Aerobic glycolysis suppresses p53 activity to provide selective protection from apoptosis upon loss of growth signals or inhibition of BCR-Abl

Unlike the growth factor-dependence of normal cells, cancer cells can maintain growth factor-independent glycolysis and survival through expression of oncogenic kinases, such as BCR-Abl. While targeted kinase inhibition can promote cancer cell death, therapeutic resistance develops frequently and fu...

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Main Authors: Mason, Emily F., Zhao, Yuxing, Goraksha-Hicks, Pankuri, Coloff, Jonathan L., Gannon, Hugh, Jones, Stephen N., Rathmell, Jeffrey C.
Formato: Artigo
Idioma:Inglês
Publicado: 2010
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Article
Acceso en liña:https://ncbi.nlm.nih.gov/pmc/articles/PMC2955844/
https://ncbi.nlm.nih.gov/pubmed/20876800
https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1158/0008-5472.CAN-10-0608
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