PTEN maintains haematopoietic stem cells and acts in lineage choice and leukaemia prevention

Jiwang Zhang, Justin C. Grindley, Tong Yin, Sachintha Jayasinghe, Xi C. He, Jason T. Ross, Jeffrey S. Haug, Dawn Rupp, Kimberly S. Porter-Westpfahl, Leanne M. Wiedemann, Hong Wu and Linheng Li ()
Additional contact information
Jiwang Zhang: Stowers Institute for Medical Research
Justin C. Grindley: Stowers Institute for Medical Research
Tong Yin: Stowers Institute for Medical Research
Sachintha Jayasinghe: Stowers Institute for Medical Research
Xi C. He: Stowers Institute for Medical Research
Jason T. Ross: Stowers Institute for Medical Research
Jeffrey S. Haug: Stowers Institute for Medical Research
Dawn Rupp: Stowers Institute for Medical Research
Kimberly S. Porter-Westpfahl: Stowers Institute for Medical Research
Leanne M. Wiedemann: Stowers Institute for Medical Research
Hong Wu: UCLA School of Medicine
Linheng Li: Stowers Institute for Medical Research

Nature, 2006, vol. 441, issue 7092, 518-522

Abstract: Cancer stem cell function Stem cells that initiate and maintain cancers are so like normal stem cells that it's hard to design drugs to target them specifically. This is a serious problem as, for example, damaging blood stem cells in leukaemia therapy can cause haematopoietic failure and death. Now a study of the tumour suppressor PTEN, often inactivated in leukaemia and other cancers, pinpoints a major difference between self-renewal in normal and cancer stem cells. PTEN normally inhibits the phosphatidylinositol-3-OH kinase signalling pathway, limiting cell proliferation and survival. In the absence of PTEN, leukaemic stem cells proliferate, but normal stem cells are depleted. This suggests that PTEN-mimicking drugs may act against leukaemia yet preserve blood stem cells. Indeed, in Pten-deficient mice rapamycin kills leukaemic stem cells but rescues normal stem cell function. A separate study confirms PTEN's role in blood stem cell regulation.

Date: 2006
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DOI: 10.1038/nature04747

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