Jian Chen, Ph.D., from the University of Texas Southwestern Medical Center in Dallas, and colleagues examined how recurrence occurs in a genetically engineered mouse model of glioblastoma. The researchers found that, on arrest of tumor cell proliferation with temozolomide, a subset of endogenous tumor cells were identified as the source of new tumor growth. In a second study, Gregory Driessens, Ph.D., from the Université Libre de Bruxelles, and colleagues used genetic labeling to mark and trace individual squamous skin tumor cells at different stages in progression. While the majority of cells in benign papilloma had a limited proliferative potential, the researchers found that a fraction of the cells had the capacity to persist in the long term. These cells gave rise to progeny that comprised a considerable part of the tumor.

In a third study, Arnout G. Schepers, from the Hubrecht Institute in Utrecht, Netherlands, and colleagues used lineage retracing to examine the cancer stem cell hypothesis in a mouse model of primary intestinal adenomas. The researchers found that the crypt stem cell marker (Lgr5) marked a subpopulation of adenoma cells, representing about 5 to 10 percent of the cells in an adenoma. This subpopulation generated additional Lgr5+ cells and all other adenoma cell types.

"Combined with the observation that large parts of an adenoma can emerge from a single Lgr5+ adenoma cell, these observations qualify these cells as the multipotent stem cells of the adenoma," Schepers and colleagues write.

Abstract - Chen
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Abstract - Driessens
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Abstract - Schepers
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