Pten, tumorigenesis, and stem cell self-renewal.
Self-renewal pathways crucial for maintaining stem cells are deregulated in cancer, raising the spectre that cancer therapies targeting such pathways might also ablate normal stem cells. As Yilmaz et al. (2006) report in a recent Nature paper, this may not be the case for the tumor suppressor protein Pten, which drives the self-renewal of normal hematopoietic stem cells and the formation of leukemia cells through different mechanisms.
Rossi
Derrick J
DJ
Department of Pathology, Stanford University School of Medicine, Beckman Center B259, 279 Campus Drive, Stanford, CA 94305, USA. drossi@stanford.edu
Weissman
Irving L
IL
D000818:Animals; D002453:Cell Cycle / Q000502:physiology*; D006412:Hematopoietic Stem Cells / Q000502:physiology*; D006706:Homeostasis; D006801:Humans; D015470:Leukemia, Myeloid, Acute / Q000378:metabolism* / Q000503:physiopathology; D051059:PTEN Phosphohydrolase / Q000235:genetics / Q000378:metabolism*; D015398:Signal Transduction / Q000502:physiology
D051059:PTEN Phosphohydrolase