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Open AccessJournal ArticleDOI

Live or let die: the cell's response to p53

TLDR
Understanding the complex mechanisms that regulate whether or not a cell dies in response to p53 will ultimately contribute to the development of therapeutic strategies to repair the apoptotic p53 response in cancers.
Abstract
Compared with many normal tissues, cancer cells are highly sensitized to apoptotic signals, and survive only because they have acquired lesions — such as loss of p53 — that prevent or impede cell death. We are now beginning to understand the complex mechanisms that regulate whether or not a cell dies in response to p53 — insights that will ultimately contribute to the development of therapeutic strategies to repair the apoptotic p53 response in cancers.

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Mitochondrial Membrane Permeabilization in Cell Death

TL;DR: Once MMP has been induced, it causes the release of catabolic hydrolases and activators of such enzymes (including those of caspases) from mitochondria, meaning that mitochondria coordinate the late stage of cellular demise.
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Robbins and Cotran pathologic basis of disease

TL;DR: The pathologic basis of disease is determined by X-ray diffraction analysis of the granuloma with an Higgs–Cotran–Bouchut–Seiden ratio of 3:1.
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Malignant astrocytic glioma: genetics, biology, and paths to treatment.

TL;DR: The recent confluence of advances in stem cell biology, cell signaling, genome and computational science and genetic model systems have revolutionized understanding of the mechanisms underlying the genetics, biology and clinical behavior of glioblastoma.
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Integrating cell-signalling pathways with NF-kappaB and IKK function.

TL;DR: This work has shown that crosstalk constitutes a decision-making process that determines the consequences of NF-κB and IKK activation and, ultimately, cell fate.
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p53 in health and disease.

TL;DR: It is now becoming clear that p53 can have a much broader role and can contribute to the development, life expectancy and overall fitness of an organism.
References
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Journal ArticleDOI

WAF1, a potential mediator of p53 tumor suppression

TL;DR: A gene is identified, named WAF1, whose induction was associated with wild-type but not mutant p53 gene expression in a human brain tumor cell line and that could be an important mediator of p53-dependent tumor growth suppression.
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Surfing the p53 network

TL;DR: The p53 tumour-suppressor gene integrates numerous signals that control cell life and death, and the disruption of p53 has severe consequences when a highly connected node in the Internet breaks down.
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Tumor suppressor p53 is a direct transcriptional activator of the human bax gene

TL;DR: The bax gene promoter region contains four motifs with homology to consensus p53-binding sites and wild-type but not mutant p53 protein bound to oligonucleotides corresponding to this region of the bax promoter, suggesting that bax is a p53 primary-response gene, presumably involved in a p 53-regulated pathway for induction of apoptosis.
Journal Article

Mutations in the p53 Tumor Suppressor Gene: Clues to Cancer Etiology and Molecular Pathogenesis

TL;DR: The p53 tumor suppressor gene has become a paradigm in cancer research because it is commonly mutated in human cancer and the spectrum of p53 mutations in these cancers is providing clues to the etiology and molecular pathogenesis of neoplasia as discussed by the authors.
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Proliferation, cell cycle and apoptosis in cancer

TL;DR: Deregulated cell proliferation provides a minimal 'platform' necessary to support further neoplastic progression and should be targeted withroit targeting to have potent and specific therapeutic consequences.
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