Cancer: A Dysmethylation Syndrome ?

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John Libbey Eurotext, 2005 - 117 pages
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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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Contents

Introduction
1
controls that might be perturbed
17
cause or consequence?
35
Phosphatase PP2A failure and mitosis
49
Histone status and gene transcription in normal
63
Do oncogenes prove the metabolic tumorigenic model?
69
urate or ascorbate protection
75
Chemotaxis or ancient hunger signals involved in cancer
81
Cell adhesionproteolysis and the control of differentiation
87
metabolic cycles run amok
95
Conclusion
101
References
107
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