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1.
Article in Chinese | WPRIM | ID: wpr-771897

ABSTRACT

OBJECTIVE@#To investigate the predictive value of CD45CD117 phenotype-abnormal cells (hereinafter referred to as "abnormal cells") for relapse and prognosis in adult patients with acute myeloid leukemia (AML) within 2 weeks after the first complete remission (CR1).@*METHODS@#The clinical data of patients with newly diagnosed AML (non-acute promyelocytic leukemia) admitted in our department from July 1, 2014 to June 30, 2017 were analyzed retrospectively, and the relationship between clinical features at the initial diagnosis and the abnormal phenotype cells of CD45CD117 within 2 weeks after CR1 with the prognosis were analyzed.@*RESULTS@#A total of 91 patients with CD45CD117 abnormal cells were detected. The median age was 51 years old, the median WBC count was 11.60×109/L, and the median ratio of bone marrow blast cells was 0.35 at initial diagnosis. According to the FAB classification, 1 (1.1%), 7 (7.7%), 38 (41.7%), 20 (22.0%), 21 (23.1%) and 4 (4.4%) patients were classifice as M0, M1, M2, M4, M5, and M6, respectively. According to the NCCN risk stratification, 30 (33.0%), 51 (56.0%), and 10 (11.0%) patients were determined as good, moderate, and poor prognosis, respectively. The median ratio of abnormal cells within 2 weeks after CR1 was 1.8500 (0.0236-8.0000)%. The median time from initiation of induction therapy to the acquisition of CR was 46 days, median recurrence-free survival time was 319 days, and median overall survival time was 352 days. A total of 45 patients relapsed, of which 14 died; 46 patients did not relapse, of which 3 died. The cutoff of abnormal cells by receiver operating characteristic curve (ROC) analysis was 2.055% (Se=0.733,Sp=0.761). The abnormal cell ratio was>2.055% in 44 patients, the median ratio of abnormal cells was 3.075%, among which 33 patients relapsed and 12 patients died; the abnormal cell ratio was <2.055% in 47 patients, the median ratio of abnormal cells was 1.150%, 12 patients relapsed and 5 patients died. Regression analysis showed that WBC count>50×10/L and abnormal cell ratio>2.055% were independent risk factors for recurrence. The abnormal cell ratio>2.055% group had a 2-year RFS rate of 54.3% and a 2-year OS rate of 52.8%. The abnormal cell ratio<2.055% group had a 2-year RFS rate of 86.6% (P=0.018), and a 2-year OS rate of 85.3% (P<0.05).@*CONCLUSION@#For adult AML patients, CD45CD117 phenotypical abnormal cells ratio>2.055% within 2 weeks after CR1 is an independent risk factor for recurrence, which also is an dverse factor for RFS and OS.


Subject(s)
Humans , Leukemia, Myeloid, Acute , Leukocyte Common Antigens , Leukocyte Count , Middle Aged , Prognosis , Proto-Oncogene Proteins c-kit , Remission Induction , Retrospective Studies
2.
Article in Chinese | WPRIM | ID: wpr-771896

ABSTRACT

OBJECTIVE@#To investigate the effect of stably down-regulating the FMI expression of K562 cells on the sensitivity of K562 cells to Imatinib (IM) and its possible mechanism.@*METHODS@#Western-blot was used to detect the expression of FMI protein in K562 cells and peripheral blood mononuclear cells from the patients with chronic myelogenous leukemia, chronic myeloid blast crisis and healthy volunteers. The specific interference sequences targeting at the human FMI gene were designed and ligated into the lentiviral vector LV3; the three plasmid system-packaged lentivirus particles were used to transfect K562 cells to screen K562 cells that stably down-regulated FMI. CCK-8 assay and flow cytometry were used to determine effect of IM on cell proliferation and apoptosis. The transcription level of FMI and Fz8 in leukemia cells was detected by fluorescent quantitative PCR. The protein expression levels of FMI, Fz8, NFAT1, BCR-ABL and β-catenin in leukemia cells were detected by Western-blot.@*RESULTS@#The expression of FMI protein could be detected in peripheral blood mononuclear cells of the patients with CML-BC and K562 cells, the FMI expression could not be detected in all the patients with CML-CP and healthy volunteers. The recombinant lentiviral vector LV3/FMI had been successfully constructed the lentivirus was packaged, and the K562 cells stably down-regulating the FMI protein were screened. After stable down-regulation of FMI expression in K562 cells, the proliferation rate of leukemia cells decreased and the apoptosis rate was increased under the same drug concentration. Both the transcription and protein expression levels of Fz8 decreased. The NFAT1 total protein level increased, as well as the nuclear translocation of protein was enhanced. There was no significant change in the expression level of BCR-ABL fusion protein. The expression level of β-catenin protein decreased.@*CONCLUSION@#After the stable down-regulation of FMI expression, the sensitivity of K562 cells to IM and apoptosis of cells increase, which are performed possibly by inhibiting the FMI-Fz8 signaling pathway and activating the Ca-NFAT and Wnt/β-catenin signaling pathway.


Subject(s)
Apoptosis , Drug Resistance, Neoplasm , Fusion Proteins, bcr-abl , Humans , Imatinib Mesylate , K562 Cells , Leukemia, Myelogenous, Chronic, BCR-ABL Positive , Leukocytes, Mononuclear
3.
Article in Chinese | WPRIM | ID: wpr-771895

ABSTRACT

OBJECTIVE@#To explore the role of Ca-NFAT signaling pathway in Ph-ALL drug resistance mediated by bone marrow stromal cells.@*METHODS@#The transcription level of NFAT mRNA in Sup-B15 cells and Ph ALL primary cells was detected by polymerase chain reaction. The expression of P-glycoprotein in Sup-B15 cells was detected by flow cytometry. The change of NFAT protein in Sup-B15 cells was detected by Western blot. AnnexinV/7-AAD was used to label cells. Flow cytometry was used to detect cell apoptosis; Fluo 3-AM dye was used to label cells, and flow cytometry used to detect changes of Ca concentration in leukemia cells.@*RESULTS@#NFAT expression could be detected in both Sup-B15 and Ph ALL primary cells; P-glycoprotein could not be detected by flow cytometry; CAS could significantly inhibit NFAT protein expression in clinically applied drug concentrations (2.5, 5 μmol/L); Clinically applied concentration of CAS (2.5, 5 μmol / L) has no significant effect on the apoptosis of Sup-B15 cells, while higher concentration of CAS (10 μmol / L) could induce apoptosis of Sup-B15 cells. Bone marrow stromal cells OP9 could, decrease the sensitivity of Sup-B15 cells and Ph ALL primary cells to imatinib (IM); After co-culture with bone were marrow stromal cells, the Ca concentration in Sup-B15 cells was enhanced, the levels of NFAT protein and nullear protein in sup-B15 cells also were enhanced. The addition of CAS in co-culture system could inlibit the Ca-NFAT signaling pathway, reduce the protective effect of OP9 on Sup-B15 cells.Conclution:The Ca-NFAT sigualing pathway, contributes to the survival of Ph ALL cells. Bone marrow stromal cells can mediate the resistance of Ph ALL cells to IM by activating Ca-NFAT signaling pathway.


Subject(s)
Bone Marrow Cells , Cell Line, Tumor , Humans , Imatinib Mesylate , Mesenchymal Stem Cells , NFATC Transcription Factors , Precursor Cell Lymphoblastic Leukemia-Lymphoma , Signal Transduction
4.
Journal of Experimental Hematology ; (6): 1174-1179, 2018.
Article in Chinese | WPRIM | ID: wpr-689510

ABSTRACT

<p><b>OBJECTIVE</b>To analyze the risk factors and prognosis of hepatic chronic GVHD after allogeneic hematopoietic stem cell transplantation (allo-HSCT).</p><p><b>METHODS</b>The clinical data of 147 patients undergoing allo-HSCT from January 2013 to December 2016 were analyzed, the correlation between recipient age and sex, disease state, matched degree of HLA, donor sex, stem cell sources, ATG in GVHD prophylaxis, liver dysfunction during conditioning period, pre-transplant HBsAg, prior aGVHD and hepatic cGVHD were studied, and the correlation between hepatic cGVHD and prognosis were analysed.</p><p><b>RESULTS</b>Thirty-two patients had hepatic cGVHD, cumulative incidence of 26.4%. In univariate analysis, pre-transplant HBsAgand liver dysfunction during conditioning period were not significantly related with hepatic cGVHD (P>0.05). In multivariate analysis, prior acute GVHD (HR=2.087, P=0.045) was the independent risk factor for hepatic cGVHD, ATG (HR=0.231, P=0.000) was significantly related with a lower incidence of hepatic cGVHD. In univariate analysis, patients with hepatic cGVHD had a lower 2 years relapse rate (P=0.038).</p><p><b>CONCLUSION</b>Prior acute GVHD is the independent risk factor for hepatic cGVHD, the ATG can significantly reduce the incidence of hepatic cGVHD. Hepatic cGVHD has been found to relate with a lower 2 years relapse rate.</p>


Subject(s)
Graft vs Host Disease , Hematopoietic Stem Cell Transplantation , Humans , Prognosis , Retrospective Studies , Risk Factors , Transplantation Conditioning
5.
Journal of Experimental Hematology ; (6): 1281-1287, 2018.
Article in Chinese | WPRIM | ID: wpr-689490

ABSTRACT

@#<p><b>OBJECTIVE</b>To evaluate the long-term prognosis of CML patients whose BCR-ABL transcript level was warning and best response at 12 months of treatment with tyrosine kinase inhititor (TKI), and to investigate the factors affecting therapeutic efficacy and prognosis.</p><p><b>METHODS</b>The clinical data of patients with newly diagnosed CML were analyzed retrospectively. According to BCR-ABL transcript level, the 80 patients were divided into group A and group B, the patients with BCR-ABL >0.1% and ≤ 1% (warning response) were entolled in group A, and the patients with BCR-ABL ≤ 0.1% (best response) were enrolled in group B as control. The ratio of patients with main molecular response (MMR) and deep molecular response (DMR), as well as aquistation rate and cummulative rate of MR (DMR) at specified fine points in 2 groups were compared, the independent risk factors affecting the therapeutic efficacy and prognosis were analyzed.</p><p><b>RESULTS</b>The MMR and MR of the B group at 15, 18 and 24 months after TKI treatment were significantly higher than those of the A group, and the patients in the B group reached MR faster. In the 3 months, 6 months and 12 months after the demarcation point (TKI 12 months), the A group was much less easy to obtain MR (P<0.05) than the B group. Through survival analysis, there were more patients in the B group than the A group at different time points to reach MR, and the difference was statistically significant (P<0.01). The single factor analysis showed that the splenomegaly (below rib edge)> 10cm (P<0.01) and lactate dehydrogenase > 400 U/L (P<0.05) were the long-term warning factors for patients. Multivariate analysis showed that the size of the spleen was an independent factor (P<0.01) to affect the prognosis of the patients who had been warned for 12 months.</p><p><b>CONCLUSION</b>Patients at 12 months warning effect are slower and less easier to get DMR, which has a poor long-term prognosis. The size of the spleen in the patient at warning for 12 months of treatment effect can predict the relatively poor long-term prognosis. For a patient with a 12 months response to the warning, an early replacement therapy is available on the basis of combining other factors..</p>

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