ArticleJournal of gastrointestinal cancer2019
Molecular Alterations Associated with DNA Repair in Pancreatic Adenocarcinoma Are Associated with Sites of Recurrence.
Article in Journal of gastrointestinal cancer, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 14 citations in OpenAlex.
- Is survival influenced by metastatic site in synchronous metastatic pancreatic adenocarcinoma (PDAC)? A prospective real-world BACAP study.ESMO gastrointestinal oncology · 2025Article
- Cancer Cachexia.Advances in experimental medicine and biology · 2025Review
- Prognostication for recurrence patterns after curative resection for pancreatic ductal adenocarcinoma.Annals of hepato-biliary-pancreatic surgery · 2024Article
- Clinical and genomic characterization of pancreatic ductal adenocarcinoma patients with lung oligometastasis.ESMO gastrointestinal oncology · 2023Article
- Bromo- and Extra-Terminal Domain Inhibitors Induce Mitochondrial Stress in Pancreatic Ductal Adenocarcinoma.Molecular cancer therapeutics · 2023Article
- Do patients with metastatic pancreatic adenocarcinoma to the lung have improved survival?Cancer medicine · 2023Article
- Molecular Landscape and Prognostic Biomarker Analysis of Advanced Pancreatic Cancer and Predictors of Treatment Efficacy of AG Chemotherapy.Frontiers in oncology · 2022Article
- TGF-β Alters the Proportion of Infiltrating Immune Cells in a Pancreatic Ductal Adenocarcinoma.Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract · 2022Article
- Role of TGF-β in pancreatic ductal adenocarcinoma progression and PD-L1 expression.Cellular oncology (Dordrecht, Netherlands) · 2021Article
- TGF-β Inhibitors in Metastatic Pancreatic Ductal Adenocarcinoma.Journal of gastrointestinal cancer · 2019Review
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPancreatic ductal adenocarcinoma (PDAC) remains one of the deadliest malignancies with a rising incidence. Mutational analysis of PDAC has provided valuable information but has not yet dramatically changed the therapeutic landscape due to the number of variations detected in any one individual. The pattern of molecular alterations-gene mutations, variations in copy number, and changes in gene expression-has been described in the literature. The purpose of this study is to further investigate the molecular alterations in recurrent or metastatic PDAC based on the site of disease.
methodsMolecular alterations in patients with recurrent or metastatic PDAC from 2007 to 2015 were analyzed. The most common molecular alterations found in PDAC tumors from the pancreas were compared to metastatic PDAC specimens from the liver, lung, peritoneum, and other locations. Means were compared with a two-tailed Student's t test or ANOVA as appropriate. Rates of molecular alterations among the different groups were compared with Pearson's χ
resultsTwo thousand five hundred fifty-two patients with PDAC were identified in a retrospective database, and the 15 most common molecular alterations were utilized for analysis. The most common alterations among all patients were mutations in KRAS and PTEN (59 and 62%, respectively), with differences in prevalence by site of metastasis (p = 0.042 and p = 0.037, respectively). KRAS mutations were more commonly found in metastasis in the lung (72%) than in other sites (59%, p = 0.042). Low expression of ERCC1 was found in 49% of lung metastases from PDAC but only 15% in PDAC in the pancreas (p < 0.001). Five of the 8 molecular alterations significantly associated with site of metastatic disease were involved in DNA maintenance, repair, replication, or transcription (each p < 0.001).
conclusionsAberrant expression or mutation in genes involved in DNA maintenance is found in association with specific sites of metastatic PDAC. Personalizing therapy for metastatic PDAC based on site of disease and their associated molecular alterations warrants further investigation.
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