A UCLA-led study of DNA patterns in tumor cells suggests that the abundance of aberrant genetic signatures common in more aggressive cancers is not random but reflects selective forces in tumor evolution. The findings also demonstrate that these changes drive glucose metabolism in cells, which can lead to accelerated cancer growth. Less aggressive cancers are known to have an intact genome — the complete set of genes in a cell — while the genome of more aggressive cancers tends to have a great deal of abnormalities. Modern research has focused largely on individual cancer genes, specifically oncogenes and tumor-suppressor genes, as the primary targets for DNA mutations and copy number alternations. Mutation or amplification in oncogenes can turn healthy cells into tumor cells. When tumor-suppressor genes are not working properly cells can grow out of control. However, scientists continue to observe many recurrent copy number alteration patterns in tumors that cannot be fully explained by these canonical cancer genes. It has long been known that a fundamental difference between healthy cells and tumor-forming cells is reprogrammed cellular metabolism. An altered metabolism benefits a transformed cell in many ways, particularly in the ability to convert glucose into energy. This process, known as glycolysis, can fuel tumor growth the most-aggressive cancers. In the five-year study, Thomas Graeber, Ph.D., UCLA Professor of Molecular and Medical Pharmacology, and his colleagues used a cross-cancer analysis of copy number alterations data from human tumors, cancer cell lines and mouse models of cancer.
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