Myelodysplastic syndromes (MDS), are a heterogenic group of hematopoietic disorders caused by changes in pluripotent cells, common in the elderly, and a high rate of progression to acute myeloid leukemias (AML). These syndromes are characterized by ineffective hematopoiesis resulting in present dysplasia, impaired differentiation and peripheral blood cytopenias and result from multiple changes in the bone marrow stem cells that determine the differentiation deregulation and apoptosis of hematopoietic cells. There is no specific treatment for MDS, and the bone marrow transplantation corresponds to the unique alternative healing, but it is not applicable for most patients.. These syndromes have been described less than three decades and the molecular mechanisms involved in its pathogenesis have been elucidated only recently. In recent years a crescent interest has been given to the interaction of the progenitor cells with the stromal bone marrow, called hematopoietic niches. There are several indications that the curative treatment of diseases is correlated with interaction and mobilization of the quiescent cells. Microarray results of our research group have identified two particular interesting genes that could be involved in the physiopathology of MDS: Hematopoietic cell kinase genes (HCK) and serine peptidase inhibitor, Kunitz type 2 (SPINT2), which are relate to changes in tumor environment of different cancer and the hematopoiesis regulation. The HCK, whose expression is specific for hematopoietic cells, showed increased expression in CD34+ cells from patients with MDS and possibly participates in transduction processes signaling related to the self-renewal, differentiation dysfunction and increased apoptosis in the hematopoietic MDS cells. The SPINT2, is an inhibitor of HGF production, and an inducer of SDF-1 secretion, which is related to angiogenesis and apoptosis in MDS. This gene is related to solid invasive tumors and was hipoexpressed in stromal cells of patients with MDS. Given the absence of data in the literature, this study aims to investigate the function of HCK and SPINT2 in the biology of Myelodysplastic Syndromes and Acute Myeloid Leukemia.
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