ArticleThe American journal of pathology2000
Molecular analysis of microdissected tumors and preneoplastic intraductal lesions in pancreatic carcinoma.
Article in The American journal of pathology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.
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Who cites it
29 citing papers in PubMed, 1 synthesis or guideline pooled it, 121 citations in OpenAlex.
- Frequency of K-ras mutations in pancreatic intraductal neoplasias associated with pancreatic ductal adenocarcinoma and chronic pancreatitis: a meta-analysis.Neoplasia (New York, N.Y.) · 2005Pooled it
- Analysis of Donor Pancreata Defines the Transcriptomic Signature and Microenvironment of Early Neoplastic Lesions.Cancer discovery · 2023Article
- Multifaceted role for p53 in pancreatic cancer suppression.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Analysis of donor pancreata defines the transcriptomic signature and microenvironment of early pre-neoplastic pancreatic lesions.bioRxiv : the preprint server for biology · 2023Article
- Protein tyrosine phosphatases: promising targets in pancreatic ductal adenocarcinoma.Cellular and molecular life sciences : CMLS · 2019Review
- Combating pancreatic cancer with PI3K pathway inhibitors in the era of personalised medicine.Gut · 2019Review
- Genetic Alterations of Periampullary and Pancreatic Ductal Adenocarcinoma: An Overview.Current genomics · 2018Review
- Cells of origin of pancreatic neoplasms.Surgery today · 2018Review
- Pancreatic cancer stromal biology and therapy.Genes & diseases · 2015Article
- The Mdm network and its regulation of p53 activities: a rheostat of cancer risk.Human mutation · 2014Review
- Beyond laser microdissection technology: follow the yellow brick road for cancer research.American journal of cancer research · 2014Review
- High prevalence of BRCA1 and BRCA2 germline mutations with loss of heterozygosity in a series of resected pancreatic adenocarcinoma and other neoplastic lesions.Clinical cancer research : an official journal of the American Association for Cancer Research · 2013Article
- Study human pancreatic cancer in mice: how close are they?Biochimica et biophysica acta · 2013Review
- Targeted destruction of the orchestration of the pancreatic stroma and tumor cells in pancreatic cancer cases: molecular basis for therapeutic implications.Cytokine & growth factor reviews · 2012Review
- Two sides of the story? Smad4 loss in pancreatic cancer versus head-and-neck cancer.FEBS letters · 2012Review
- Increased alternative splicing of the KLF6 tumour suppressor gene correlates with prognosis and tumour grade in patients with pancreatic cancer.European journal of cancer (Oxford, England : 1990) · 2008Article
- Emerging molecular biology of pancreatic cancer.Gastrointestinal cancer research : GCR · 2008Article
- Update on pancreatic intraepithelial neoplasia.International journal of clinical and experimental pathology · 2008Article
- Both p16(Ink4a) and the p19(Arf)-p53 pathway constrain progression of pancreatic adenocarcinoma in the mouse.Proceedings of the National Academy of Sciences of the United States of America · 2006Article
- Transcriptome analysis of microdissected pancreatic intraepithelial neoplastic lesions.Oncogene · 2005Article
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Authors and funding
8 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Little or no data exist concerning the inactivation of tumor suppressor genes in intraductal lesions surrounding invasive ductal pancreatic carcinomas. Using a novel improved primer extension and preamplification polymerase chain reaction, we analyzed microdissected paraffin-embedded specimens of pancreatic carcinoma (n = 29) and their corresponding pancreatic intraductal lesions (PIL, n = 331) for loss of heterozygosity (LOH) of p16(INK4), DPC4, and p53 by microsatellite analysis and for p53 protein by immunohistochemistry. LOH at the p16(INK4) locus (9p21) was found in nine of 22 informative tumors (41%), in 15 of 25 tumors (60%) at the DPC4 locus (18q21.1), and in 22 of 27 tumors (81%) at the p53 locus (17p13). Homozygous deletions of p16(INK4) and DPC4 were found in eight of 22 (36%) and four of 25 tumors (16%), respectively. Furthermore, 24 of 29 tumors (83%) revealed considerable intratumoral genetic heterogeneity. In 165 of 277 PILs (60%) having suitable DNA for microsatellite analysis, alterations in at least one tumor suppressor gene were found. In individual PILs, up to three alterations were detected, and p53 LOH occurred even in morphologically normal-appearing ductal epithelium near the tumor. Although deletions of all three tumor suppressor genes were found in PILs without nuclear atypia, there was a tendency toward earlier LOH of p16(INK4) compared to DPC4 and p53 in these lesions. LOH in tumors accompanied positive p53 immunohistochemistry in 81% but only in 38% in PILs.
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