Intrinsic tumour suppression

By Scott W. Lowe, E. Cepero, G. Evan. Nature, 2004

1,382 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/f699a2e9854fc2ebf43a70d9122898c6b691a913

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Citations in the corpus

Hallmarks of cancer: the next generation. (2011, positive): “Although the cellular conditions that trigger apoptosis remain to be fully enumerated, several abnormality sensors that play key roles in tumor development have been identified (Adams and Cory, 2007; Lowe et al., 2004).”
Metastasis: a question of life or death (2006, background): “The classic view is that the induction of apoptosis is important because it limits the time available for the accumulation of tumorigenic alterations, and because it balances the pro-oncogenic potential of many proto-oncogenes like MYC”
Identification and validation of oncogenes in liver cancer using an integrative oncogenomic approach. (2006, background): “In any case, the antiapoptotic activity of cIAP1 would be unlikely to cooperate with Akt or Ras, which already transmit prosurvival signals (Lowe et al., 2004).”
Tumour suppression by p53: a role for the DNA damage response? (2009, background): “jpg" NDATA ITEM> ]> p53 is a short-lived transcription factor that has been most extensively studied in its capacity to mediate innate tumour suppression”
DNA damage response as a candidate anti-cancer barrier in early human tumorigenesis (2005, methodology): “To validate this concept for early tumorigenesis in vivo, three predictions should be verified: (1) tumorigenic abnormalities that deregulate entry into S phase must occur with high frequency; (2) there should be evidence for replicational stress; and (3) activation of a functional checkpoint should”
microRNAs join the p53 network — another piece in the tumour-suppression puzzle (2007, background): “jpg" NDATA ITEM> ]> Three decades of intensive investigation have placed p53 at the center of a complex molecular network regulating diverse physiological responses to cancer-related stresse”
Oncogene-induced senescence relayed by an interleukin-dependent inflammatory network. (2008, background): “Several mechanisms including apoptosis and lack of vessel formation account for their failure to continue expanding and undergo full malignant transformation (Lowe et al., 2004; Sherr, 2004).”
Hippo signaling in organ size control. (2007, background): “In most circumstances, these two processes are coupled in a manner so that unscheduled cell proliferation, such as that caused by myc activation, is countered by increased cell death (for review, see Lowe et al. 2004).”
Chemokine signaling via the CXCR2 receptor reinforces senescence. (2008, background): “Senescence is therefore a first-line defense against potentially dangerous mutations (Lowe et al., 2004), locking the afflicted cells into a permanent state of arrest (Mooi and Peeper, 2006).”
Senescence in tumours: evidence from mice and humans (2010, background): “In this manner, the concept of oncogene-induced senescence emerged as a putative tumour suppressor mechanism, similar to the better known phenomenon of oncogene-induced apoptosi”
Tumor heterogeneity: causes and consequences (2009, background): “These mechanisms include intrinsic tumor-suppressive mechanisms, wherein activation of strong oncogenes triggers activation of tumor-suppressive networks, resulting in senescence or death of mutated cells [127].”