BCL-2 dependence and ABT-737 sensitivity in acute lymphoblastic leukemia
Open Access
- 15 February 2008
- journal article
- Published by American Society of Hematology in Blood
- Vol. 111 (4) , 2300-2309
- https://doi.org/10.1182/blood-2007-06-098012
Abstract
Cancer cells acquire disruptions in normal signal transduction pathways and homeostatic mechanisms that would trigger apoptosis in normal cells. These abnormaliKeywords
This publication has 55 references indexed in Scilit:
- Tumor Growth Need Not Be Driven by Rare Cancer Stem CellsScience, 2007
- New therapeutic strategies for the treatment of acute lymphoblastic leukaemiaNature Reviews Drug Discovery, 2007
- Chronic lymphocytic leukemia requires BCL2 to sequester prodeath BIM, explaining sensitivity to BCL2 antagonist ABT-737Journal of Clinical Investigation, 2007
- The BH3 mimetic ABT-737 targets selective Bcl-2 proteins and efficiently induces apoptosis via Bak/Bax if Mcl-1 is neutralizedCancer Cell, 2006
- A novel Bcl-2/Bcl-XL/Bcl-w inhibitor ABT-737 as therapy in multiple myelomaOncogene, 2006
- Evasion of the p53 tumour surveillance network by tumour-derived MYC mutantsNature, 2005
- EGFR Mutations in Lung Cancer: Correlation with Clinical Response to Gefitinib TherapyScience, 2004
- Cell Death: Critical Control PointsPublished by Elsevier ,2004
- Proapoptotic BAX and BAK: A Requisite Gateway to Mitochondrial Dysfunction and DeathScience, 2001
- Cloning the chromosomal breakpoint of t(14;18) human lymphomas: clustering around Jh on chromosome 14 and near a transcriptional unit on 18Cell, 1985