Archasappawat, S.; Al-Musawi, F.; Liu, P.; Lee, E.; Hwang, C.-I. Familial Pancreatic Cancer Research: Bridging Gaps in Basic Research and Clinical Application. Preprints2024, 2024080282. https://doi.org/10.20944/preprints202408.0282.v1
APA Style
Archasappawat, S., Al-Musawi, F., Liu, P., Lee, E., & Hwang, C. I. (2024). Familial Pancreatic Cancer Research: Bridging Gaps in Basic Research and Clinical Application. Preprints. https://doi.org/10.20944/preprints202408.0282.v1
Chicago/Turabian Style
Archasappawat, S., EunJung Lee and Chang-il Hwang. 2024 "Familial Pancreatic Cancer Research: Bridging Gaps in Basic Research and Clinical Application" Preprints. https://doi.org/10.20944/preprints202408.0282.v1
Abstract
Familial pancreatic cancer (FPC) represents a significant yet underexplored area in pancreatic cancer research. Basic research efforts are notably limited, and when present, they are predominantly centered on BRCA1 and BRCA2 mutations due to the scarcity of other genetic variants associated with FPC, leading to a limited understanding of the broader genetic landscape of FPC. This review examines the current state of FPC research, focusing on the molecular mechanisms driving pancreatic ductal adenocarcinoma (PDAC) progression. It highlights the role of homologous recombination (HR) and its therapeutic exploitation via synthetic lethality with PARP inhibitors in BRCA1/2-deficient tumors. The review discusses various pre-clinical models of FPC, including conventional two-dimensional (2D) cell lines, patient-derived organoids (PDOs), patient-derived xenografts (PDXs), and genetically engineered mouse models (GEMMs) as well as new advancements in FPC research.
Biology and Life Sciences, Biochemistry and Molecular Biology
Copyright:
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
