ArticleMolecular biology reports2020
Pancreatic ductal adenocarcinomas from Mexican patients present a distinct genomic mutational pattern.
Article in Molecular biology reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 6 citations in OpenAlex.
- A Pilot Study: Contrasting Genomic Profiles of Lung Adenocarcinoma Between Patients of European and Latin American Ancestry.International journal of molecular sciences · 2025Article
- Cancer genomics and bioinformatics in Latin American countries: applications, challenges, and perspectives.Frontiers in oncology · 2025Review
- Subtype-WGME enables whole-genome-wide multi-omics cancer subtyping.Cell reports methods · 2024Article
- The high expression of FOXE1 in colorectal cancer predicts a promising prognosis: a retrospective study.Clinical and experimental medicine · 2023Article
- The Role of lncRNAs in the Stem Phenotype of Pancreatic Ductal Adenocarcinoma.International journal of molecular sciences · 2021Review
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Pancreatic ductal adenocarcinoma (PDAC) is one of the deadliest cancers in humans, with less than 5% 5-year survival rate. PDAC is characterized by a small number of recurrent mutations, including KRAS, CDKN2A, TP53, and SMAD4 and a long "tail" of infrequent mutated genes. Most of the studies have been performed in US and European populations, so new studies are needed to describe the mutational landscape of these tumors in other cohorts. The present study analyzed the exome and transcriptome of four PDAC tumors from Mexican patients. We found a paucity of the previously described recurrent mutations, with mutations in only three genes (HERC2, CNTNAP2 and HMCN1) previously reported in PDAC with a frequency > 1%. In addition, we discovered several recurrent putative copy number aberrations in SKP2, BRAF, CSSF1R, FOXE1, JAK2 and MET genes and in genes previously reported as putative drivers in PDAC, including KRAS, SF3B1, BRAF, MYC and MET. Although a larger cohort is needed to validate these findings, our results could be pointing toward potential differences in contributing factors for PDAC in Latin-American populations.
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