ABSTRACT
OBJECTIVE@#To investigate the clinical characteristics, laboratorial and bone marrow pathological features of primary thrombocytopenia (ET) patients with different mutations of CALR, JAK2 and MPL genes.@*METHODS@#The chinical data of 120 cases of ET in Jiangsu provincial people's hospital/ The First Affiliated Hospital of Nanjing Medical University from January 2015 to December 2017 were collected and analyzed, including 76 cases with JAK2 gene mutation, 40 cases with CALR gene mutation, 2 cases with MPL gene mutations, 2 cases without gene mutation.@*RESULTS@#Among the ET patients, compared with the JAK2 gene mutation, CALR gene mutation showed statistically significant deareament of white blood cells and hemoglobin (P=0.001, P=0.01) and the male platelets in CALR group showed significant increament (P=0.04). Fourthermore, the average number of megakaryocytes and its cluster numbers in each hight power field of vision showed statistically significant decreament in CALR group as compared with JAK2 group (P=0.001, P=0.001), and thrombotic events in CALR group were signicantly lower than those in JAK2 group (7.5% vs 18.4%) (P=0.03).@*CONCLUSION@#Mutations of CALR, JAK2 have different clinical characteristics and blood pathological changes of Chinese ET patients, and their clinical significance is worth to explore.
Subject(s)
Humans , Male , Bone Marrow , Calreticulin , Genetics , China , Janus Kinase 2 , Genetics , Mutation , Receptors, Thrombopoietin , Genetics , Thrombocythemia, EssentialABSTRACT
Objective To explore the clinical characteristics,diagnosis and treatment of polycythemia vera(PV) transforming to acute myeloid leukemia(AML).Methods The clinical features and process of diagnosis and treatment in 4 cases of PV transforming to AML were analyzed.Results The case 1 had 10 years history of PV,after experiencing PV,had myelofibrosis and transformed to AML at the end stage of natural disease course;the case 2 had 7 years history of PV,orally took hydroxyurea(HU) treatment in recent 2 years and transformed to AML at present,his chromosome karyotype analysis showed 46,XY,del(7)(q31q36),del (18) (q22)[10],which was considered as treatment-related AML;the case 3 and 4 orally took H U for a long time after diagnosing HU,and respectively turned into AML during the pathologic polyemia stage after 6 and 7 years.Conclusion PV can be transformed to AML,the safety of HU in treatment should by paid attention to.
ABSTRACT
The purpose of this study was to investigate the effect of salidroside on human bone marrow mesenchymal stem cell (hBMMSC) apoptosis induced by cytarabine C (Ara-C) and its mechanism, hBMMSC were cultured in vitro and isolated by Fircoll density gradient centrifugation; cell surface antigens were measured by flow cytometry; the osteogenic and adipogenic differentiation of MSC was tested and evaluated by specific staining methods. The proliferation and apoptosis of cells exposed to Ara- C were detected by MTT and flow cytometry respectively. The experiments were divided into 4 groups: control group, Ara-C group, salidroside group and Ara-C+salidroside group. The mRNA expression of BCL-2 and BAX was assayed by RT-PCR. The results showed that the adherent cells displayed spindle and fibroblast cell-like shape; the hBMMSC expressed CD44, CD71 and HLA-ABC, not expressed CD34, CD45 and HLA-DR; the hBMMSC successfully differentiated into osteogenic and adipogenic lineages, which showed mineralization with von Kossa staining. Furthermore, liquid vacuoles were detected by oil red O staining; Ara- C exhibited a less inhibitory effect on the proliferation of hBMMSC treated with salidroside. The apoptosis of hBMMSC treated with salidroside were significantly higher as compared with control group (P < 0.05); RT-PCR results demonstrated that the BCL-2 expression was significantly down regulated but BAX mRNA expressions was up-regulated in Ara- C group as compared with those in the control group. Salidroside significantly inhibited the apoptosis of MSC and reversed the mRNA expression of BCL-2 and BAX. It is concluded that salidroside can inhibit the apoptosis of hBMMSC induced by Ara-C, its mechanism may be related with the regulation of BCL-2/BAX expression.