Bmi1 controls tumor development in an Ink4a/Arf-independent manner in a mouse model for glioma
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. Howeve...
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| Published in: | Cancer cell Vol. 12; no. 4; p. 328 |
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| Main Authors: | , , , , , , , |
| Format: | Journal Article |
| Language: | English |
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United States
01.10.2007
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| ISSN: | 1535-6108 |
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| 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. |
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| AbstractList | 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.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. 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. |
| Author | van Lohuizen, Maarten van Tellingen, Olaf Hulsman, Danielle Buckle, Tessa Tanger, Ellen Zevenhoven, John Blom, Marleen Bruggeman, Sophia W M |
| Author_xml | – sequence: 1 givenname: Sophia W M surname: Bruggeman fullname: Bruggeman, Sophia W M organization: Division of Molecular Genetics, The Netherlands Cancer Institute, 1066CX, Amsterdam, the Netherlands – sequence: 2 givenname: Danielle surname: Hulsman fullname: Hulsman, Danielle – sequence: 3 givenname: Ellen surname: Tanger fullname: Tanger, Ellen – sequence: 4 givenname: Tessa surname: Buckle fullname: Buckle, Tessa – sequence: 5 givenname: Marleen surname: Blom fullname: Blom, Marleen – sequence: 6 givenname: John surname: Zevenhoven fullname: Zevenhoven, John – sequence: 7 givenname: Olaf surname: van Tellingen fullname: van Tellingen, Olaf – sequence: 8 givenname: Maarten surname: van Lohuizen fullname: van Lohuizen, Maarten |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/17936558$$D View this record in MEDLINE/PubMed |
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| SubjectTerms | 3T3 Cells Animals Astrocytes - metabolism Astrocytes - pathology Brain Neoplasms - genetics Brain Neoplasms - metabolism Brain Neoplasms - pathology Cell Differentiation Cell Proliferation Cell Transformation, Neoplastic - metabolism Cell Transformation, Neoplastic - pathology Cells, Cultured Cyclin-Dependent Kinase Inhibitor p16 - deficiency Cyclin-Dependent Kinase Inhibitor p16 - genetics Cyclin-Dependent Kinase Inhibitor p16 - metabolism Gene Expression Regulation, Neoplastic Glioblastoma - genetics Glioblastoma - metabolism Glioblastoma - pathology Mice Mice, Inbred BALB C Mice, Knockout Mice, Nude Mutation Neoplasm Staging Neoplasms, Experimental - metabolism Neoplasms, Experimental - pathology Neurons - metabolism Neurons - pathology Nuclear Proteins - deficiency Nuclear Proteins - genetics Nuclear Proteins - metabolism Phenotype Polycomb Repressive Complex 1 Proto-Oncogene Proteins - deficiency Proto-Oncogene Proteins - genetics Proto-Oncogene Proteins - metabolism Receptor, Epidermal Growth Factor - genetics Receptor, Epidermal Growth Factor - metabolism Repressor Proteins - genetics Repressor Proteins - metabolism Signal Transduction - genetics Stem Cells - metabolism Stem Cells - pathology Time Factors Transduction, Genetic |
| Title | Bmi1 controls tumor development in an Ink4a/Arf-independent manner in a mouse model for glioma |
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