via the methionine metabolism cycle. a near ubiquitous feature of cancer is a maladaption of the methionine metabolic pathway in response to genetic or environmental conditions resulting in depletion of sam and/or sam-dependent methylation. whether it is deficiency in enzymes such as methylthioadenosine phosphorylase, methionine-dependency of cancer cells, high levels of polyamine synthesis in cancer, or induction of cancer through a diet deprived of extrinsic methyl donors or enhanced in methylation inhibitors, tumor formation is strongly correlated with a decrease in levels of sam in mice, rats and humans. according to a 2012 review, the effect of methionine restriction on cancer has yet to be studied directly in humans and "there is still insufficient knowledge to give reliable nutritional advice". ampk ampk is thought to be a major element or mechanism in cancer-related effects of diet. it modulates the activity of cellular survival signaling such as mtor and akt, leading to cell growth inhibition which is relevant to cancer growth. targeting ampk has become a novel strategy for cancer prevention and treatment. potential complementary or preventive options under investigation include periods of caloric restriction and ampk agonists (typically mtor inhibitors). however, ampk can also promote cancer in some settings.