Genetic Damage or Epigenetic Change as a More Important Cause of Cancer?
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Cancer is an age-related disease. It can happen at any age, but the odds are very low until you start into later life. There are many possible reasons as to why this is the case: the progressive decline in effectiveness of the immune system, which detects and destroys cancerous and potentially cancerous cells; rising levels of stochastic damage to nuclear DNA; greater inflammation and disarray in metabolism resulting from other forms of cellular and molecular damage associated with aging.

How about epigenetic changes, however? The number, type, and position of molecules attached to nuclear DNA continually alter in response to environment, health, and age. Much of this is presumably a response to the above noted damage and dysfunction, a reaction to circumstances. These decorating molecules act to alter gene expression, the rate at which proteins are produced from each blueprint gene, and thus alter the behavior of cells. Epigenetic patterns are different in every cell and tissue and between individuals, but characteristic differences between old people and young people can be discerned given enough data and computing power.

NIH Study Offers Insight into Why Cancer Incidence Increases with Age

Scientists have known for years that age is a leading risk factor for the development of many types of cancer, but why aging increases cancer risk remains unclear. Researchers suspect that DNA methylation, or the binding of chemical tags, called methyl groups, onto DNA, may be involved. Methyl groups activate or silence genes, by affecting interactions between DNA and the cell's protein-making machinery.

[Researchers] identified DNA methylation sites across the human genome that changed with age. They demonstrated that a subset of those sites - the ones that become increasingly methylated with advancing age - are also disproportionately methylated in a variety of human cancers. "You can think of methylation as dust settling on an unused switch, which then prevents the cell from turning on certain genes. If a cell can no longer turn on critical developmental programs, it might be easier for it to become a cancer cell."

You might recall that in recent years researchers have started to make inroads in using DNA methylation patterns as a measure of chronological and biological age. If that works - and it appears to - it shouldn't be surprising to also find associations with cancer.

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"You might recall that in recent years researchers have started to make inroads in using DNA methylation patterns as a measure of chronological and biological age. If that works - and it appears to - it shouldn't be surprising to also find associations with cancer."

DNA methylation could serve as a biomarker of cancer risk, but I don't think the scientists have ruled out whether methylation of certain sites is the cause of increased cancer rates, or if increased methylation is merely correlated with aging which is the cause of increased cancer rates.

The only way to be sure is to alter the DNA methylation patterns comprehensively in an old mouse or monkey model and see if that reduces or increases rates of cancer.

I don't know if that is possible yet? It would be good if someone could do a review of the current state of genetic engineering.

Posted by: Jim at February 4, 2014 12:39 AM
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