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2008;295:E78E84

63 Together, these findings indicate that (i) the sensitivity of tumors to insulin and IGF-1 parallels their response to CR, and (ii) neither the activation status of PI3KAKT per se nor mutation status of individual genes predicts for the sensitivity of tumors to both growth factors and CR

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Additionally, it is now known that pro-inflammatory cytokines also hijack IGF-1 intracellular signalling by phosphorylating serine residues on insulin related substrate (IRS) molecules and hence impeding their binding to IGF-1R [124]

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