent advances in molecular profiling, our understanding of GBC remains fragmented, with most studies focusing on isolated genetic or epigenetic events rather than integrating the broader molecular interplay. Frequently altered genes—including TP53, KRAS, ERBB2, and CDKN2A—impact critical signaling cascades such as Ras/MAPK, PI3K/AKT/mTOR, Wnt/β-catenin, and p53, with aberrant ERK pathway activation emerging as a pivotal driver. Epigenetic modifications, dysregulated non-coding RNAs, and immune microenvironmental factors add further layers of complexity but remain underexplored in a unified context. Currently, no comprehensive framework links these alterations into a generalized molecular mechanism that could accelerate biomarker discovery and therapeutic innovation. This review integrates genomic, epigenomic, and immunologic data, complemented by KEGG pathway enrichment analysis, to present a consolidated molecular landscape of GBC. By mapping converging oncogenic hubs and signaling cross-talk, we aim to identify actionable targets—particularly within the ERK axis—that could inform early detection, guide precision therapy, and direct future translational research.