The Influence Of JAK2 Expression In Patients With MDS Caused By Decitabine And Its Clinical Significance

ObjectiveMyelodysplastic syndromes(MDS) is a group of disease in pluripotent hematopoietic stem cell stage heterogeneity and cloning, which can turn to acute leukemia because of genetic instability. Recently more and more reports show that JAK2 gene may be involved in the pathogenesis of MDS and its malignant transformation, and it is one of the signaling pathways by which MDS-RA changes to high risk MDS-RAEB and then to the AL. JAK normal expression depends on the normal methylation. To consider decitabine as the representative for competitive nucleotide methyltransferase inhibitors, has been widely used to reverse the abnormal methylation of tumor cells, it is the first drug used to treat MDS of epigenetics demethylation approved by FDA. So whether JAK2 gene can be used as a positive molecular markers of MDS curative effect caused by decitabine? This research will get the answer by studying the expression of JAK2 gene caused by decitabine, in order to provide help for clinical treatment. MethodsThis research review 22 patients diagnosed with myelodysplastic syndrome from November 2012 to November 2013,including outpatient and hospitalized patients. All the patients were classified with the 2001 WHO classification standards, including 12 cases of RA type and 10 cases of RAEB. 20 cases of normal control group are healthy ones. 10 patients with MDS-RAEB type were given decitabine(20 mg/m2 / d x 5 d) single-agent chemotherapy for at least four cycles. WE get 2-3 ml peripheral blood and put them into EDTA anticoagulant tubes, and then store them in a environment of 4-25 ℃, finish the inspection in 48 hours. FQ- PCR method is applied to monitor the peripheral blood JAK2-V617 F real-time quantitative PCR copy number of general population, patients with MDS- RAEB before treatment, patients with MDS-RAEB after 2 cycles of chemotherapy of decitabine,patients with MDS-RAEB after 4 cycles of chemotherapy of decitabine.Obs- erve whether there are significant differences, and then research the effects of JAK2-V617 F gene expression caused by decitabine in patients with MDS from the level of molecular biology. ResultsThe peripheral blood JAK2-V617 F gene real time quantitative PCR copy number of patients with MDS-RAEB reduced from 22545.98±11084.87 to 14654.88±7205.16 after 2 cycles of chemotherapy by decitabine single-agent chemotherapy.The two groups before and after treatment comparison difference was statistically significant(P < 0.0 l). The peripheral blood JAK2-V617 F gene real time quantitative PCR copy number reduced from 14654.88±7205.16 to 9469.31±4655.64 after two more cycles of chemotherapy by decitab- ine single-agent chemotherapy.The comparison difference was statistically significant(P < 0.0 l). Conclusions1.JAK2-V617 F involved in the pathogenesis of MDS and its malignant transformation,JAK2 may be one of the signal pathes that low-risk MDS cells transfrom to high-risk type.2. Decitabine can reduce JAK2 V617 F gene expression significantly in patients with MDS RAEB.3. The longer decitabine chemotherapy cycle can further reduce the JAK2-V617 F expression of peripheral blood.