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Paper Information

Journal:   GENETICS IN THE 3RD MILLENNIUM   WINTER 2016 , Volume 13 , Number 4; Page(s) 4100 To 4105.
 
Paper: 

TGF-B AND TGF-BRII FLUCTUATION IN HLA-DR NEGATIVE AML PATIENTS

 
 
Author(s):  MOHAMMADI MOHAMMAD HOSSEIN, AMIRIZADEH NASER, ALLAHBAKHSHIAN FARSANI MEHDI, AGHAEE NEZHAD HAMIDEH, AHMADZADEH AHMAD, NAJAFI SAFA, AZARKEIVAN AZITA*
 
* PEDIATRIC HEMATOLOGIST AND ONCOLOGIST, FACULTY OF TRANSFUSION RESEARCH CENTER, HIGH INSTITUTE FOR RESEARCH AND EDUCATION IN TRANSFUSION MEDICINE, DEPARTMENT OF THALASSEMIA CLINIC. TEHRAN, IRAN
 
Abstract: 

Acute myeloblastic leukemia is the most frequent cancer in adults and the patients have a wide range of sub-classes. HLA DR negative cases represent one of the major immune-phenotypic classes. HLA-DR is routinely used to distinguish acute promyelocytic leukemia (APL) from other AML subclasses based on the immunophenotype. The TGF-b signaling pathway, as a critical regulator, guides different vital and sometimes opposite aspects of cell processes, including cell proliferation, apoptosis, differentiation quiescence, and malignancy expansion. A review of previous studies regarding the role of TGF-b in human malignancies made us interested in the evaluation of the role of the TGF signaling pathway in leukemia. We evaluated TGF-b / TGF-bRII fluctuant in “HLA-DR negative AML”, at expression level in bone marrow and peripheral blood samples. Forty-six patients were consecutively diagnosed with HLA-DR negative AML by flow cytometry, morphology, cytochemistry, and molecular analysis. By using Ficoll density centrifugation, mononuclear cells were isolated from the peripheral blood and bone marrow from both patients and controls, then, TGF-b, TGFbRII, and ABL1 genes were amplified by quantitative Real Time PCR. The results revealed that the TGF-b expression level was not different between patients and controls while TGF-b R was higher in patients than control cases, the expression of TGF-b and TGF-bRII was significantly lower in non M3-AML (M0, M1, M2) than M3-AML (APL) (P<0.05). We conclude that despite the conventional role of the TGF-b/TGF-bRII pathway to induce quiescence, anther role was defined for leukemic cells expansion in HLA-DR negative AML.
Currently we are studying this pathway to find the downstream target of leukemogenesis activity.

 
Keyword(s): HLA-DR NEGATIVE, LEUKEMIA, MYELOID, ACUTE, TRANSFORMING GROWTH FACTOR BETA, TGF-BRII
 
 
References: 
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Click to Cite.
APA: Copy

MOHAMMADI, M., & AMIRIZADEH, N., & ALLAHBAKHSHIAN FARSANI, M., & AGHAEE NEZHAD, H., & AHMADZADEH, A., & NAJAFI, S., & AZARKEIVAN, A. (2016). TGF-B AND TGF-BRII FLUCTUATION IN HLA-DR NEGATIVE AML PATIENTS. GENETICS IN THE 3RD MILLENNIUM, 13(4), 4100-4105. https://www.sid.ir/en/journal/ViewPaper.aspx?id=508648



Vancouver: Copy

MOHAMMADI MOHAMMAD HOSSEIN, AMIRIZADEH NASER, ALLAHBAKHSHIAN FARSANI MEHDI, AGHAEE NEZHAD HAMIDEH, AHMADZADEH AHMAD, NAJAFI SAFA, AZARKEIVAN AZITA. TGF-B AND TGF-BRII FLUCTUATION IN HLA-DR NEGATIVE AML PATIENTS. GENETICS IN THE 3RD MILLENNIUM. 2016 [cited 2021May08];13(4):4100-4105. Available from: https://www.sid.ir/en/journal/ViewPaper.aspx?id=508648



IEEE: Copy

MOHAMMADI, M., AMIRIZADEH, N., ALLAHBAKHSHIAN FARSANI, M., AGHAEE NEZHAD, H., AHMADZADEH, A., NAJAFI, S., AZARKEIVAN, A., 2016. TGF-B AND TGF-BRII FLUCTUATION IN HLA-DR NEGATIVE AML PATIENTS. GENETICS IN THE 3RD MILLENNIUM, [online] 13(4), pp.4100-4105. Available: https://www.sid.ir/en/journal/ViewPaper.aspx?id=508648.



 
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