Journal article
Modulation of NOXA and MCL-1 as a strategy for sensitizing melanoma cells to the BH3-mimetic ABT-737
KM Lucas, N Mohana-Kumaran, D Lau, XD Zhang, P Hersey, DC Huang, W Weninger, NK Haass, JD Allen
Clinical Cancer Research | AMER ASSOC CANCER RESEARCH | Published : 2012
Abstract
Purpose: Drug resistance in melanoma is commonly attributed to ineffective apoptotic pathways. Inhibiting antiapoptotic BCL-2 and its relatives is an attractive strategy for sensitizing lymphoid malignancies to drugs but it has been largely unsuccessful for melanoma and other solid tumors. ABT-737, a small-molecule BH3-mimetic, selectively inhibits BCL-2, BCL-XL, and BCL-w and shows promise for treating leukemia, lymphoma, and small-cell lung cancer. Melanoma cells are insensitive to ABT-737, but MCL-1 inhibition reportedly increases the sensitivity of other tumors to the compound. Experimental Design: The efficacy of MCL-1 and BFL-1 inhibition for sensitizing melanoma cells to ABT-737 was i..
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Awarded by Cancer Institute New South Wales
Awarded by Cancer Council New South Wales
Awarded by Cancer Australia/Cure Cancer Australia Foundation
Funding Acknowledgements
K.M. Lucas and N. Mohana-Kumaran are Cancer Institute New South Wales Scholar Award recipients. K.M. Lucas received an Australian Postgraduate Award. N. Mohana-Kumaran was supported by the Government of Malaysia. X.D. Zhang and J.D. Allen are Cancer Institute New South Wales Fellows. N.K. Haass is a recipient of the Cameron Fellowship from the Melanoma and Skin Cancer Research Institute, Australia. N.K. Haass is CIA on Project Grant RG 09-08 (Cancer Council New South Wales), Project Grant 570778 (Priority-driven collaborative cancer research scheme/Cancer Australia/Cure Cancer Australia Foundation), and Research Innovation Grant 08/RFG/1-27 (Cancer Institute New South Wales) and Project Grant 1003637 (National Health and Medical Research Council).