Bmi1 controls tumor development in an Ink4a/Arf-independent manner in a mouse model for glioma - PubMed (original) (raw)
Bmi1 controls tumor development in an Ink4a/Arf-independent manner in a mouse model for glioma
Sophia W M Bruggeman et al. Cancer Cell. 2007 Oct.
Free article
Abstract
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.
Comment in
- Bmi1 and cell of origin determinants of brain tumor phenotype.
Dirks P. Dirks P. Cancer Cell. 2007 Oct;12(4):295-7. doi: 10.1016/j.ccr.2007.10.003. Cancer Cell. 2007. PMID: 17936553
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