Pten dependence distinguishes haematopoietic stem cells from leukaemia-initiating cells

By Ömer H. Yilmaz, R. Valdez, Brian K. Theisen, Wei Guo, D. Ferguson, Hong Wu, S. Morrison. Nature, 2006

1,334 citations recorded by the source corpus.

Subfields: Molecular Biology

View Paper: https://www.semanticscholar.org/paper/eda6ec35aa01090b537e83706b93cab79b00c52b

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In Molecular Biology

1. David M. Sabatini
2. J. Massagué
3. Zena Werb
4. M. Laplante
5. S. Morrison
6. M. Clarke
7. R. DePinho
8. Hongjun Song

Citations in the corpus

• Leptin Receptor-expressing mesenchymal stromal cells represent the main source of bone formed by adult bone marrow (2014, neutral): “PTEN Regulates Quiescence, Maintenance, and Differentiation of LepR Cells Pten is cell-autonomously required for the maintenance of HSCs (Kalaitzidis et al., 2012; Lee et al., 2010; Magee et al., 2012; Yilmaz et al., 2006; Zhang et al., 2006) and neural stem cells (Bonaguidi et al.”
• The Cancer Stem Cell Niche: How Essential is the Niche in Regulating Stemness of Tumor Cells? (2015, neutral): “Although the histological evidence of leukemia persisted, the mice were overtly healthy (Yilmaz et al., 2006).”
• Phenotypic heterogeneity among tumorigenic melanoma cells from patients that is reversible and not hierarchically organized (2010, background): “…Jamieson et al., 2004; Neering et al., 2007; Oravecz-Wilson et al., 2009) and acute myeloid leukemias (Bonnet and Dick, 1997; Lapidot et al., 1994; Yilmaz et al., 2006) do follow a cancer stem cell model in which leukemogenic cells are rare, phenotypically distinct from the vast majority of other…”
• mTOR signaling in growth control and disease (2012, positive): “This result confirmed previous observations showing that inhibition of mTORC1 prevents stem cell exhaustion and increases stem cell function in vivo (Castilho et al., 2009; Yilmaz et al., 2006).”
• Metabolic regulation of hematopoietic stem cells in the hypoxic niche. (2011, background): “In contrast, deletion of Pten, a PIP3 phosphatase, induces constitutively activated PI3K/Akt signaling, resulting in an accelerated cell cycle, and eventually leads to HSC exhaustion (Yilmaz et al., 2006; Zhang et al., 2006).”