Genetic Mutations of Pancreatic Cancer and Genetically Engineered Mouse Models
Open accessAbstract
Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive malignancy, and the seventh leading cause of cancer-related deaths worldwide. An improved understanding of tumor biology and novel therapeutic discoveries are needed to improve overall survival. Recent multi-gene analysis approaches such as next-generation sequencing have provided useful information on the molecular characterization of pancreatic tumors. Different types of pancreatic cancer and precursor lesions are characterized by specific molecular alterations. Genetically engineered mouse models (GEMMs) of PDAC are useful to understand the roles of altered genes. Most GEMMs are driven by oncogenic Kras, and can recapitulate the histological and molecular hallmarks of human PDAC and comparable precursor lesions. Advanced GEMMs permit the temporally and spatially controlled manipulation of multiple target genes using a dual-recombinase system or CRISPR/Cas9 gene editing. GEMMs that express fluorescent proteins allow cell lineage tracing to follow tumor growth and metastasis to understand the contribution of different cell types in cancer progression. GEMMs are widely used for therapeutic optimization. In this review, we summarize the main molecular alterations found in pancreatic neoplasms, developed GEMMs, and the contribution of GEMMs to the current understanding of PDAC pathobiology. Furthermore, we attempted to modify the categorization of altered driver genes according to the most updated findings.
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Pancreatic cancer commonly features mutations in key genes KRAS, p16/CDKN2A, TP53 and SMAD4/DPC4.
“Pancreatic cancer commonly features mutations in key genes, such as KRAS, p16/CDKN2A, TP53 and SMAD4/DPC4 [3,4,5] (Table 1).”
From Significance of TP53, CDKN2A, SMAD4 and KRAS in Pancreatic Cancer (2024) · cites this paper as [4]
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Significance of TP53, CDKN2A, SMAD4 and KRAS in Pancreatic Cancer
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TGFβ in Pancreas and Colorectal Cancer: Opportunities to Overcome Therapeutic Resistance
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Targeting Neoantigens in Pancreatic Ductal Adenocarcinoma
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An Updated Review of the Anticancer Mechanisms and Therapeutic Potential of Naringenin
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Inflammation, microbiota, and pancreatic cancer
Chen, X., Sun, F., Wang, X., Feng, X., Aref, A. R., Tian, Y., Ashrafizadeh, M., & Wu, D. (2025) · Cancer Cell International · doi:10.1186/s12935-025-03673-6 · Cited by 13 · see citing works
Precision immune regulation in KRAS-mutated cancers: the final piece of the puzzle?
Fu, S., Ma, J., Cai, C., Tan, J., Deng, X., Shen, H., Zeng, S., Chen, Y., & Han, Y. (2025) · Journal of Experimental & Clinical Cancer Research · doi:10.1186/s13046-025-03444-1 · Cited by 11 · see citing works
Zhang, F., Yan, Y., Liang, Q., Liu, Y., Wu, G., Xu, Z., & Yang, K. (2023) · Heliyon · doi:10.1016/j.heliyon.2023.e13456 · Cited by 10 · see citing works
The Road Ahead in Pancreatic Cancer: Emerging Trends and Therapeutic Prospects
Do, C. T. P., Prochnau, J. Y., Domínguez, A. M., Wang, P., & Rao, M. K. (2024) · Biomedicines · doi:10.3390/biomedicines12091979 · Cited by 9 · see citing works
Prognostic utility of TME-associated genes in pancreatic cancer
Nie, Y., Xu, L., Bai, Z., Liu, Y., Wang, S., Zeng, Q., Gao, X., Xia, X., & Chang, D. (2023) · Frontiers in Genetics · doi:10.3389/fgene.2023.1218774 · Cited by 8 · see citing works
Functionalized Nanomaterials In Pancreatic Cancer Theranostics And Molecular Imaging
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Polysaccharides as therapeutic vehicles in pancreatic cancer
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The RAS Signaling Network and Cancer
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- Authors
- Saiki, Y., Jiang, C., Ohmuraya, M., & Furukawa, T.
- Affiliations
- Tohoku University (JP)
- Hyogo Medical University (JP)
- Corresponding author
- Furukawa, Toru
- Venue
- Cancers
- Publisher
- MDPI AG
- Published
- 2021-12-24
- Volume
- 14
- Issue
- 1
- Pages
- 71
- ISSN
- 2072-6694 (ISSN-L)
- PMC
- PMC8750056
- OpenAlex
- W4200062746
- Cited by
- 38
- References
- 126
- Citations by year
- 2026: 2 · 2025: 13 · 2024: 11 · 2023: 9 · 2022: 3
- FWCI
- 0.70
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Cancers (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Japan Society for the Promotion of Science (20K07386)
- Topics
- Health Sciences › Medicine › Oncology › Pancreatic and Hepatic Oncology Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer Genomics and Diagnostics
- Health Sciences › Medicine › Surgery › Pancreatitis Pathology and Treatment
- Keywords
- pancreatic ductal adenocarcinoma, pancreatic cancer, genetic mutations, genetically engineered mouse models, KRAS mutation, driver genes, precancerous lesions, CRISPR/Cas9 genome editing, fluorescent protein reporter, lineage tracing, metastasis
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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