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Myelodysplastic syndrome Mechanism of
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Myelodysplastic syndrome Mechanism of
Keywords: Myelodysplastic syndromes
Myelodysplastic syndrome (Myelodysplastic Syndromes, MDS) is a group originated in hematopoietic stem / progenitor cells acquired clonal disease, to proliferation is characterized by abnormal and ineffective hematopoiesis. Characterized by the performance of the peripheral blood for more than one department or a series of cells decreased, bone marrow hyperplasia of hyperthyroidism, and has morphological abnormalities, including pathological erythroid, granulocyte, or pathological pathological thrombopoietin. MDS is a multi-gene, multi-stage involving the pathological process, stem cell genetic abnormalities, hematopoietic micro-environment changes and defects in the pathogenesis of immune mechanisms play an important role in both. With the MDS carried out in recent years, a more extensive and in-depth study found that MDS disease process, an increasing number of genetic abnormalities play a different role in the pathogenesis. The pathogenesis of MDS constant awareness of new treatment programs provide the basis. The pathogenesis of MDS will now be the new progress summarized as follows:
A stem cell gene abnormalities
Existence of proto-oncogene mutations in MDS bone marrow in vitro cytogenetic abnormalities as well as the variation of both tips are clonal disorders of this disease in recent years, along with in-depth research, more and more genetic abnormalities have been discovered.
1.1 The growth-regulating genes
Ras gene (ras genes) family and its signal transduction role in tumorigenesis has been confirmed, Ha Thanh Nishino et al [1] studies have shown that in MDS in 10% ~ 40% is ras gene point mutation, ras gene mutation rates vary by the type of MDS, with chronic bone marrow mononuclear cell leukemia (Chronic Myelomonocytic Leukemia, CMML) the mutation rate is highest. ras gene mutation and the prognosis is closely relat
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