Proliferation, cell cycle and apoptosis in cancer

By G. Evan, Karen H. Vousden. Nature, 2001

3,534 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/434eb48cfa6e631c9b04b793ca2e827a2d29dc97

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Citations in the corpus

Death and anti-death: tumour resistance to apoptosis (2002, positive): “This assumption is confirmed by the finding that deregulated proliferation alone is not sufficient for tumour formation, but leads to cell death (reviewed in Ref”
Scatter-factor and semaphorin receptors: cell signalling for invasive growth (2002, background): “On the one hand, cancer cells must proliferate to expand the colonizing population, migrate to reach remote targets, and survive to limit attrition and senescenc”
Transcription factor YY1: structure, function, and therapeutic implications in cancer biology (2006, background): “Moreover, the same molecular components are targets for oncogenic changes that frequently drive cell proliferation to cooperate with those that uncouple proliferation from apoptosis during transformation and tumorigenesis (Evan and Vousden, 2001; Fridman and Lowe, 2003).”
FK866, a highly specific noncompetitive inhibitor of nicotinamide phosphoribosyltransferase, represents a novel mechanism for induction of tumor cell apoptosis. (2003, background): “Deregulation of apoptosis is consequently associated with various diseases like cancer and immune dysfunction (6, 7).”
Survivin, versatile modulation of cell division and apoptosis in cancer (2003, background): “This is consistent with the general paradigm that deregulated apoptosis inhibition contributes to malignancy by favoring the accumulation of additional ‘cancer traits’ (Hanahan and Weinberg, 2000), codifying more aggressive disease behaviors (Evan and Vousden, 2001).”
Control of apoptosis by p53 (2003, background): “However, as indicated above, p53 is now known to act in many cellular processes, including cell-cycle checkpoints, DNA repair, senescence, angiogenesis, surveillance of genomic integrity, and apoptosis (Ko and Prives, 1996; Evan and Vousden, 2001).”
Live or let die: the cell's response to p53 (2002, background): “Yet, our increasing understanding of the molecular evolution of the cancer cell has revealed that many of the alterations that make a cell malignant and dangerous, such as oncogene-driven deregulated proliferation and invasion, are hard-wired to signals that prevent cell growth — in many cases, by s”
Ovarian cancer: strategies for overcoming resistance to chemotherapy (2003, background): “A number of oncogenic transcription factors — such as c-MYC, c-JUN and c-FOS — have also been shown to alter the threshold for apoptosis, to be involved in the response to paclitaxel and cisplatin in vitro , and have been implicated in resistanc”
A Review on a Deep Learning Perspective in Brain Cancer Classification (2019, background): “(i) The first category is known as tumor suppressors that controls the cell death cycle (apoptosis) [14].”
p63 and p73 are required for p53-dependent apoptosis in response to DNA damage (2002, background): “jpg" NDATA ITEM> ]> The tumour-suppressor gene p53 is frequently mutated in human cancers and is important in the cellular response to DNA damage”
Acetylation of the C terminus of Ku70 by CBP and PCAF controls Bax-mediated apoptosis. (2004, neutral): “Here, we identify eight by apoptosis (reviewed by Evan and Vousden, 2001).”