Acute myeloid leukemia (AML) is a disease of the elderly.Treating acute myeloid leukemia in the elderly is the highlight in the 56th American Society of Hematology (ASH) annual meeting.The question of which elderly patients with AML benefit from conventional intensive chemotherapy versus hypomethylating therapy or novel agent remains uncertain.This article reviews the latest research presented at the 56th ASH annual meeting on the elderly AML.

Acute lymphoblastic leukemia (ALL) is a heterogeneous disease affected by many factors,including age,immunologic subtype,and clinical,genetic and molecular features,Improved tools can identify patients in remission based on morphology but those with active disease based on molecular biology or immunophenotype (minimal residual disease).B-cell antigen panels,clone-specific immunoglobulins,or T-cell receptor rearrangements is used to detect positivity at thresholds at least.There are 13 ALL clinical related abstracts (poster) in the 19th European Hematology Association annual congress which reflected recent progress of research ALL.

Objective To investigate the effect of arsenic trioxide (As2O3) and imatinib mesylate (imatinib) or in combination with imatinib with different concentration on Raji cells and the mechanisms.Methods The inhibition of cell proliferation was measured by MTT assay to assess the cells survival after As2O3 and imatinib or in combination with imatinib treatment with different concentration at indicated time.Caspase-3 activity changes and the relative number of cells in different phases and the percentages of cells calculated in G1 and S phase of the cell cycle were assessed by FCM. The expression of p16 protein was analyzed by SABC immunohistochemical method. Results The results of MTT assay showed that As2O3 and imatinib or in combination with imatinib could inhibit Raji cells growth. There was clear statistical significance between the union groups and the single-drug group (P<0.05). As2O3 inducing apoptosis was accompanied by up-regulation and activation of apoptosis protein Caspase-3. The mean percentage of apoptosis cells was both in time-and dosage-dependent form (P<0.0001). While Raji cell lines were less sensitive to imatinib than arsenic trioxide (P >0.05). Further more, Combination of imatinib with As2O3 had not a synergistic inducing apoptosis effect on Raji cells (P >0.05). The optical density of p16 protein increased both in time-and dosage-dependent form with As2O3 by immunohistochemical method (P<0.05). While at higher concentration and for a longer time, imatinib could up-regulated the optical density of p16 protein. There was no obvious statistic significance for p16 protein in Raji cells with using As2O3 only compared with the unions group(P >0.05). The cell cycle was arrested at G1 phase, the number of cells G1 period increased significantly,and S phase decreased on Raji cells after As2O3 treatment. The relationship between the cellular DNA contents and the concentration of As2O3 showed a dose-and time-dependent manner (P<0.0001). But it was found that imatinib had no effect on Raji cell cycle. There was no the obvious difference (P >0.05) between two drugs unions group with only using As2O3 group. Conclusion The results showed that As2O3 exerted variable and definite effects on lymphoma Raji cells, and suggested that As2O3 might induce apoptosis and up-regulate the optical density of p16 protein and arrest cell cycle. As for Raji cells, imatinib might affect the expression of p16 protein at higher concentration. Two drugs unions had no effective and synergistic effect.

Objective To investigate the impact of triptolide (TP) on proliferation and apoptosis of imatanib resistant CML cell (K562/G01) and its regulating effect on Wnt/β3-catenin signal pathway.Methods A series of 10,20,40,and 80 nmol/L of triptolide were used in CML cells K562/G01 for 12,24,and 48 hours.The cell proliferation was detected with methyl thiazolyl tetrazolium (MTT) test.The apoptosis was assessed with flow cytometry (FCM).The mRNA expressions of breakpoint cluster region-c-abl (BCR-ABL),β-catenin and its down-stream targets Lef-1,and cyclinD1 were analyzed with real-time quantitative polymerase chain reaction (RT-PCR),respectively.Results Triptolide significantly inhibited K562/G01 cell growth ability and induced apoptosis in a dose-dependent manner.Mter being treated with 20,40 nmol/L TP for 24 hours,the cell growth inhibition rates were (22.62 ± 1.33) ％,and (51.41 ±1.39) ％,respectively.The late apuptosis rates were (6.91 ± 0.14) ％,and (7.64 ± 0.47) ％,respectively.Meanwhile,PCR data showed that the mRNA levels of BCR-ABL were decreased,compared to the control group,the mRNA levels of β-catenin,Lef-1,and cyclinD1 were also decreased obviously after treatment.Conclusions Our data indicated that the triptolide could inhibit the proliferation and induce the apoptosis of K562/G01,and the mechanism might be related to the blockade of Wnt/β-catenin signal pathway.

Objeetive To observe NB4 cells that is treated with both ATO and BOR.Methods MTT assay demonstrated that NB4 cell lines,growth inhibiting effect after interfered with BOR alone or BOR plus ATO.Flow cytometry detect cell cycle and apoptosis.RT-PCR method detect the expression of survivin mRNA.Results MTT assay showed depressant effect by BOR.BOR can strengthen cells,lethal effect by ATO.Flow cytometry investigate obvious apoptosis and cycle blockage of G2/M stage.RT-PCR discover that ATO or BOR can downregulate the expression of survivin mRNA alone,there is an additional effect if used them at the same time.Conclusion Combination of BOR and ATO have stronger inflictive and apoptosisinducing activity.The blockage of G2/M stage and degression of survivin mRNA is a possible mechanism that leads to cell apoptosis treated with BOR and ATO.

Objective To investigate the effect of bortezomib alone and in combination with imatinib on apoptosis of human chronic myeloid leukemia cells of the line K562 ,what is more, to explore the mechanism. Methods K562 was cultured and treated with bortezomib and (or) imatinib in different concentrations for 12, 48, 72 hours. Cell proliferation was analyzed by MTT assay, the apoptosis of K562 cells was observed by flow cytometry, and the expression of Livin mRNA was determined by reverse transcription polymerase chain reaction (RT-PCR). Results MTT assay and flow cytometry showed that bortezomib could inhibit K562 cell proliferation and induce its apoptosis, and it can strengthen cells' lethal effect by imatinib. The expression of Livin mRNA was decreased by bortezomib or imatinib to some extent, and was downregulated significantly when combined treatment was given. Conclusion Bortezomib alone and in combination with imatinib can induce K562 cells apoptosis, in which decrease of the expression of Livin mRNA is the possible mechanism.

Proteasomes is a multienzyme complex.It can degradate cyclin,which control the process of cell cycle and cell apoptosis.Proteasome inhibitor regulate cell cycle and promote cell apoptosis through suppressing UP pathway.Proteasome inhibitor can stimulate apoptosis of various hematological systemetic malignant tumor and cause cell apoptosis through different mechanism in vivo and vitro.Therefore,proteasome inhibitor is a new-style tumor targeted therapy drug.

CD+4 CD+25 regulatory T cell (Treg) has immune incompetent and immune suppression functions, and is a kind of suppressor T-cell subsets. It can inhibit the activation and proliferation of CD+4 T cells and CD+8 T cells, so as to effectively suppress the immune system to foreign organ and reduce the graftversus-host disease (GVHD) after hematopoietic stem cell transplantation (HSCT), without affecting the role of graft-versus-leukemia (GVL), which plays an important role in the transplantation immune tolerance.

The incidence of elderly patients with acute myeloid leukemia (AML) is increased year by year, and the median onset age is 67 years old. As old patients often have the viscera dysfunction, it is still lack of unified treatment clinically. This article summarizes the latest research progress of elderly patients with AML in the 58th American Society of Hematology Annual Meeting.

Objective To explore the apoptosis of K562/G01 cells induced by triptolide through MDM2/p53 signaling pathway. Methods K562/G01 cell line was treated with different concentrations of triptolide. MTT was used to detect the cell proliferation inhibition rate. FCM was used to determine the apoptosis rate changes in 12 h and 24 h. The mRNA expression levels of bcr-abl, XIAP, MDM2, p53 were detected by real-time quantitative PCR. Results After treatment by 10, 20, 40, 80, 100 nmol/L TP in 12, 24, 48 h, the viability of K562/G01 cells was inhibited in time-dose dependence manner. K562/G01 cells was treated by 20 nmol/L, 40 nmol/L TP after 12 h, 24 h, the cell apoptosis rate was rising with drug concentration and time. The bcr-abl, XIAP, MDM2 mRNA expression was down-regulated and p53 mRNA expression was up-regulated by TP. Conclusion TP can inhibit the growth of K562/G01 cell line and induce apoptosis through XIAP-MDM2-p53 signaling pathway.