Cited by 717Pancreatic and Hepatic Oncology ResearchCancer Genomics and DiagnosticsPancreatitis Pathology and Treatment

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Pancreatic Cancer

Open access

Maitra, Anirban, Hruban, Ralph H.·2008·Annual Review of Pathology: Mechanisms of Disease

DOI 10.1146/annurev.pathmechdis.3.121806.154305PMC PMC2666336

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Abstract

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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Authors: Maitra, A., & Hruban, R. H.
Affiliations: Johns Hopkins University (US)
ORCID: Maitra, Anirban
Hruban, Ralph H.
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
DOI: 10.1146/annurev.pathmechdis.3.121806.154305
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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