Chronic lymphocytic leukemia requires BCL2 to sequester prodeath BIM, explaining sensitivity to BCL2 antagonist ABT-737.

By Victoria Del Gaizo Moore, Jennifer R. Brown, Michael T. Certo, Tara M. Love, C. Novina, A. Letai. Journal of Clinical Investigation, 2007

614 citations recorded by the source corpus.

Subfields: Genetics, Immunology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/f776e94c99c8689ab1e697267f612477b229d726

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In Immunology

1. Stephen W. Fesik

In Molecular Biology

1. A. Letai
2. J. Brunelle
3. Stephen W. Fesik
4. D. Huang
5. Jerry M. Adams
6. Douglas R. Green
7. Suzanne Cory

Citations in the corpus

• Control of mitochondrial apoptosis by the Bcl-2 family (2009, background): “The anti-apoptotic proteins of such cells are already burdened with significant amounts of activator BH3-only proteins, such as Bim (Del Gaizo Moore et al., 2007), and can be killed merely by inhibiting anti-apoptotic function.”
• Targeting BCL2 with Venetoclax in Relapsed Chronic Lymphocytic Leukemia (2015, neutral): “Small lymphocytic lymphoma 7 (12) 7 (12) 14 (12)”
• ABT-263: a potent and orally bioavailable Bcl-2 family inhibitor. (2008, background): “In addition to established human tumor cell lines, ABT-737 effectively induces apoptosis in primary patient-derived lymphoma and chronic lymphocytic leukemia cells ex vivo (12, 17).”
• Substantial susceptibility of chronic lymphocytic leukemia to BCL2 inhibition: results of a phase I study of navitoclax in patients with relapsed or refractory disease. (2012, background): “Navitoclax is thought to kill MCL1expressing cells by displacing BIM from a stable complex with BCL2, thereby freeing BIM to antagonize MCL1.”