ArticleOncogene2017
TGFβ promotes mesenchymal phenotype of pancreatic cancer cells, in part, through epigenetic activation of VAV1.
Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
20 citing papers in PubMed, 33 citations in OpenAlex.
- The Role of Epigenetic Mechanisms in the Treatment of GI Cancers.Current cancer drug targets · 2025Review
- Smad4 restricts injury-provoked biliary proliferation and carcinogenesis.Disease models & mechanisms · 2024Article
- Epigenetic priming targets tumor heterogeneity to shift transcriptomic phenotype of pancreatic ductal adenocarcinoma towards a Vitamin D susceptible state.Cell death & disease · 2024Article
- Review
- Vav1 Promotes B-Cell Lymphoma Development.Cells · 2022Article
- A new era: tumor microenvironment in chemoresistance of pancreatic cancer.Journal of cancer science and clinical therapeutics · 2022Article
- Identification of prognostic alternative splicing events in sarcoma.Scientific reports · 2021Article
- Vav1 Sustains the In Vitro Differentiation of Normal and Tumor Precursors to Insulin Producing Cells Induced by all-Trans Retinoic Acid (ATRA).Stem cell reviews and reports · 2021Article
- Comparative genomic analysis of head and body/tail of pancreatic ductal adenocarcinoma at early and late stages.Journal of cellular and molecular medicine · 2021Article
- Vav1 Down-Modulates Akt2 Expression in Cells from Pancreatic Ductal Adenocarcinoma: Nuclear Vav1 as a Potential Regulator of Akt Related Malignancy in Pancreatic Cancer.Biomedicines · 2020Article
- Epigenetic silencing of AATK in acinar to ductal metaplasia in murine model of pancreatic cancer.Clinical epigenetics · 2020Article
- Vav1 and mutant K-Ras synergize in the early development of pancreatic ductal adenocarcinoma in mice.Life science alliance · 2020Article
- A New Fusion Peptide Targeting Pancreatic Cancer and Inhibiting Tumor Growth.OncoTargets and therapy · 2020Article
- Vav1 mutations identified in human cancers give rise to different oncogenic phenotypes.Oncogenesis · 2018Article
- Review
- Article
- miR-3656 expression enhances the chemosensitivity of pancreatic cancer to gemcitabine through modulation of the RHOF/EMT axis.Cell death & disease · 2017Article
- Alterations of Epigenetic Regulators in Pancreatic Cancer and Their Clinical Implications.International journal of molecular sciences · 2016Review
- Suppression of Tumor Growth and Muscle Wasting in a Transgenic Mouse Model of Pancreatic Cancer by the Novel Histone Deacetylase Inhibitor AR-42.Neoplasia (New York, N.Y.) · 2016Article
- Pancreatic Cancer, A Mis-interpreter of the Epigenetic Language.The Yale journal of biology and medicine · 2016Review
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The highly homeostasis-resistant nature of cancer cells leads to their escape from treatment and to liver metastasis, which in turn makes pancreatic ductal adenocarcinoma (PDAC) difficult to treat, especially the squamous/epithelial-to-mesenchymal transition (EMT)-like subtype. As the molecular mechanisms underlying tumour heterogeneity remain elusive, we investigated whether epigenetic regulation might explain inter-individual differences in the progression of specific subtypes. DNA methylation profiling performed on cancer tissues prior to chemo/radiotherapy identified one hypermethylated CpG site (CpG6882469) in the VAV1 gene body that was correlated with demethylation of two promoter CpGs (CpG6772370/CpG6772811) in both PDAC and peripheral blood. Transforming growth factor β treatment induced gene-body hypermethylation, dissociation of DNMT1 from the promoter, and VAV1 expression via SMAD4 and mutant Kras
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.