tgf-b and tgf-brii fluctuation in hla-dr negative aml patients

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, tgf-brii, 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.