Wenhai  Ye , Haidan Yan

Department of Bioinformatics, Fujian Key Laboratory of Medical Bioinformatics, School of Medical Technology and Engineering, Fujian Medical University, Fuzhou, 350122, Fujian, China
Author    Correspondence author
International Journal of Molecular Medical Science, 2024, Vol. 14, No. 5   
Received: 19 Aug., 2024    Accepted: 26 Sep., 2024    Published: 10 Oct., 2024

This is an open access article published under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Pancreatic ductal adenocarcinoma (PDAC) is the most common and lethal type of pancreatic cancer, with KRAS gene mutations present in over 90% of PDAC cases, serving as a major driver of the disease's progression. This study systematically reviews the genomic mechanisms of KRAS mutations and their impact on tumor initiation, progression, and therapeutic resistance. KRAS mutations promote tumor cell proliferation, invasion, and survival by activating multiple signaling pathways, such as MAPK and PI3K, and interact with other oncogenes and tumor suppressor genes, further exacerbating the aggressiveness of pancreatic cancer and its resistance to treatment. Although significant progress has been made in detecting KRAS mutations, effective targeted therapies against KRAS remain challenging. The study also explores the current status and future prospects of KRAS-targeted therapies, including novel KRAS inhibitors, combination therapies, and personalized treatment strategies. With the continuous advancement of genomic technologies, KRAS-targeted therapies are expected to play a more critical role in the treatment of pancreatic cancer.

KRAS mutations; Pancreatic ductal adenocarcinoma; Targeted therapy; Genomic mechanisms; Resistance mechanisms