Attacking a nexus of the oncogenic circuitry by reversing aberrant eIF4F-mediated translation.

ABSTRACT: Notwithstanding their genetic complexity, different cancers share a core group of perturbed pathways converging upon a few regulatory nodes that link the intracellular-signaling network with the basic metabolic machinery. The clear implication of this view for cancer therapy is that instead of targeting individual genetic alterations one by one, the next generation of cancer therapeutics will target critical hubs in the cancer network. One such hub is the translation-initiation complex eIF4F, which integrates several cancer-related pathways into a self-amplifying signaling system. When hyperactivated by apical oncogenic signals, the eIF4F-driven translational apparatus selectively switches the translational repertoire of a cell toward malignancy. This central integrative role of pathologic

SUBMITTER: Bitterman PB 

PROVIDER: S-EPMC3349966 | biostudies-literature | 2012 May

REPOSITORIES: biostudies-literature