ArticleBMC cancer2019
SMAD4 Y353C promotes the progression of PDAC.
Article in BMC cancer, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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Who cites it
19 citing papers in PubMed, 23 citations in OpenAlex.
- Unexpected Long-Term Survival in Resected Pancreatic Ductal Adenocarcinoma Harboring KRAS G12R with an Ultra-Low-VAF SMAD4 Mutation: A Case Report and Mini-Review.Reports (MDPI) · 2026Article
- An integrative mutational and network analysis of pancreatic cancer reveals key genes, and signalling pathways.Functional & integrative genomics · 2026Article
- Targeting Triple NK Cell Suppression Mechanisms: A Comprehensive Review of Biomarkers in Pancreatic Cancer Therapy.International journal of molecular sciences · 2025Review
- Significance of TP53, CDKN2A, SMAD4 and KRAS in Pancreatic Cancer.Current issues in molecular biology · 2024Review
- The Epstein-Barr virus-miRNA-BART6-5p regulates TGF-β/SMAD4 pathway to induce glycolysis and enhance proliferation and metastasis of gastric cancer cells.Oncology research · 2024Article
- Histone Modifications Represent a Key Epigenetic Feature of Epithelial-to-Mesenchyme Transition in Pancreatic Cancer.International journal of molecular sciences · 2023Review
- Juvenile polyposis diagnosed with an integrated histological, immunohistochemical and molecular approach identifying new SMAD4 pathogenic variants.Familial cancer · 2022Article
- An EGFR/HER2-targeted conjugate sensitizes gemcitabine-sensitive and resistant pancreatic cancer through different SMAD4-mediated mechanisms.Nature communications · 2022Article
- Proscillaridin A induces mitochondrial damage and autophagy in pancreatic cancer and reduces the stability of SMAD4 in Panc-1 cells.Annals of translational medicine · 2022Article
- Smad4 Deficiency Promotes Pancreatic Cancer Immunogenicity by Activating the Cancer-Autonomous DNA-Sensing Signaling Axis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- The Role ofCancers · 2022Review
- TGFβ Signaling in the Pancreatic Tumor Microenvironment.Cancers · 2021Review
- Article
- Transcript annotation tool (TransAT): an R package for retrieving annotations for transcript-specific genetic variants.BMC bioinformatics · 2021Article
- Diagnostic, Predictive and Prognostic Molecular Biomarkers in Pancreatic Cancer: An Overview for Clinicians.Cancers · 2021Review
- Upregulated MicroRNA-483-3p is an Early Event in Pancreatic Ductal Adenocarcinoma (PDAC) and as a Powerful Liquid Biopsy Biomarker in PDAC.OncoTargets and therapy · 2021Article
- Mutational drivers of cancer cell migration and invasion.British journal of cancer · 2021Review
- SMAD4 and the TGFβ Pathway in Patients with Pancreatic Ductal Adenocarcinoma.International journal of molecular sciences · 2020Review
- Tumor-Infiltrating Immune Cell Signature Predicts the Prognosis and Chemosensitivity of Patients With Pancreatic Ductal Adenocarcinoma.Frontiers in oncology · 2020Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundSMAD4 is frequently inactivated and associated with a poor prognosis in pancreatic ductal adenocarcinoma (PDAC). Abnormal SMAD4 expression also plays an important role in the malignant progression of PDAC.
methodsWe investigated SMAD4 status in PDAC by immunohistochemical methods to explore the relationships between SMAD4 expression and clinicopathological features and then detected SMAD4 mutations by Sanger sequencing in 95 patients with PDAC to identify new mutation sites in PDAC. We further evaluated the effects of a missense mutation, Y353C, in the SMAD4 MH2 domain, on cell proliferation and migration in vitro.
resultsImmunohistochemistry showed that the expression of SMAD4 in PDAC carcinoma tissue was significantly lower than that in normal pancreatic tissue, and negative SMAD4 expression was closely related to tumour diameter, staging, lymph node metastasis and differentiation. Sanger sequencing analysis showed that the rate of SMAD4 mutation was 11.8% in 85 PDAC cases, and the novel SMAD4 Y353C missense mutation identified in this study promoted cell migration and invasion without affecting cell proliferation in vitro. Furthermore, SMAD4 Y353C resulted in reduced expression of E-cadherin and increased expression of Vimentin compared with wild-type SMAD4 overexpression.
conclusionThis study supports the key role of SMAD4 as a tumour suppressor gene in PDAC and shows that SMAD4 Y353C is associated with poor progression of PDAC.
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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.