ArticlePathology oncology research : POR2013
The predictive role of p16 deletion, p53 deletion, and polysomy 9 and 17 in pancreatic ductal adenocarcinoma.
Article in Pathology oncology research : POR, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 17 citations in OpenAlex.
- Nanoliposomal irinotecan with fluorouracil for the treatment of advanced pancreatic cancer, a single institution experience.BMC cancer · 2018Trial
- Exploring the Common Mutational Landscape in Cutaneous Melanoma and Pancreatic Cancer.Pigment cell & melanoma research · 2025Review
- CT Radiomics and Whole Genome Sequencing in Patients with Pancreatic Ductal Adenocarcinoma: Predictive Radiogenomics Modeling.Cancers · 2022Article
- Mutations in key driver genes of pancreatic cancer: molecularly targeted therapies and other clinical implications.Acta pharmacologica Sinica · 2021Review
- Article
- LMNA functions as an oncogene in hepatocellular carcinoma by regulating the proliferation and migration ability.Journal of cellular and molecular medicine · 2020Article
- The Mutational Landscape of Pancreatic and Liver Cancers, as Represented by Circulating Tumor DNA.Frontiers in oncology · 2019Review
- Development and validation of a novel clinical fluorescence in situ hybridization assay to detect JAK2 and PD-L1 amplification: a fluorescence in situ hybridization assay for JAK2 and PD-L1 amplification.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2017Article
- Review
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In this study, we investigated p53 and p16 deletions, and chromosome 9 and 17 amplifications in pancreatic ductal adenocarcinoma (PDAC), and further analyzed their associations with clinical characteristics and prognosis of PDAC. A total of 32 PDAC and 23 peritumoral tissues were collected. Molecular abnormalities of CEP9/p16 and CEP17/p53 were detected using Fluorescence in situ hybridization (FISH). Deletions of p16 and p53 were detected in 50 % and 65.7 % of PDAC, respectively. Polysomy 9 and 17 were identified in 75 % and 71.8 % of PDAC, respectively. No p16 and p53 deletion, polysomy 9 and 17 were identified in peritumoral tissues. We also observed significant correlations of p16 deletion, polysomy 9 and 17 with shorter survival of PDAC. P16 deletion, polysomy 9 and 17 are predictive markers for poor prognosis of PDAC patients, but p53 deletion is not associated with the clinical characteristics and prognosis of PDAC.
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