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
Open accessAbstract
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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In the citing paper
“KRAS mutations were found in 10% of CP lesions and 44% of PDAC lesions, with an increase in frequency with the progression of PanIN grade [102].”
From Significance of TP53, CDKN2A, SMAD4 and KRAS in Pancreatic Cancer (2024) · cites this paper as [102]
Experimental — accuracy not yet measuredIn the citing paper
“KRAS mutations are often early events in tumourigenesis in lung and pancreatic cancers [41, 42].”
From Drugging KRAS: Current perspectives and state-of-art review (2022) · cites this paper as [42]
In the citing paper
“KRAS mutation is readily detectable in 25% and 38% of PanIN-1A and PanIN-1B, respectively (55).”
From KRAS mutation in pancreatic cancer (2021) · cites this paper as [55]
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Self-citationK-ras mutations and allelic loss at 5q and 18q in the development of human pancreatic cancers
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Self-citationWhat Is the True Rate of K-ras Mutation in Carcinoma of the Pancreas?
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ResultImmortalized bovine pancreatic duct cells become tumorigenic after transfection with mutant k-ras
Löhr, M. J., Müller, P., Zauner, I., Schmidt, C., Trautmann, B., Thévenod, F., Capellá, G., Farré, A., Liebe, S., & Jesnowski, R. (2001) · Archiv für Pathologische Anatomie und Physiologie und für Klinische Medicin · doi:10.1007/s004280100397 · Cited by 29 · cited 1×
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“were classified [10,21] by two independent pathologists”
Self-citationMultiple K‐ras Mutations in Hyperplasia and Carcinoma in Cases of Human Pancreatic Carcinoma
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Self-citationDistribution of genetic variants in preneoplastic areas of colorectal tumours
Lindforss, U., Papadogiannakis, N., Zetterquist, H., Lindberg, G., & Olivecrona, H. (2003) · European Journal of Surgical Oncology · doi:10.1016/s0748-7983(03)00075-1 · Cited by 10 · cited 1×
“Similar results were obtained in extrapancreatic adenocarcinomas, which were also found to have an elevated K-ras mutation rate [14].”
ResultSystematic review and meta‐analysis in anatomic pathology
Heatley, M. K. (2000) · Histopathology · doi:10.1046/j.1365-2559.2000.00943.x · Cited by 4
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Background
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)
- PMC
- PMC1490318
- 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
- gold
- doi.org
- Licence
- 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
About these checks
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.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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