Dynamic and transient cancer stem cells nurture melanoma.

Abstract

A popular—and controversial—theory is that tumors are initiated and maintained by a fixed population of stem cell–like tumor cells. Research on human cells and mice adds a twist to this theory, suggesting that such stem cell–like cells might be more plastic than previously thought. Alexander Roesch <i>et al.</i> find that a group of cells, which divide slowly, can sustain melanoma growth and self-renew—hallmarks of cancer stem cells. However, the cells can switch phenotype through epigenetic changes mediated by JARID1B, a histone modifier, suggesting a plastic process. They found that human cells expressing JAR1D1B could initiate and sustain melanoma growth when implanted into mice, whereas JARD1B-negative cells could only initiate tumors. JARD1B-negative cells, however, could switch on JARD1B to support tumor growth. Might cancer stem cells be ‘moving’ targets? What, then, are the therapeutic implications?