Author/Authors :
Bruggeman، نويسنده , , Sophia W.M. and Hulsman، نويسنده , , Danielle and Tanger، نويسنده , , Ellen and Buckle، نويسنده , , Tessa and Blom، نويسنده , , Marleen and Zevenhoven، نويسنده , , John and van Tellingen، نويسنده , , Olaf and van Lohuizen، نويسنده , , Maarten، نويسنده ,
Abstract :
Summary
lycomb group and oncogene Bmi1 is required for the proliferation of various differentiated cells and for the self-renewal of stem cells and leukemic cancer stem cells. Repression of the Ink4a/Arf locus is a well described mechanism through which Bmi1 can exert its proliferative effects. However, we now demonstrate in an orthotopic transplantation model for glioma, a type of cancer harboring cancer stem cells, that Bmi1 is also required for tumor development in an Ink4a/Arf-independent manner. Tumors derived from Bmi1;Ink4a/Arf doubly deficient astrocytes or neural stem cells have a later time of onset and different histological grading. Moreover, in the absence of Ink4a/Arf, Bmi1-deficient cells and tumors display changes in differentiation capacity.
