The DOI matches its Crossref record; 185 of the 185 references it cites were found in a registry or an index.
Pancreatic Cancer
Open accessAbstract
The past two decades have witnessed an explosion in our understanding of pancreatic cancer, and it is now clear that pancreatic cancer is a disease of inherited (germ-line) and somatic gene mutations. The genes mutated in pancreatic cancer include KRAS2, p16/CDKN2A, TP53, and SMAD4/DPC4, and these are accompanied by a substantial compendium of genomic and transcriptomic alterations that facilitate cell cycle deregulation, cell survival, invasion, and metastases. Pancreatic cancers do not arise de novo, and three distinct precursor lesions have been identified. Experimental models of pancreatic cancer have been developed in genetically engineered mice, which recapitulate the multistep progression of the cognate human disease. Although the putative cell of origin for pancreatic cancer remains elusive, minor populations of cells with stem-like properties have been identified that appear responsible for tumor initiation, metastases, and resistance of pancreatic cancer to conventional therapies.
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“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 [3]
In the citing paper
“Germline CDKN2A mutation is associated with an increased risk of melanoma and pancreatic cancer, and somatic CDKN2A loss is common in pancreatic cancer49–51.”
From Impact of KRAS mutations and co-mutations on clinical outcomes in pancreatic ductal adenocarcinoma (2024) · cites this paper as [50]
In the citing paper
“Germline CDKN2A mutation is associated with an increased risk of melanoma and pancreatic cancer, and somatic CDKN2A loss is common in pancreatic cancer49–51.”
From Impact of KRAS mutations and co-mutations on clinical outcomes in pancreatic ductal adenocarcinoma (2024) · cites this paper as [50]
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Cited by
Sorted by citations
Core Signaling Pathways in Human Pancreatic Cancers Revealed by Global Genomic Analyses
Jones, S., Zhang, X., Parsons, D. W., Lin, J. C.-H., Leary, R. J., Angenendt, P., Mankoo, P., Carter, H., Kamiyama, H., Jimeno, A., et al. (2008) · Science · doi:10.1126/science.1164368 · Cited by 3,969
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Distant metastasis occurs late during the genetic evolution of pancreatic cancer
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Early Detection of Pancreatic Cancer: Opportunities and Challenges
Singhi, A. D., Koay, E. J., Chari, S. T., & Maitra, A. (2019) · Gastroenterology · doi:10.1053/j.gastro.2019.01.259 · Cited by 841
Self-citation
Metadata
- Authors
- Maitra, A., & Hruban, R. H.
- Affiliations
- Johns Hopkins University (US)
- Venue
- Annual Review of Pathology: Mechanisms of Disease
- Publisher
- Annual Reviews
- Published
- 2008-02-01
- Volume
- 3
- Issue
- 1
- Pages
- 157-188
- ISSN
- 1553-4006 (ISSN-L)
- 1553-4014
- PMC
- PMC2666336
- OpenAlex
- W4211122150
- Cited by
- 707
- References
- 185
- Citations by year
- 2026: 16 · 2025: 10 · 2024: 31 · 2023: 29 · 2022: 55 · 2021: 46 · 2020: 46 · 2019: 39 · 2018: 43 · 2017: 42 · 2016: 41 · 2015: 53 · 2014: 59 · 2013: 48 · 2012: 32
- FWCI
- 3.60
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Annual Review of Pathology Mechanisms of Disease (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Cancer Institute (R01CA113669, P50CA062924)
- 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 cancer, germline mutations, somatic mutations, KRAS2, CDKN2A, TP53, genetic alterations, transcriptomic alterations, cell cycle dysregulation, metastasis, precursor lesions, genetically engineered mouse models, tumor progression, cancer stem cells, treatment resistance
- MeSH terms
- Animals, Disease Models, Animal, Humans, Pancreatic Neoplasms, Mice
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