In this book, the authors suggest that a "dysmethylation syndrome" disrupts essential regulations controlling cellular growth, metabolism and mitosis, and may then cause cancer. Dysmethylations (hyper or hypomethylations) affect not only the expression of genes controlling growth and mitosis, but also the activity of enzymes such as (PP2A) phosphatase, which is assembled after methylation, PP2A limits the action of trophic kinases activated by growth factors or by oncogenes.

In neurones, the syndrome associated to a poor methylation of the phosphatase and other substrates, leads to hyperphosphorylated proteins, as found in Alzheimer's disease. Cancer, Alzheimer's disease may possibly have, like Biermer's anemia, essential links with methylation processes.

• Introduction
• Cancer as a disease of the genome
• Cancer cannot be summarized as a disease of the genome
• Major anti-cancer drugs are not cytotoxic
• Cancer as a metabolic disease: back to Otto Warburg
• Cytotoxic chemotherapy changes the metabolism
• Glucose metabolism: controls that might be perturbed in tumors
• Glycolysis, gluconeogenesis, in normal tissues and tumors: the malate-aspartate shuttle
• The special metabolism of tumors: cause or consequence? Pyruvate kinase blockade, role of PP2A phosphatase
• Hexokinase: the first enzyme of glycolysis, its control by oxidative mitochondrial metabolism
• Phosphatase PP2A failure and mitosis
• Histone status and gene transcription in normal and tumor cells
• Do oncogenes prove the metabolic tumorigenic model?
• Inflammation and cancer: urate or ascorbate protection
• Chemotaxis or ancient hunger signals, involved in cancer and inflammation
• Cell adhesion-proteolysis and the control of differentiation
• Cytotoxic drugs that change either gene methylations,
• or protein methylations, exemplified by PP2A phosphatase
• Resistance to chemotherapy: metabolic cycles run amok
• The metabolic disturbances caused by chemotherapy are carcinogenic
• Conclusion
• The dysmethylation hypothesis and cancer
• References