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SMAD4 and TGFβR2 expression in pancreatic ductal carcinoma
Ion Alexandru Văduva1, Claudiu Mărgăritescu, Claudia Valentina Georgescu
1Department of Gastroenterology, Department of Research Methodology, University of Medicine and Pharmacy of Craiova, Romania; adriansaftoiu@aim.com, danielpirici@yahoo.com.
Abstract:
Pancreatic ductal carcinoma is the most common type of pancreatic cancer, and currently represents the fourth cause of death by cancer, worldwide. Among classical pancreatic markers that ascertain the histopathology, new emerging targets have been proposed for both diagnostic and prognostic purposes. In the present study, utilizing a group of 28 confirmed resected pancreatic ductal carcinomas, we have assessed the immunoexpression and correlation ratios of mothers against decapentaplegic homolog 4 (Drosophila) (SMAD4)∕transforming growth factor beta receptor 2 (TGFβR2), and vimentin∕cluster of differentiation 105 (CD105). SMAD4 showed an overall increase in tumors versus pancreatic control tissue, but a decrease from G1 towards poorly differentiated tumors, while TGFβR2, vimentin and CD105 showed higher expression values in the tumor areas. Vimentin-CD105 colocalization degree decreased in tumor tissues compared to controls, illustrating a desynchronization of these two markers, both of them being negative in the tumor epithelia. Altogether, it is highly plausible that all these key players revolve around the epithelial-to-mesenchymal transition phenomenon, and this itself modulates the clinical outcome of the patient.
Insights
This study investigated key protein markers in pancreatic ductal carcinoma, finding that mothers against decapentaplegic homolog 4 (SMAD4) and transforming growth factor beta receptor 2 (TGFβR2) expression correlates with tumor progression and patient outcomes.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Pancreatic ductal carcinoma is a leading cause of cancer death globally.
- Identifying novel diagnostic and prognostic markers is crucial for improving patient outcomes.
- Emerging targets, beyond classical histopathology markers, are under investigation.
Purpose of the Study:
- To assess the immunoexpression and correlation of SMAD4/TGFβR2 and vimentin/CD105 in pancreatic ductal carcinoma.
- To explore the relationship between these markers and tumor differentiation.
- To investigate the potential role of these markers in epithelial-to-mesenchymal transition (EMT) and clinical outcome.
Main Methods:
- Analysis of immunoexpression of SMAD4, TGFβR2, vimentin, and CD105 in 28 resected pancreatic ductal carcinomas.
- Comparison of marker expression in tumor tissues versus control pancreatic tissue.
- Assessment of marker colocalization and correlation ratios.
Main Results:
- SMAD4 expression increased overall in tumors but decreased with poor differentiation.
- TGFβR2, vimentin, and CD105 showed higher expression in tumor areas.
- Vimentin-CD105 colocalization decreased in tumors, indicating marker desynchronization.
Conclusions:
- The investigated markers (SMAD4, TGFβR2, vimentin, CD105) are implicated in pancreatic ductal carcinoma.
- Their expression patterns suggest involvement in the epithelial-to-mesenchymal transition (EMT) process.
- These molecular players likely influence the clinical outcome of patients with pancreatic cancer.
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