A new genetic link between the rapid growth of healthy fetuses and the uncontrolled cell division in cancer was discovered by two researchers at the National Institutes of Health. The findings shed light on normal development and on the genetic underpinnings of common cancers.
The work, conducted using mouse and human tissue, appears in today's issue of the Proceedings of the National Academy of Sciences. The authors, Julian C. Lui, Ph.D., and Jeffrey Baron, M.D., work at the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD).
"We've long known that some of the genes that promote rapid growth in prenatal and early postnatal life become reactivated in cancer cells," said Dr. Baron. "Now we've identified a molecular switch that appears to turn on some of these genes, taking us a step forward in understanding normal body growth and the abnormal growth in some types of cancer."
For years, scientists did not know what turned IGF2 on and off. Now, using a variety of techniques and tissue types, Drs. Lui and Baron found evidence that a protein known as E2F3 activates the IGF2 gene in normal development and in cancer—in particular, in bladder and metastatic prostate cancers. More broadly, E2F3 appears to regulate not just IGF2, but also many other genes on the body-growth team. When E2F3 levels are high, these genes are active. When E2F3 takes a dive, so do these genes. The upshot is that E2F3 may function as one of the master switches that limit body growth. As such, it is of great interest as researchers seek to understand the complex genetic choreography responsible for normal growth and the diseases that result when it goes awry.