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Updated: May 15, 2026

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Published on: October 27, 2020
Transforming growth factor β repressor, SnoN, is overexpressed in human gastrointestinal stromal tumors
V Bravou1, P Papanastasopoulos, D Verras
1Department of Pathology, General Hospital of Patras, Agios Andreas, Patras, Greece. vibra@upatras.gr
Purpose:
The transforming growth factor bgr; (TGF-β)/ Smad pathway is implicated in the development of interstitial cells of Cajal. The aim of this study was to examine the role of this pathway in human gastrointestinal stromal tumors (GISTs).
Methods:
The expression of TGF-β receptor II (TβRII), phosphorylated Smad2 (p-Smad2), SnoN, p21(WAF17sol;CIP1) and p27(KIP1) was examined by immunohistochemistry in 30 hu-man GISTs in relation to prognostic factors.
Results:
TβRII was expressed in 76.9% of the cases. All cases were positive for p-Smad2 and SnoN, with significantly higher expression levels in small intestinal compared to gastric GISTs. Downregulation of p21(WAF1/CIP1) and p27(KIP1) was found in 78.6% and 46.4% of the cases respectively, while cytoplasmic expression of p27(KIP1) was also noted in 50% of GISTs.
Conclusions:
TGF-β/Smad pathway may contribute to GIST pathogenesis. SnoN overexpression and low levels of p21(WAF1)/CIP1 and p27(KIP1) may be of importance in GISTs.
Insights
The transforming growth factor-beta (TGF-β)/Smad pathway is involved in gastrointestinal stromal tumors (GISTs). SnoN overexpression and reduced p21/p27 expression may play a role in GIST development.
Area of Science:
- Oncology
- Molecular Biology
- Gastroenterology
Background:
- The transforming growth factor-beta (TGF-β)/Smad pathway is crucial for interstitial cells of Cajal development.
- Understanding this pathway's role in human gastrointestinal stromal tumors (GISTs) is essential.
Purpose of the Study:
- To investigate the involvement of the TGF-β/Smad pathway in the pathogenesis of human GISTs.
- To correlate pathway component expression with GIST prognostic factors.
Main Methods:
- Immunohistochemistry was used to assess the expression of TGF-β receptor II (TβRII), phosphorylated Smad2 (p-Smad2), SnoN, p21(WAF1/CIP1), and p27(KIP1).
- Analysis was performed on 30 human GIST samples.
Main Results:
- TβRII expression was observed in 76.9% of GISTs.
- All GISTs showed positive expression for p-Smad2 and SnoN, with higher levels in small intestinal GISTs compared to gastric ones.
- Downregulation of p21(WAF1/CIP1) and p27(KIP1) was noted in 78.6% and 46.4% of cases, respectively, with 50% exhibiting cytoplasmic p27(KIP1).
Conclusions:
- The TGF-β/Smad pathway may contribute to GIST pathogenesis.
- SnoN overexpression and decreased p21(WAF1/CIP1) and p27(KIP1) levels are potentially significant in GISTs.
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