The epigenetic gene regulator BMI1 induces neural stem cell self-renewal in vitro and in vivo, a function that could be useful in regenerative medicine. However, increased expression of BMI1 in medulloblastoma, a brain tumour that can arise from cerebellar granule cell progenitors (CGPs), suggests that BMI1 is oncogenic in some circumstances. Behesti et al. investigated this possibility by generating transgenic mice that overexpress Bmi1 in the granule cell lineage. Bmi1 overexpression in CGPs decreased cerebellar size by decreasing CGP proliferation, whereas its overexpression in postmitotic granule cells improved cell survival under stress. No medulloblastomas developed in the transgenic mice, but Bmi1 overexpression in a Trp53−/− background produced a low incidence of medulloblastomas. Thus, BMI1 overexpression is not sufficient to induce neoplastic transformation but can improve neuronal survival under stress. These results have implications for regenerative therapies. Page 49
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IN THIS ISSUE| 01 January 2013
Bmi1, medulloblastoma and regenerative therapy
Online Issn: 1754-8411
Print Issn: 1754-8403
Written by Jane Bradbury. © 2012. Published by The Company of Biologists Ltd.
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial Share Alike License (http://creativecommons.org/licenses/by-nc-sa/3.0), which permits unrestricted non-commercial use, distribution and reproduction in any medium provided that the original work is properly cited and all further distributions of the work or adaptation are subject to the same Creative Commons License terms.
Dis Model Mech (2013) 6 (1): 1.
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Bmi1, medulloblastoma and regenerative therapy. Dis Model Mech 1 January 2013; 6 (1): 1. doi:
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