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My "take" on the article:
The association between mutations that activate IGF1R,
Ras, or Akt and many human cancers prompted the authors of this study to formulate the hypothesis
that normal but not cancer cells would respond to starvation or
down-regulation of Ras/Akt signaling by entering a stress-
resistance mode.
They described one of the major hallmarks of cancer
cells as having self-sufficiency of growth signals and described that
in the majority of cancers this ability to grow or remain in a growth
mode even in the absence of growth factors is provided by the
hyperactivation of one or several components of the IGF1R,
Ras, Akt, and mTor pathways.
They particularly singled out the IGF1R pathway.
Put simply, cancer often outgrows its blood supply and has the ability
to keep growing under very adverse and stressful conditions. Thus it uses means such as activating heat shock proteins, IGF1R, RAS, Akt and mTor pathways to survive such stress whereas normal cells just go into a dormant state until the "stress" passes.
These authors hope to exploit that difference
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