Bmi1 controls tumor development in an Ink4a/Arf-independent manner in a mouse model for glioma.

Autor: Bruggeman SW; Division of Molecular Genetics, The Netherlands Cancer Institute, 1066CX, Amsterdam, the Netherlands., Hulsman D, Tanger E, Buckle T, Blom M, Zevenhoven J, van Tellingen O, van Lohuizen M
Jazyk: angličtina
Zdroj: Cancer cell [Cancer Cell] 2007 Oct; Vol. 12 (4), pp. 328-41.
DOI: 10.1016/j.ccr.2007.08.032
Abstrakt: The Polycomb 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.
Databáze: MEDLINE