Newswise \u2014 As we age, our cells replicate, and the DNA in these cells can acquire mistakes \u2014 or mutations \u2014 every time the sequence is copied. Most newly acquired mutations are harmless, but some can tip the balance toward cancer development later in life.<\/p>\n
Now, a new study led by researchers at Washington University School of Medicine in St. Louis shows that such newly acquired mutations interact with our inherited mutations \u2014 those passed down by our parents \u2014 in important ways that influence a person\u2019s lifetime cancer risk. Understanding such interactions could guide development of new methods for early detection and prevention of cancer.<\/p>\n
The research, published in Nature Genetics, focused specifically on the risk of blood cancers such as acute myeloid leukemia (AML), although interactions between inherited and acquired mutations likely have roles in other types of cancer.<\/p>\n
Inherited mutations are carried in the egg and sperm and are therefore present in every cell starting at birth, whereas acquired mutations accumulate gradually with age in different cells. Led by Kelly Bolton, MD, PhD<\/a>, an assistant professor of medicine in the Division of Oncology<\/a> at WashU Medicine and the study\u2019s senior author, the research team set out to understand how interactions between these two types of mutations influence a person\u2019s risk of developing blood cancer.<\/p>\n In particular, they focused on a blood condition called clonal hematopoiesis that is known to increase a person\u2019s risk of developing blood cancer. Clonal hematopoiesis is caused by a mutation in blood stem cells \u2014 cells that give rise to all the different cell types in the blood \u2014 that gives those cells a slight survival advantage over the normal stem cells. Such stem cell clones multiply more and are at risk of transforming to blood cancer.<\/p>\n