Bmi1 is essential for cerebellar development and is overexpressed in human medulloblastomas

By C. Leung, Merel Lingbeek, O. Shakhova, James Liu, Ellen Tanger, P. Saremaslani, Maarten van Lohuizen, S. Marino. Nature, 2004

596 citations recorded by the source corpus.

Subfields: Molecular Biology

View Paper: https://www.semanticscholar.org/paper/c76fd1c659af76aeceee1158a4cf9a2007277022

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In Molecular Biology

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Citations in the corpus

• Bmi-1 promotes neural stem cell self-renewal and neural development but not mouse growth and survival by repressing the p16Ink4a and p19Arf senescence pathways. (2005, background): “C; van der Lugt et al. 1994; Leung et al. 2004).”
• Regulation of the INK4b–ARF–INK4a tumour suppressor locus: all for one or one for all (2006, background): “Similarly, although it has been shown that BMI1 expression is activated by Sonic hedgehog signalling during cerebellar developmen”
• Microarray analysis identifies a death-from-cancer signature predicting therapy failure in patients with multiple types of cancer. (2005, result): “Consistent with our findings, an increased BMI-1 expression in human medulloblastomas was demonstrated in a recent study (37).”
• The Polycomb group proteins bind throughout the INK4A-ARF locus and are disassociated in senescent cells. (2007, background): “…of both adult (hematopoetic and neural) and cancer stem cell populations (Lessard and Sauvageau 2003; Molofsky et al. 2003; Park et al. 2003; Leung et al. 2004), and this has primarily been attributed to its ability to repress the Ink4a-Arf locus (Bruggeman et al. 2005; Molofsky et al.…”
• Stem cells and cancer: two faces of eve. (2006, background): “For example, Sonic hedgehog (Shh) signaling, which has been implicated in the self-renewal of stem cells in both the brain and blood, can upregulate Bmi1 expression in primitive neural stem or progenitor cells (Leung et al., 2004).”
• Bmi1 is essential in Twist1-induced epithelial–mesenchymal transition (2010, background): “, and overexpression of BMI1 is frequently observed in tumour-initiating cell”
• The biology of cancer stem cells. (2007, background): “It is likely that some oncogenic mutations, such as the activation of Bmi-1 or the inactivation of some of its downstream targets, play a role in cancer stem cell maintenance.”
• Gene silencing in cancer by histone H3 lysine 27 trimethylation independent of promoter DNA methylation (2008, background): “BMI-1 is overexpressed frequently in human medulloblastoma cell lines and primary tumor”
• The intestinal stem cell. (2008, background): “The Bmi1 gene has recently attracted significant attention because of its role in selfrenewal of neuronal, hematopoietic, and leukemic cells (Lessard and Sauvageau 2003; Molofsky et al. 2003; Leung et al. 2004).”
• Mechanisms of stem cell self-renewal. (2009, background): “Nonetheless, this is not a black and white difference as granule precursor cells in the cerebellum and lymphocytes in the hematopoietic system also require Bmi-1 for their proliferation (Leung et al. 2004, van der Lugt et al. 1994).”
• Tissue repair and stem cell renewal in carcinogenesis (2004, background): “, is dependent on Hh pathway activity in Hh-dependent tumour”