Bmi-1 determines the proliferative capacity of normal and leukaemic stem cells
By J. Lessard, G. Sauvageau. Nature, 2003
1,603 citations recorded by the source corpus.
Subfields: Molecular Biology, Oncology
View Paper: https://www.semanticscholar.org/paper/478a43c77a33d02af638d3d53e3ccffa413fb671
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Citations in the corpus
- Tumour-initiating cells: challenges and opportunities for anticancer drug discovery (2009, background): “Several studies show that BMI1 polycomb ring finger oncogene ( BMI1 ) and the Wnt signalling molecule β-catenin regulate the self-renewal of haematopoietic stem cells (HSCs) and the proliferation of leukaemia-initiating cell”
- SSEA-1 Is an Enrichment Marker for Tumor-Initiating Cells in Human Glioblastoma (2009, background): “Similar to the GBM lines containing CD133+ cells, these cell lines are highly tumorigenic, grew as neurospheres (see Figure S1A available online), and expressed high levels of stem cell-associated proteins such as Nestin (Lendahl et al., 1990), Sox2 (Suh et al., 2007; Yuan et al., 1995), Bmi1 (Lessa”
- Hmga2 promotes neural stem cell self-renewal in young, but not old, mice by reducing p16Ink4a and p19Arf expression (2008, background): “Bmi-1-deficient mice are born with normal numbers of stem cells but exhibit postnatal self-renewal defects that lead to the depletion of adult stem cells (Lessard and Sauvageau, 2003; Molofsky et al., 2003; Park et al., 2003).”
- Bmi1 is essential for cerebellar development and is overexpressed in human medulloblastomas (2004, background): “This extends the recently reported essential role of Bmi1 in renewal of adult haematopoietic stem cell”
- Regulation of the INK4b–ARF–INK4a tumour suppressor locus: all for one or one for all (2006, background): “More detailed analyses of the neurological and haematological problems encountered in Bmi1 −/− mice revealed that one of the underlying reasons is a failure in the self-renewal capacity of the relevant stem cells, rather than a failure of these cells to give rise to differentiated progen”
- 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).”
- Slug and Sox9 Cooperatively Determine the Mammary Stem Cell State (2012, background): “Although accumulating evidence has begun to support this notion (Dick, 2008; Lessard and Sauvageau, 2003; Lobo et al., 2007; Reya et al., 2001; Shimono et al., 2009), direct evidence has remained scarce thus far.”
- Therapeutic implications of cancer stem cells. (2004, background): “Post-natal mice deficient in the expression of Bmi-1 display failure of hematopoiesis and fetal liver and bone marrow stem cells from Bmi / mice are able to contribute to recipient hematopoiesis only transiently indicating a primary defect in adult HSC self-renewal [14 ,15,16 ].”
- MLL translocations, histone modifications and leukaemia stem-cell development (2007, background): “Gene_RVDocSum">PRC1 that binds H3K27 marks) in HSC, point to a fine balance between the action of TrxG proteins that maintain and PcG proteins that suppress transcriptio”
- Plzf is required in adult male germ cells for stem cell self-renewal (2004, background): “BMI1 is required to maintain adult self-renewing hematopoietic and leukemic stem cell”
- Tissue repair and stem cell renewal in carcinogenesis (2004, methodology): “Consistent with this model, the Bmi-1 gene required for HSC renewal is also required for the propagation of leukaemias in transfer experiment”
- An essential switch in subunit composition of a chromatin remodeling complex during neural development. (2007, background): “, 2003) and hemopoietic stem cells (Lessard and Sauvageau, 2003; Park et al., 2003).”