An interesting paper in Nature revealed why some some tumours are resistant to dietary restriction. Normally, restricting food intake will lead to tumour shrinkage but some tumours grow despite limiting calorific intake.  The answer?  PI3K activation is permanently turned "on" via a mutation, so the tumours grow and proliferate independent of the amount of food consumed:

"Substitution of an activated mutant allele of PI3K with wild-type PI3K
in otherwise isogenic cancer cells, or the restoration of PTEN
expression in a
PTEN-null cancer cell line, is sufficient to
convert a dietary-restriction-resistant tumour into one that is
dietary-restriction-sensitive."

Further information can be found on the institution's website at MIT:

Meanwhile, there are a number of PI3K and PTEN inhibitors in development, but if these only affect the wild-type, not mutant, mutation, then they may only have a limited effect in overcoming the proliferation.  This blog has covered PI3 Kinase and PTEN in tumourigenesis in the past.   Companies with active research in PI3 kinase pr PTEN inhibitors include Genentech, Exelixis, Calistoga, Semafore, EMD and others.  It will be interesting to see how the research pans out. 

Finally, some thoughts from the researchers on what they found from their studies:

“We already know that the United States has an epidemic of obesity and
that obesity is probably the biggest contributor to cancer in the U.S.,
even more so than smoking. Does this research have anything to do with
that correlation between obesity and cancer, that if we make animals
really obese, that this pathway is also involved in determining their
sensitivity to cancer?  Answering that question is the next step.”

rb2 large gray Cell pathway on overdrive prevents normal cancer response to dietary restriction
Kalaany, N., & Sabatini, D. (2009). Tumours with PI3K activation are resistant to dietary restriction Nature DOI: 10.1038/nature07782