Scholarlink

Purpose of review <p>Gallbladder cancer (GBC) is a highly aggressive malignancy with limited therapeutic options and poor prognosis. This review explores the multifaceted etiology and molecular mechanisms underlying GBC, highlighting key pathways and biomarkers associated with its progression.</p> Recent findings <p>Central to GBC pathogenesis are genetic mutations, epigenetic modifications, and the interplay between chronic inflammation and gallstone disease. Molecular markers such as TP53, EGFR, and PI3KCA mutations, alongside epigenetic alterations like DNA methylation, play pivotal roles in disease development. Non-coding RNAs, including miRNAs and lncRNAs, modulate oncogenic and tumor suppressor pathways, impacting proliferation, invasion, and chemoresistance. Chronic inflammation driven by bacterial infections and bile acid dysregulation fosters a tumor-promoting microenvironment, with the epithelial-mesenchymal transition (EMT) and cancer stem cells (CSCs) contributing to metastasis and drug resistance. Advances in understanding the tumor microenvironment, signaling pathways, and exosome-mediated communication offer insights into novel therapeutic targets.</p> Summary <p>This review underscores the need for personalized medicine approaches, leveraging high-throughput sequencing and biomarker discovery to develop tailored diagnostic and therapeutic strategies. By unraveling the complex molecular landscape of GBC, this work provides a foundation for innovative treatments, improving outcomes for patients facing this formidable disease.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Signaling Pathways and Molecular Biomarkers in Gallbladder Cancer: A State-of-the-Art Review

  • 期刊论文

  • 发表日期：

    2025年8月5日

查看全文
  • Tanusree Saha,
  • Naoshad Muhammad

摘要

Purpose of review

Gallbladder cancer (GBC) is a highly aggressive malignancy with limited therapeutic options and poor prognosis. This review explores the multifaceted etiology and molecular mechanisms underlying GBC, highlighting key pathways and biomarkers associated with its progression.

Recent findings

Central to GBC pathogenesis are genetic mutations, epigenetic modifications, and the interplay between chronic inflammation and gallstone disease. Molecular markers such as TP53, EGFR, and PI3KCA mutations, alongside epigenetic alterations like DNA methylation, play pivotal roles in disease development. Non-coding RNAs, including miRNAs and lncRNAs, modulate oncogenic and tumor suppressor pathways, impacting proliferation, invasion, and chemoresistance. Chronic inflammation driven by bacterial infections and bile acid dysregulation fosters a tumor-promoting microenvironment, with the epithelial-mesenchymal transition (EMT) and cancer stem cells (CSCs) contributing to metastasis and drug resistance. Advances in understanding the tumor microenvironment, signaling pathways, and exosome-mediated communication offer insights into novel therapeutic targets.

Summary

This review underscores the need for personalized medicine approaches, leveraging high-throughput sequencing and biomarker discovery to develop tailored diagnostic and therapeutic strategies. By unraveling the complex molecular landscape of GBC, this work provides a foundation for innovative treatments, improving outcomes for patients facing this formidable disease.