| First Author | Peng C | Year | 2010 |
| Journal | Blood | Volume | 115 |
| Issue | 3 | Pages | 626-35 |
| PubMed ID | 19965668 | Mgi Jnum | J:156831 |
| Mgi Id | MGI:4421478 | Doi | 10.1182/blood-2009-06-228130 |
| Citation | Peng C, et al. (2010) PTEN is a tumor suppressor in CML stem cells and BCR-ABL-induced leukemias in mice. Blood 115(3):626-35 |
| abstractText | The tumor suppressor gene phosphatase and tensin homolog (PTEN) is inactivated in many human cancers. However, it is unknown whether PTEN functions as a tumor suppressor in human Philadelphia chromosome-positive leukemia that includes chronic myeloid leukemia (CML) and B-cell acute lymphoblastic leukemia (B-ALL) and is induced by the BCR-ABL oncogene. By using our mouse model of BCR-ABL-induced leukemias, we show that Pten is down-regulated by BCR-ABL in leukemia stem cells in CML and that PTEN deletion causes acceleration of CML development. In addition, overexpression of PTEN delays the development of CML and B-ALL and prolongs survival of leukemia mice. PTEN suppresses leukemia stem cells and induces cell-cycle arrest of leukemia cells. Moreover, PTEN suppresses B-ALL development through regulating its downstream gene Akt1. These results demonstrate a critical role of PTEN in BCR-ABL-induced leukemias and suggest a potential strategy for the treatment of Philadelphia chromosome-positive leukemia. |
