The tumor suppressor p53 regulates polarity of self-renewing divisions in mammary stem cells.
By Angelo Cicalese, G. Bonizzi, C. Pasi, M. Faretta, S. Ronzoni, B. Giulini, C. Brisken, S. Minucci, Pier Paolo Di Fiore, Pier Giuseppe Pelicci. Cell, 2009
746 citations recorded by the source corpus.
Subfields: Cell Biology, Oncology
View Paper: https://www.semanticscholar.org/paper/d70d24c4ecc55561e103148a3f1107e2e6826041
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Citations in the corpus
- Cancer stem cells: current status and evolving complexities. (2012, background): “…has elicited a response against putative CSCs. undergo more frequent symmetrical division than normal mammary stem cells in mammosphere cultures (Cicalese et al., 2009), it is tempting to speculate that the long period between primary tumor detection and relapse in patients with ER-positive…”
- Cancer heterogeneity—a multifaceted view (2013, positive): “Reciprocally, genetic mutations such as inactivation of TP53 can influence the CSC content [45].”
- BRCA1 basal-like breast cancers originate from luminal epithelial progenitors and not from basal stem cells. (2010, background): “It is formally possible that use of the p53 heterozygote background in the tumor models may alter the predicted cell type specificity of the promoters used to drive Cre expression, given the role of p53 in controlling polarity in mammary stem cell division (Cicalese et al., 2009).”
- Biological and molecular heterogeneity of breast cancers correlates with their cancer stem cell content. (2010, background): “We have previously shown that skewing self-renewal division from an asymmetric (one stem / one stem + one progenitor) to a symmetric (one stem / two stems) mode is a critical step in a model of murine mammary cancerogenesis (Cicalese et al., 2009).”
- Notch signalling in solid tumours: a little bit of everything but not all the time (2011, background): “that can self-renew symmetrically or that can divide asymmetrically to produce daughter cells that continue to proliferate and so sustain tumour growt”
- Senescence impairs successful reprogramming to pluripotent stem cells. (2009, background): “Related mechanisms may exist, as shown by the fact that p53 loss increases the pool of CSCs by promoting the symmetrical cell divisions of cancer stem cells (Cicalese et al., 2009).”