Application BCL-2 inhibitors in treatment of acute myeloid leukemia

[biokit]

Recently, scientists from Stanford University School of Medicine in the international journal nature medicine online published their latest research advances them through large-scale RNAi screening methods found in acute myeloid leukemia, IDH1R132H against apoptotic gene mutation BCL- 2 has a strong dependence, with BCL-2 inhibitor treatment, will lead to apoptosis of cells containing the mutant IDH1R132H more likely.

Prior studies have found that in patients with acute myeloid leukemia cells, isocitrate dehydrogenase 1 and 2 mutations can lead to changes in the apparent intracellular genetic map. Large-scale RNAi screening by researchers trying to find cause cells containing IDH1R132H fatal genetic mutations, eventually locking research focuses on the anti-apoptotic gene BCL-2. The experimental results show, IDH-1 and IDH-2 mutation primary AML cells specific inhibitor ABT-199 BCL-2 has a greater sensitivity, and ABT-199 is highly specific for BCL-2 inhibitor, has conducted clinical validation by in vitro and in xenograft models. Further research found that the sensitivity function is mainly by (R) -2-HG mitochondrial electron transport chain in cytochrome c oxidase activity regulation to achieve, inhibition of cytochrome c oxidase activity will reduce the trigger mitochondrial inhibition of BCL-2 mediated apoptosis threshold value, so that primary AML cells containing IDH-1 and IDH-2 mutation of ABT-199 having more sensitive.

In summary, the results of this study indicate that patients carry Human insulin autoantibodies ELISA Kit http://www.cusabio.com/ELISA_Kit-114614/ in acute myeloid leukemia BCL-2 inhibitors might generate response, which is the combination of blocking the activity of the mitochondrial electron transport chain drug and ABT-199 treatment AML provides a clear molecular basis.