Cancer Stem Cells Self-Renewal Capacity Is Independent Of Their Ability To Initiate Leukemia

Date: May-28-2012In leukemia, specialized cells called cancer stem cells are thought to proliferate to generate tumor cells. These cancer stem cells are rare in the tumor population and have unique properties from other tumor cells, including increased resistance to conventional drug therapy. Defects in regulating the mammalian target of rapamycin mTOR complex 1 (mTORC1), formed by several proteins including mTOR and Raptor, are common in leukemia. Although ablation of mTOR and Raptor have shown that mTORC1 is indispensable for normal cell proliferation and survival during embryogenesis, the role of mTORC1 in cancer stem cells and established leukemia is unclear.

In the May 24, 2012 issue, Atsushi Hirao and colleagues from Kanazawa University in Japan have demonstrated in adult mice that Raptor deficiency impairs granulocyte and B cell development without affecting normal hematopoietic progenitor cell survival or proliferation. Furthermore, in a model of acute myeloid leukemia, mTORC1 inactivation by Raptor deficiency does not affect the ability of cancer stem cells to self-renew but halts their capacity to initiate leukemia. Reactivation of mTORC1 restores the leukemia-initiating capacity of these cancer stem cells.

Their findings are unique in showing that the ability of cancer stem cells to self-renew is different from the capacity to initiate and propagate tumors. Accounting for this difference can significantly impact future studies geared towards improved therapeutic strategies to target cancer cells resistant to conventional treatment.
Courtesy: Medical News Today Note: Any medical information available in this news section is not intended as a substitute for informed medical advice and you should not take any action before consulting with a health care professional.