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Genetic Mutation and Regulation in Pancreatic Ductal Adenocarcinoma Cancer: Developing Relevant Molecular Biomarkers
- 1 Department of Biology, New York University, New York, United States
* Author to whom correspondence should be addressed.
Abstract
Pancreatic ductal adenocarcinoma (PDAC) is a highly invasive and highly lethal malignant tumor. Due to the difficulty in early diagnosis and limited treatment options, the 5-year survival rate is less than 10%. Traditional treatments such as surgery, chemotherapy, and radiotherapy have limited effects on PDAC, which is mainly attributed to its unique tumor microenvironment (TME), common gene mutations (such as KRAS, and TP53), and immunosuppressive properties. In recent years, with the advancement of molecular biology and genomics technologies, the molecular mechanisms of PDAC have been studied more deeply, revealing the gene mutations and regulatory networks associated with its pathogenesis. In particular, KRAS mutations have become an important research direction for targeted therapy. However, the effect of immunotherapy in PDAC is limited by the immune escape characteristics of TME. This article systematically summarizes the key gene mutations in PDAC and their regulatory mechanisms, including epigenetic regulation, microRNA, histone modification and other influencing factors. CRISPR-Cas9 shows great potential in correcting gene mutations and reshaping TME. In addition, combining immunotherapy with targeted drug delivery (such as nanotechnology) can improve the precision of treatment and reduce side effects. These advances provide a comprehensive reference for future personalized and effective treatment options for PDAC
Keywords
Pancreatic ductal adenocarcinoma, mutation, genetic regulation, target therapy
[1]. Sarantis, P., Koustas, E., Papadimitropoulou, A., et al. (2020). Pancreatic ductal adenocarcinoma: Treatment hurdles, tumor microenvironment and immunotherapy. World Journal of Gastrointestinal Oncology, 12(2), 173.
[2]. Orth, M., Metzger, P., Gerum, S., et al. (2019). Pancreatic ductal adenocarcinoma: Biological hallmarks, current status, and future perspectives of combined modality treatment approaches. Radiation Oncology, 14(1), 1-20.
[3]. Luo, J. (2021). KRAS mutation in pancreatic cancer. In Seminars in Oncology (Vol. 48, No. 1, pp. 10-18). WB Saunders.
[4]. Eser, S., Schnieke, A., Schneider, G., et al. (2014). Oncogenic KRAS signalling in pancreatic cancer. British Journal of Cancer, 111(5), 817-822.
[5]. Schofield, H. K., Zeller, J., Espinoza, C., et al. (2018). Mutant p53R270H drives altered metabolism and increased invasion in pancreatic ductal adenocarcinoma. JCI Insight, 3(2).
[6]. McCubrey, J. A., Yang, L. V., Abrams, S. L., et al. (2022). Effects of TP53 mutations and miRs on immune responses in the tumor microenvironment important in pancreatic cancer progression. Cells, 11(14), 2155.
[7]. Stefanoudakis, D., Frountzas, M., Schizas, D., et al. (2024). Significance of TP53, CDKN2A, SMAD4 and KRAS in pancreatic cancer. Current Issues in Molecular Biology, 46(4), 2827-2844.
[8]. Venkat, S., Alahmari, A. A., & Feigin, M. E. (2021). Drivers of gene expression dysregulation in pancreatic cancer. Trends in Cancer, 7(7), 594-605.
[9]. Won, E. J., Park, H., Yoon, T. J., et al. (2022). Gene therapy using nanocarriers for pancreatic ductal adenocarcinoma: Applications and challenges in cancer therapeutics. Pharmaceutics, 14(1), 137.
[10]. Yang, H., Bailey, P., & Pilarsky, C. (2019). CRISPR Cas9 in pancreatic cancer research. Frontiers in Cell and Developmental Biology, 7, 239.
Cite this article
Ai,X. (2025). Genetic Mutation and Regulation in Pancreatic Ductal Adenocarcinoma Cancer: Developing Relevant Molecular Biomarkers. Theoretical and Natural Science,90,54-60.
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The datasets used and/or analyzed during the current study will be available from the authors upon reasonable request.
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Volume title: Proceedings of ICMMGH 2025 Workshop: Computational Modelling in Biology and Medicine
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