Tyrosine kinase inhibitor (TKI) may significantly improve the treatment outcome in chronic myeloid leukemia (CML).It is the most frequent question about whether the patients with durable complete molecular response (CMR) can safely discontinue TKI treatment without relapse.This has focused attention on the strategies to eradicate residual CML cells,especially the CML stem cells,which should result in long term leukemia-free survival and permanent cure.Here,the progress on discontinuation of TKI therapy and alternative approaches to eradicating CML stem cells in the 55th ASH annual meeting is reviewed.

Objective To explore the drainage effect of drainage tube with different materials on the basis of a constant nega tive pressure drainage,and its impact on flap survival.Methods The most common clinical used Polyvinyl chloride resin (PVC)pipe,latex tubes,silicone tube drainage tubes,and flaps were compared at different phases of the drainage,to determine the best clinical flap with drainage material.After three groups of flaps were designed,including a constant negative pressure drainage device,without a constant negative pressure drainage system,and drainage alone (no negative pressure) drainage flap,the flap survival was observed at different phase space.Three different drainage drainage ways of the flap and the flap survival area of effect were statistically analyzed.Results The silicone tube drainage was more fully and effectively.Constant negative pressure drainage volume of liquid was up to the flap with drainage to the fullest,the highest rate of skin flap healing,and better healing.Conclusions The constant negative pressure in the drainage of the flap makes drainage more fully,and promotes rapid healing of wounds,while the silicone tube is suitable for flap drainage.

With the great success of imatinib mesylate(IM) and other tyrosine kinase inhibitor (TKI),chronic myelogenous leukemia (CML) is taken as a successful model of targeted therapies for human cancer.Although the emergence of TKI has greatly improved the prognosis of CML,the long-term TKI treatment may bring the problems of drug resistance,serious side effects,poor compliance,and heavy economic burden.Recently,people focus on whether patients would be cured after discontinuation of TKI treatment.Here,the progresses on discontinuation of TKI therapy in CML presented in the 54th American Society of Hematology (ASH) annual meeting were reviewed.

Induced pluripotent stem (iPS) cell based on recently developed stem cell reprogramming technique holds great hope for regenerative medicine,in vitro disease modeling and drug evaluation.Recent progress on clinical hematology includes in vitro generation of hematopoietic progenitors and mature blood cells from somatic cells,iPS cells derived from chronic myeloid leukemia cells for the better understanding of the resistance mechanisms of bcr-abl inhibitor imatinib,and moreover,correction the monogenic inherited disease using gene-targeted strategies.However,whether the iPS cells can fully replace human embryonic stem cells still needs further investigation.

It is a crucial question whether it is necessary to continue the treatment after the patients with chronic myeloid leukemia (CML) who have achieved a complete molecular response (CMR) on imatinib (IM) treatment. If tyrosine kinase inhibitor (TKI) therapy was required indefinitely to maintain CMR, the problems of financial burden and adverse effects would be increased. Approximately 40 ％ of patients with a stable CMR for at least 2 years could stop IM treatment and remain in molecular remission for at least 2 years without IM treatment. Therefore, the ultimate aim should be to give the patients long-term disease control without the need for ongoing treatment. Here the studies progresses of discontinuation of TKI therapy in CML reported in the 53th American Society of Hematology (ASH) annual meeting were reviewed.

Since the identification of BCR-ABL fusion gene and the advent of targeted tyrosine kinase inhibitors (TKI), patients with chronic myeloid leukemia (CML) have been "walking" on the path of chronic disease for around twenty years. In recent years, the second - and third -generation TKI have provided further protection for the long-term survival of CML patients. However, TKI discontinuation and the prognostic situation of a small number of patients with TKI resistance or carrying poor prognostic genes are still hot issues in CML-related researches. This article reviews the research progress of CML at the 62nd American Society of Hematology Annual Meeting.

Objective: To investigate the expression of Cyclin G mRNA in leukemia patients and its clinical significance. Methods: RT-PCR was used to analyze the expression of Cyclin G mRNA in the mononuclear cells of 129 leukemia patients and 10 healthy controls. Results: (1) The expression of Cyclin G in acute leukemia (AL) and chronic leukemia (CL) patients was significantly higher than that in healthy controls (both P 50?109/L in AL and AML groups were significantly higher than those with WBC ≤ 50?109/L. (4) Fifty-three of the newly diagnosed cases were Cyclin G positive. The remission rate of patients with high Cyclin G expression(51.7%)was significantly lower than that with low Cyclin G expression(79.1%)(P

AIM:To study the effect of bcr - abl gene antisense phosphorothioate oligonucleotides(Aspo) on K562 cell line and explore its significance in chronic myelogencous leukemia (CML) gene therapy. METHODS: Cells were exposed to oligomers, observed by inverted microscope. Cells inhibitory rate were determined by 0.4% trypan blue exclusion. CFU - K562 were cultured in 0.8% methylcellulose. P210 was measured by flow cytometry. RESULTS:K562 cells were treated with Aspo, they still grew in clone state and show antisense sequence specific and dose dependent. When the concentration of Aspo was more than 5?mol/L, the growth of cells was inhibited and P210 was down regulated or completely suppressed, and the greatest growth inhibition was at 120h. There was significant inhibition of cell proliferation in a rang of cells number from 1 ? 10-4/mL to 5 ? 10-4/mL after treatment with 10?mol/L Aspo. b2a2 Aspo was also effect on K562 cells which expressing b3a2 mRNA. CONCLUSION: bcr - abl Aspo has a specific growth inhibition effect on K562 cells, and worths further study in CML gene therapy.

AIM:To investigate the effects of baicalin on proliferation inhibition and apoptosis induction in human Burkitt lymphoma cell line CA46 and to explore its underlying mechanisms.METHODS:CA46 cells were exposed to baicalin at different dosages and its proliferation inhibition was detected by MTT assay.The ability of baicalin to induce CA46 cell apoptosis was examined by Annexin V-FITC/PI double staining analysis,TUNEL labeling method and DNA fragmentation.The mRNA expressions of c-myc and bcl-2 were detected by RT-PCR,and the protein expressions of c-Myc,Bcl-2,caspase-3 precursor(procaspase-3) and poly ADP-ribose polymerase(PARP) were detected by Western blotting.RESULTS:Baicalin remarkably inhibited the CA46 cell proliferation,with an IC50 value of 10 ?mol/L.Apoptosis was remarkably induced by baicalin in a dose-dependent manner,and its earlier and later stages were detected by annexin V-FITC/PI double staining analysis,TUNEL labeling method and DNA fragmentation,respectively.Furthermore,RT-PCR showed that the mRNA expressions of c-myc and bcl-2 in treated CA46 cells decreased in a time-dependent manner.Western blotting showed that the protein expressions of c-Myc,Bcl-2,procaspase-3 and PARP(116 kD) in baicalin treated CA46 cells were down-regulated in a time-dependent manner,while the expression of PARP(85 kD) was up-regulated.CONCLUSION:Baicalin efficiently induces proliferation inhibition and apoptosis in CA46 cells,which may be related with the down-regulation of c-Myc and Bcl-2 expressions,as well as the up-regulation of caspase-3 activity.

Objective:To investigate the effect of SU11248 proliferation and apoptosis of multiple myeloma cell line U266 in vitro and analyze its mechanisms.Methods:Effect of SU11248 on proliferation of U266 cells was detected by MTT assay.The ability of SU11248 to induce apoptosis of U266 cells was examined by cell cycle analysis,TUNEL and DNA fragmentation.Expression of c-myc,hTERT,Bcl-2 and Bax mRNA in U266 cells was assessed by RT-PCR analysis.Results:The proliferation of U266 cells was inhibited by SU11248 in dose-and time-dependent manners (P