Interferon recovery CML Mechanism of adhesion defects.docVIP

 PAGE \* MERGEFORMAT 14 Interferon recovery CML Mechanism of adhesion defects Keywords:: chronic myeloid leukemia adhesion defects in interferon Chronic myeloid leukemia (cML) is a clonal proliferation of hematopoietic stem cell diseases, in order to mark their ph chromosome characteristics. Allogeneic hematopoietic stem cell transplantation (allo-HSCT) is the only cure cML means, subject to age and source of donor restrictions, only about 15% ~ 25% of patients have the opportunity to receive such treatment. Conventional chemotherapy such as busulfan, hydroxyurea, although the disease can control symptoms, but can not clear the ph + cells. From the early 80s to interferon (iFN) for the treatment of cML has affirmed iNF a variety of clinical observation of the efficacy of the treatment cML. iNF not only make the treatment of hematologic cML achieved complete remission (cHR), but also to achieve cytogenetic complete remission (cCR), can significantly prolong survival in patients with chronic phase and time [1 ~ 5], which is any kind of conventional chemotherapy drugs is difficult to achieve therapeutic effect. Therefore, iFN more and more blood, scientists attention. But people iFN how to play to selectively kill the tumor cells, the mechanism of normal hematopoiesis is unclear. The past 20 years, it is recognized that cML hematopoietic stem / progenitor cell adhesion defect in cML play an important role in the pathogenesis and thus iFN correct cML mechanism of adhesion defects has become more in-depth. Now on the iFN treatment cML resume cML the role of adhesion defects are reviewed. A hematopoietic stem / progenitor cells and bone marrow hematopoiesis in normal adhesion between the significance of Hematopoietic stem / progenitor cells and bone marrow stromal adhesion between the hematopoietic function in normal play an important role [6,7]. Hematopoietic stem / progenitor cell proliferation, differentiation, mature and orderly manner from the bone marrow ar