Senescence and tumour clearance is triggered by p53 restoration in murine liver carcinomas

By W. Xue, Lars Zender, C. Miething, R. Dickins, E. Hernando, V. Krizhanovsky, C. Cordon-Cardo, Scott W. Lowe. Nature, 2007

2,392 citations recorded by the source corpus.

Subfields: Biotechnology, Oncology, Physiology

View Paper: https://www.semanticscholar.org/paper/9736760f7a17ecf251e25e9b120be1f6b97a2655

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Citations in the corpus

Cellular senescence and its effector programs (2014, background): “Xue et al. (2007) first showed that senescent cells can also be eliminated in vivo.”
The tumor suppressor p53 regulates polarity of self-renewing divisions in mammary stem cells. (2009, background): “Therapeutic Efficacy of p53 Restoration in Cancer SCs Three groups have recently reported that re-expression of p53 causes regression of different p53 null tumors, including lymphomas, sarcomas, and hepatocellular carcinomas (Martins et al., 2006; Ventura et al., 2007; Xue et al., 2007).”
Mechanisms of Cellular Senescence: Cell Cycle Arrest and Senescence Associated Secretory Phenotype (2021, background): “…state and initiate tissue repair and regeneration by stimulating the nearby progenitor cells, or to stimulate the immune system to promote their immune clearance (Xue et al., 2007; Kang et al., 2011; Iannello et al., 2013; Tasdemir et al., 2016; von Kobbe, 2018; Mohamad Kamal et al., 2020).”
Awakening guardian angels: drugging the p53 pathway (2009, background): “A series of genetic models has, however, established that the restoration of p53 activity in established tumour cells is an exceptionally effective interventio”
Inflammatory Networks during Cellular Senescence: Causes and Consequences (2010, background): “In a mouse model of liver carcinoma, reactivation of p53 in tumor cells induces a senescence response in vivo; this response is followed by increases in expression of several inflammatory cytokines, which stimulate an infiltrating immune response to clear senescent tumor cells [41].”
Control of the senescence-associated secretory phenotype by NF-κB promotes senescence and enhances chemosensitivity. (2011, background): “…that are associated with chromatin modifications that, in some cell types, lead to marked changes in the binding of transcription factors and other chromatin modifiers, including RB, p53, and the high-mobility group A proteins (HMGA1 and HMGA2) (Narita et al. 2003, 2006; Zhang et al. 2007).”
Senescence-messaging secretome: SMS-ing cellular stress (2009, background): “For instance, in a mouse model of liver carcinoma driven by inducible shRNA-mediated depletion of p53 and HRAS V12 expression, Scott Lowe's laboratory showed that reactivation of p53 in the tumour results in a robust senescence respons”
Ca2+ signalling checkpoints in cancer: remodelling Ca2+ for cancer cell proliferation and survival (2008, background): “or that restoration of wild-type p53 causes tumour regressio”
Chemokine signaling via the CXCR2 receptor reinforces senescence. (2008, background): “Fac- tors secreted by senescent cells exert multiple effects on neighboring epithelial cells (Coppe et al., 2006; Krtolica et al., 2001; Parrinello et al., 2005) and direct the immune system to clear a senescent lesion (Xue et al., 2007).”