David J. Kerr, CBE, MD, DSc, discusses somatic mutations in normal tissue.
I'm David Kerr, professor of cancer medicine at University of Oxford. I'd like to turn your attention to a fantastic review article that I enjoyed reading recently in" and it's from an excellent group from the Francis Crick Institute in London. This is a really thoughtful, interesting article.
We assume, don't we, that normal tissue is normal genetically and phenotypically, and cancer is a collection of mutations, where eventually there's a tipping of balance in which a cell that has accumulated the most driver mutations is the one that outgrows and behaves like a cancer cell —hyperproliferative, invasive, with metastatic potential.
Think about these new tests that are coming along, like GRAIL, in which we're being persuaded that in normal individuals with low-circulating, low-copy-number DNA, if we can detect mutations in TP53, RAS, RAF, or whatever we think the important drivers might be, that these might be reflecting, especially in older people, nonmalignant changes in normal tissue.
I accept that rather than just looking for circulating fragments of DNA, you may look for patterns of methylation and so on; this might help to distinguish genuinely precancerous tissue from just quasi-passenger somatic mutations in normal tissue in healthy people.
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