What about childhood leukemias?
Dr. Morrison and his research team are studying a gene called Sox17 that regulates blood-forming stem cells in mice before they are born. They discovered that blood-forming stem cells in a fetus or newborn mouse have different self-renewal mechanisms than adult stem cells. The implication for human leukemias is that different mutations cause cancer in children than in adults, because the cancer stem cells are hijacking a different self-renewal program. One possibility is that mutations causing over-activity in Sox-17 may contribute to certain forms of childhood leukemia.
It's not unusual to see very different clinical behavior in the childhood version and the adult version of the same kind of cancer. In some cases, the childhood cancer is less deadly; in some it's more deadly. What this shows is that every cancer is different. But how they differ biologically has not been clear. The knowledge that self-renewal pathways are different between fetal and adult stem cells is likely to provide important insights into the problem.