Cancer: A Dysmethylation Syndrome ?
In this book the authors suggest that a 'dysmethylation syndrome' may affect the vital regulation of cell growth, metabolism and mitosis, and may then lead to cancer. These dysmethylations (which may be hyper- or hypo-methylations) affect not only the expression of the genes involved in growth and mitosis, but also the activity of enzymes such as phosphatase PP2A, which is assembled after methylation. This phosphatase limits the effects of the trophic kinases activated by growth factors or oncogenes. In the neurones, the syndrome associated with a deficit in the methylation of phosphatase and other substrates favours the accumulation of hyperphosphorylated proteins, as in Alzheimer's disease. This would mean that cancer and Alzheimer's disease, as well as Biermer's anaemia, are linked to cellular methylations.
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controls that might be perturbed
cause or consequence?
Phosphatase PP2A failure and mitosis
Histone status and gene transcription in normal
Do oncogenes prove the metabolic tumorigenic model?
urate or ascorbate protection
acetyl-coA action activation alanine aminoacids anti-cancer apoptosis arachidonic acid aspartate cAMP cancer cells carb kin catenin cell cycle cellular chemotactic chemotherapy citrate complex converted cytosolic cytosolic methylation cytotoxic decrease demethylase differentiation dimer disease drugs effect enzyme essential fatty acids fructose 1,6 gluconeogenesis glycogen glycolysis growth factor HDAC hexokinase histone deacetylase hormonal hypomethylation hypoxia increased induces inflammation inhibit inhibitors insulin insulin signalling interaction ketone bodies kinase bottle neck Krebs cycle lactate dehydrogenase leukemia lipids liver MAP kinase pathway mediated membrane metabolism methyl donors methylases methylated PP2A methylation deficit mitochondria mitosis mitotic NADH normal nuclear oncogene oxaloacetate oxidative phos phosphate phosphoenol phosphorylated PI3 kinase PP2A phosphatase promoter proto-oncogene PTEN pyruvate carboxylase pyruvate dehydrogenase pyruvate kinase pyruvate kinase block pyruvate kinase bottle receptor regulation released shuttle substrates subunit switch synthase synthesis target tissues treatment triggers trimers tumor tumor cells tyrosine kinase upregulation urate viral virus vitamin Warburg
Page 115 - Schneider MB, Matsuzaki H, Haorah J, Ulrich A, Standop J, Ding XZ, Adrian TE, Pour PM. Prevention of pancreatic cancer induction in hamsters by metformin.