ABT-737

04/01/2012 - "Our results also suggest that 1h could have therapeutic potential against ABT-737 refractory cancer."
01/01/2012 - "In this study, we demonstrate that ABT-737 improved the radiation sensitivity of cervical cancer HeLa cells and thereby provoked cell apoptosis. "
01/01/2013 - "A BH3 mimetic, ABT-737, has demonstrated efficacy in several forms of cancers. "
01/01/2011 - "The BH3 mimetic ABT-737, which can induce apoptosis by targeting pro-survival Bcl-2 family members, has been found to enhance the efficacy of many conventional chemotherapeutic agents in multiple cancers. "
01/15/2011 - "The current study reveals a novel mechanism whereby ABT-737 when added to apoptosis-resistant cancer cells has profound biologic effects. "

06/01/2012 - "Therapeutic efficacy of ABT-737, a Bcl-2 inhibitor, in a canine melanoma cell line."
01/01/2012 - "To determine if the anti-apoptotic BCL-2 repertoire established the cell death threshold and chemoresistance in melanoma, a novel treatment strategy was designed to inhibit the anti-apoptotic BCL-2 members with ABT-737. "
01/01/2013 - "Importantly, Maritoclax markedly enhanced the efficacy of ABT-737 against melanoma cells in both two- and three-dimensional spheroids. "
01/01/2013 - "Proteasomal degradation of Mcl-1 by maritoclax induces apoptosis and enhances the efficacy of ABT-737 in melanoma cells."
01/01/2013 - "In this study, we investigated the effects of Maritoclax, a novel Mcl-1-selective inhibitor, alone and in combination with ABT-737, on the survival of human melanoma cells. "

04/01/2012 - " control mice and CI-1040-treated mice exhibited progressive leukemia growth, ABT-737, and to a significantly greater extent, ABT-737+CI-1040 exerted major anti-leukemia activity. "
01/01/2014 - "Our study suggests that ABT-737 synergistically enhances the cytotoxic effect of DNR in AML cell lines and therefore may be useful to overcome chemoresistance of leukemia patients."
06/15/2012 - "In this study, we investigated potential mechanisms of resistance to ABT-737 in leukemia cell lines. "
03/01/2011 - "We describe the in vitro studies to demonstrate the activity and drug combinability of ABT-737 against MLL rearranged leukemia cells. "
03/01/2011 - "This study focuses on the effects of ABT-737 on leukemia cells with MLL rearrangement and identifies some of the biological correlates of its activity. "

09/01/2013 - "Importantly, BXI-61 and BXI-72 exhibit more potent efficacy against human lung cancer than ABT-737 but less degree in platelet reduction in vivo. "
07/01/2014 - "Ku70 knockdown not only promotes Mcl-1 turnover but also enhances antitumor efficacy of the BH3-mimetic ABT-737 in human lung cancer xenografts. "
08/15/2012 - "Strikingly, BCL2 expression reduced the survival of PARP inhibitor-sensitive breast cancer and lung cancer cells by 90% to 100%, and these effects were reversed by ABT-737. "
11/01/2008 - "For example, ABT-737 is able to induce apoptosis when used as a single agent to treat leukemic and lung cancer cells and has also been shown to synergize with conventional chemotherapeutic agents in several cancer types. "
09/05/2008 - "We demonstrate that a combination of ABT-737 and TRAIL induced significant cell death in multiple cancer types, including renal, prostate, and lung cancers, although each agent individually had little activity in these tumor cells. "

11/18/2008 - "In vivo efficacy of the Bcl-2 antagonist ABT-737 against aggressive Myc-driven lymphomas."
04/22/2010 - "To study potential mechanisms of resistance to ABT-737, we derived resistant lines from initially sensitive OCI-Ly1 and SU-DHL-4 lymphoma cell lines via long-term exposure. "
07/01/2009 - "Drug combination studies using a panel of conventional and novel therapeutic agents show that ABT-737 potentiates the activity of agents that have inherent anti-lymphoma activity and provide support for the evaluation of ABT-737 in the clinical setting."
04/22/2010 - "Acquired resistance to ABT-737 in lymphoma cells that up-regulate MCL-1 and BFL-1."
02/26/2009 - "Emu-myc lymphomas that expressed Bcl-2 throughout the tumorigenesis process were especially sensitive to ABT-737, while those forced to overexpress Mcl-1 were not. "