International Journal of Medical Laboratory
Shahid Sadoughi University of Medical Sciences
Thu, Apr 23, 2026
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Sedigheh Ekraminasab * 
, Mehdi Allahbakhshian Farsani , Mohsen Hamidpour , Hamideh Aghaee Nezhad , Amirmohammad Azizzadeh
, Mehdi Allahbakhshian Farsani , Mohsen Hamidpour , Hamideh Aghaee Nezhad , Amirmohammad Azizzadeh
Department of Hematology and Blood Banking, School of Allied Medical Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran
Abstract: (85 Views)
Introduction: Acute lymphoblastic leukemia (ALL) is an aggressive hematologic malignancy characterized by the clonal expansion of immature lymphoid blasts in the bone marrow, affecting both children and adults. The transforming growth factor-β/ Smad signaling pathway, a critical tumor-suppressor pathway, is frequently dysregulated in various cancers. This study aimed to investigate the expression levels of Smad3 and Smad7 in ALL patients to assess potential dysregulation.
Materials and Methods: We analyzed bone marrow and peripheral blood samples from 52 newly diagnosed ALL patients (including 20 pediatrics and 32 adults) and 15 healthy controls. Samples were assessed for morphology, immunocytochemistry, immunophenotyping, and molecular markers. Reverse transcription quantitative real-time polymerase chain reaction was used to evaluate Smad3 and Smad7 expression levels.
Results: Compared to the control group, ALL leukemia patients exhibited a statistically significant downregulation of Smad3 and upregulation of Smad7. The oncogenic role of Smad7 was more prominent in specific subtypes, with its expression being significantly higher in pediatric ALL compared to adult ALL, and in B-ALL compared to T-ALL.
Conclusions: Our findings suggest that decreased Smad3 (a key receptor-regulated Smad) and elevated Smad7 (an inhibitory Smad) may contribute to transforming growth factor-β pathway resistance, potentially playing a role in ALL pathogenesis. This study highlights the involvement of Smad dysregulation in patients with ALL, offering insights into molecular mechanisms and potential therapeutic targets. Further research is warranted to validate these findings and explore clinical applications.
Materials and Methods: We analyzed bone marrow and peripheral blood samples from 52 newly diagnosed ALL patients (including 20 pediatrics and 32 adults) and 15 healthy controls. Samples were assessed for morphology, immunocytochemistry, immunophenotyping, and molecular markers. Reverse transcription quantitative real-time polymerase chain reaction was used to evaluate Smad3 and Smad7 expression levels.
Results: Compared to the control group, ALL leukemia patients exhibited a statistically significant downregulation of Smad3 and upregulation of Smad7. The oncogenic role of Smad7 was more prominent in specific subtypes, with its expression being significantly higher in pediatric ALL compared to adult ALL, and in B-ALL compared to T-ALL.
Conclusions: Our findings suggest that decreased Smad3 (a key receptor-regulated Smad) and elevated Smad7 (an inhibitory Smad) may contribute to transforming growth factor-β pathway resistance, potentially playing a role in ALL pathogenesis. This study highlights the involvement of Smad dysregulation in patients with ALL, offering insights into molecular mechanisms and potential therapeutic targets. Further research is warranted to validate these findings and explore clinical applications.
Keywords: Acute lymphoblastic leukemia, Gene expression, Pediatric leukemia, SMAD3, SMAD7, Transforming growth factor beta
Type of Study: Research |
Subject:
Hematology & Blood Banking
Received: 2025/10/22 | Accepted: 2026/02/10
Received: 2025/10/22 | Accepted: 2026/02/10
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