Crucial role of p53-dependent cellular senescence in suppression of Pten-deficient tumorigenesis

By Zhenbang Chen, L. Trotman, D. Shaffer, Hui-Kuan Lin, Z. Dotan, M. Niki, J. Koutcher, H. Scher, T. Ludwig, W. Gerald and 2 more. Nature, 2005

2,078 citations recorded by the source corpus.

Subfields: Molecular Biology, Oncology, Physiology

View Paper: https://www.semanticscholar.org/paper/a35e3598a0f91dd62798b950d3e09243fdcd9050

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Citations in the corpus

The essence of senescence. (2010, background): “The first demonstration of tumor suppressor (PTEN) loss-induced senescence in vivo (Chen et al. 2005) is discussed below.”
PI3K pathway alterations in cancer: variations on a theme (2008, positive): “This could be due to higher expression of redundant negative regulators of this pathway such as the lipid phosphatases, SHIP and INPP4B, or due to the fact that mutations in this pathway without prior loss of p53 result in senescence (Chen et al., 2005).”
Oncogenic mutations of PIK3CA in human cancers. (2004, background): “This was especially intriguing because of the widespread belief that hyperactivation of oncogenic signaling pathways such as PI3K can thwart cancer pathogenesis by inducing p53-dependent senescence (Chen et al. 2005; Kim et al. 2007).”
The PTEN–PI3K pathway: of feedbacks and cross-talks (2008, background): “Indeed, acute Pten loss in the hematopoietic stem cell compartment leads to exhaust of the hematopoietic stem cell (Yilmaz et al., 2006; Zhang et al., 2006b) and acute Pten loss in the prostate leads to a strong p53-dependent senescence response that opposes cancer progression (Chen et al., 2005).”
Cellular Senescence: Aging, Cancer, and Injury. (2019, background): “For instance, we discussed previously in this review that Stat3 regulates the SASP of PICS, promoting an immunosuppressive tumor microenvironment (sect.”
Plasminogen activator inhibitor-1 is a critical downstream target of p53 in the induction of replicative senescence (2006, positive): “It has been reported that the levels of PTEN are crucial in determining the senescence response of fibroblasts — partial loss of PTEN confers a proliferative advantage, whereas acute loss of all PTEN induces senescenc”
Four faces of cellular senescence (2011, positive): “…al., 1991; Shay et al., 1991; Bond et al., 1994; Lin et al., 1998; Schmitt et al., 2002; Beauséjour et al., 2003; Collins and Sedivy, 2003; Oren, 2003; Herbig et al., 2004; Jacobs and de Lange, 2004; Ohtani et al., 2004; Chen et al., 2005; Campisi and d’Adda di Fagagna, 2007; Rodier et al., 2007).”
Induction of EMT by twist proteins as a collateral effect of tumor-promoting inactivation of premature senescence. (2008, background): “Indeed, senescence occurs in vivo in precancerous lesions in response to aberrant mitogenic signaling, and its inactivation is required for progression toward malignancy (Chen et al., 2005; Michaloglou et al., 2005; Collado et al., 2005).”
Mitochondrial Dysfunction Accounts for the Stochastic Heterogeneity in Telomere-Dependent Senescence (2007, positive): “Such an idea is fully consistent with the suggestion that replicative senescence serves a pleiotropic role in aging as an anti-cancer mechanism [13] for which there is growing evidence [14–17], since the damage that triggers senescence would otherwise pose an increased risk of malignancy.”