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Requirement for antiapoptotic MCL-1 in the survival of BCR-ABL B-lineage acute lymphoblastic leukemia

descriptionPublicationkeyboard_double_arrow_right Article 29 Aug 2013 English Publisher:American Society of HematologyJournal:Blood, volume 122, pages 1,587-1,598 (issn: 0006-4971, eissn: 1528-0020,

Authors: Harpreet Singh; Harpreet Singh; Joseph T. Opferman; Richard T. Williams; Jeffrey B. Morrison; Brian Koss; Jerold E. Rehg; +1 Authors

doi: 10.1182/blood-2012-06-440230

pmid: 23881917

pmc: PMC3757371

Requirement for antiapoptotic MCL-1 in the survival of BCR-ABL B-lineage acute lymphoblastic leukemia

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Abstract

Key Points Using a mouse genetic mouse model of Ph+ B-lineage ALL, endogenous antiapoptotic MCL-1 is required for leukemia survival. In BCR-ABL+ B-lineage ALL human and mouse cells, combining TKIs with small-molecule inhibitors of BCL-2 can potentiate sensitivity to cell death.

Related Organizations

University of Tennessee Health Science Center
United States
St. Jude Children's Research Hospital
United States

Keywords

B-Lymphocytes, Cell Survival, Gene Expression Regulation, Leukemic, Fusion Proteins, bcr-abl, Apoptosis, Mice, Transgenic, Precursor Cell Lymphoblastic Leukemia-Lymphoma, Mice, Inbred C57BL, Disease Models, Animal, Mice, Animals, Humans, Myeloid Cell Leukemia Sequence 1 Protein, Cell Lineage, Cells, Cultured

17 Research products, page 1 of 2

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	citations This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).	81
	popularity This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.	Top 10%
	influence This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).	Top 10%
	impulse This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.	Top 10%