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SMAD4 and TGFβR2 expression in pancreatic ductal carcinoma. | LitMetric

AI Article Synopsis

  • Pancreatic ductal carcinoma is the most prevalent form of pancreatic cancer and the fourth leading cause of cancer-related deaths globally.
  • This study examines the expression levels of specific markers (SMAD4, TGFβR2, vimentin, and CD105) in 28 tumor samples, revealing changes in these markers in relation to tumor differentiation.
  • The findings suggest that these markers are involved in the epithelial-to-mesenchymal transition process, which could influence the clinical outcomes for patients.

Article 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.

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