Cited by 346Pancreatic and Hepatic Oncology ResearchPancreatitis Pathology and TreatmentCancer Genomics and Diagnostics

The DOI matches its Crossref record; 63 of the 66 references it cites were found in a registry or an index.

Frequency of K-ras Mutations in Pancreatic Intraductal Neoplasias Associated with Pancreatic Ductal Adenocarcinoma and Chronic Pancreatitis: A Meta-Analysis

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Löhr, Matthias, Klöppel, Gunter, Maisonneuve, Patrick, Lowenfels, Albert B., Lüttges, Jutta·2005·Neoplasia

Abstract

Molecular analyses have demonstrated mutations in the K-ras gene at codon 12 in the majority of pancreatic ductal adenocarcinomas (PDACs). In order to determine whether the K-ras mutation rate increases parallel to the grade of dysplasia in duct lesions, we performed a meta-analysis of the studies published between 1988 and 2003 that provide information on K-ras mutations in hyperplastic and dysplastic duct lesions in the pancreas. The described duct lesions were reclassified according to the nomenclature for pancreatic intraepithelial neoplasia (PanIN), and the molecular methods for detecting K-ras were reviewed. In PanIN lesions from pancreata of patients with PDAC, there was a stepwise increase in K-ras mutations that correlated with the grade of dysplasia of the PanIN lesion. K-ras mutations were found in 36%, 44%, and 87% of PanIN-1a, 1b, and 2-3 lesions, respectively (trend statistic P <.001). Mutation-enriched polymerase chain reaction (PCR) resulted in higher rates of K-ras mutations in PanIN than plain PCR did. The incidence of K-ras mutations in PanIN lesions associated with chronic pancreatitis (CP) or normal pancreas was low (around 10%). In CP, K-ras mutations were only found after a disease duration of 3 years. The correlation of the incidence of K-ras mutations with the grade of dysplasia in PanIN and the occurrence of these mutations in CP with a duration of more than 3 years underlines the importance of this genetic change for the development of PDAC.

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Metadata

Authors
Löhr, M., Klöppel, G., Maisonneuve, P., Lowenfels, A. B., & Lüttges, J.
Affiliations
  • Heidelberg University (DE)
  • European Institute of Oncology (IT)
  • New York Medical College (US)
Corresponding author
Löhr, Matthias
Venue
Neoplasia
Publisher
Elsevier BV
Published
2005-01
Volume
7
Issue
1
Pages
17-23
ISSN
1476-5586 (ISSN-L)
OpenAlex
W2108100098
Cited by
343
References
66
Citations by year
2026: 6 · 2025: 7 · 2024: 15 · 2023: 15 · 2022: 16 · 2021: 16 · 2020: 17 · 2019: 13 · 2018: 24 · 2017: 22 · 2016: 15 · 2015: 18 · 2014: 26 · 2013: 21 · 2012: 16
FWCI
1.51
Type
journal article
Language
en
Open access
Locations
  • Neoplasia (publishedVersion, cc-by-nc-nd)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
  • Deutsche Forschungsgemeinschaft
  • Deutsche Krebshilfe
Topics
  • Health Sciences › Medicine › Oncology › Pancreatic and Hepatic Oncology Research
  • Health Sciences › Medicine › Surgery › Pancreatitis Pathology and Treatment
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer Genomics and Diagnostics
Keywords
KRAS mutation, pancreatic ductal adenocarcinoma, pancreatic intraepithelial neoplasia, chronic pancreatitis, pancreatic dysplasia, disease duration
MeSH terms
Adenocarcinoma, Humans, Mutation, Pancreatic Ducts, Pancreatic Neoplasms, Pancreatitis, Genes, ras, Carcinoma, Pancreatic Ductal

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