human cancer genome

Many claims have been made that nutrition has a causative or preventive role in the aetiology of cancer. . Some of these claims can be seriously considered, others dismissed as fabrications of fertile imaginations. Unfortunately this is a complex area and one to be looked at with care. However some silly claims turn out to be well founded and the reverse.
The prospect of the entire cancer genome being described offers a basis for rational thoughts and experiments for nutritionists
Abnormalities in some 350 genes have been shown to be associated with human cancer.
.A recent paper in Nature ( Greenman Nature 446, 153-158, 2007 ) has identified mutations in protein kinases, regulators of proteins through adding a phosphate and another in Science has identified the whole cancer genome in breast and colorectal cancer ( Sjoblom Science 314, 268-274, 2006 ) .
The variety of defects underlying human cancer include
Activating intragenic mutations
Gene amplification
Gene translocations
Epigenetic silencing
Gene deletions
Inactivating mutations

By the time that a cancer is diagnosed billions of cells carry the DNA abnormality which initiated the malignant transformation plus others accumulated along the way. Some of these secondary mutations are due to selective pressures ( drivers ) others incidental ( passengers). Passengers are the chance result of mutation exposures, genome instability, or through the rapid rate of proliferation.
It is the drivers that are the initiators and the subject of significant research. Mind you the passengers may turn out to be important in giving malignancy some of the significant characteristics.
Kinases have a probable role in cancer development eg BCR-ABL in chronic myeloid leukaemia. Cellular kinase mutations are common in cancer of the lung, stomach, ovary, colon and kidney and rare in breast and testes.
Each cancer genome carries many singular abnormalities and not all mutations identified contribute to the manifestations of the associated cancers.
Drivers and passengers.
From Haber and Settleman Nature 446, 145-146, 2007

Martin Eastwood
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