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We are analyzing https://www.nature.com/articles/s41420-020-0251-x.

Title:
Context is everything: extrinsic signalling and gain-of-function p53 mutants | Cell Death Discovery
Description:
The TP53 genomic locus is a target of mutational events in at least half of cancers. Despite several decades of study, a full consensus on the relevance of the acquisition of p53 gain-of-function missense mutants has not been reached. Depending on cancer type, type of mutations and other unidentified factors, the relevance for tumour development and progression of the oncogenic signalling directed by p53 mutants might significantly vary, leading to inconsistent observations that have fuelled a long and fierce debate in the field. Here, we discuss how interaction with the microenvironment and stressors might dictate the gain-of-function effects exerted by individual mutants. We report evidence from the most recent literature in support of the context dependency of p53 mutant biology. This perspective article aims to raise a discussion in the field on the relevance that context might have on p53 gain-of-function mutants, assessing whether this should generally be considered a cell non-autonomous process.
Website Age:
30 years and 10 months (reg. 1994-08-11).

Matching Content Categories {📚}

  • Education
  • Telecommunications
  • Science

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Custom-built

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🌠 Phenomenal Traffic: 5M - 10M visitors per month


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How Much Does Nature.com Make? {💰}


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$63,100 per month
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Keywords {🔍}

pubmed, mutant, google, scholar, cell, cas, cancer, death, mutants, gof, central, cells, nature, differ, mutations, tumour, effects, protein, context, expression, mechanisms, article, microenvironment, proteins, response, extrinsic, amelio, molecular, cellular, factors, stability, tumor, signalling, function, evidence, models, dna, fig, functional, stabilisation, activation, rhoa, content, gainoffunction, interaction, stressors, human, factor, transcriptional, regulation,

Topics {✒️}

nature portfolio privacy policy medical research council advertising nature 493 nature 358 nature 523 nature reprints simplistic cell-autonomous model tumour development cell death discovery empower tgfbeta-induced metastasis author information authors p53-dependent tumor suppression genetically engineered mice p53 mutant-mediated promotion p53-mediated tumor suppression p53-dependent metabolic remodelling social media conditioned media drug development vitro soft-agar assays p53-mutated cancer cells n-glycosylated membrane proteins functional wild-type version generally accepted consideration p53-mediated tumour suppression mutant p53-depedent signalling permissions author correspondence original author tp53 missense mutations feed-forward loop p53 missense mutations wild-type functional protein human breast cancer function missense mutants pluripotency factor foxh1 human breast cancers57 pro-metastatic programme hypoxia-inducible factor-1 ivano amelio breast cancer cells perspective article aims e2f2 transcriptional factor mouse model mechanosensitive hdac6 deacetylase published maps mutant p53 activity

Questions {❓}

  • Can microenvironmental factors be targeted to abolish mutant p53 GOF pro-oncogenic functions?
  • Do mutations turn p53 into an oncogene?
  • Do p53 mutants need to be activated?
  • How does p53 induce apoptosis and how does this relate to p53-mediated tumour suppression?
  • How mutant p53 empowers Foxh1 fostering leukaemogenesis?
  • How relevant is the microenvironmental context in determining mutant p53 GOF effects?
  • TP53: the unluckiest of genes?
  • What is the effective contribution of mutant p53 GOF effects to the cancer progression?
  • P53 protects cells from insults: why do cancers want to lose this benefit?

Schema {🗺️}

WebPage:
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         headline:Context is everything: extrinsic signalling and gain-of-function p53 mutants
         description:The TP53 genomic locus is a target of mutational events in at least half of cancers. Despite several decades of study, a full consensus on the relevance of the acquisition of p53 gain-of-function missense mutants has not been reached. Depending on cancer type, type of mutations and other unidentified factors, the relevance for tumour development and progression of the oncogenic signalling directed by p53 mutants might significantly vary, leading to inconsistent observations that have fuelled a long and fierce debate in the field. Here, we discuss how interaction with the microenvironment and stressors might dictate the gain-of-function effects exerted by individual mutants. We report evidence from the most recent literature in support of the context dependency of p53 mutant biology. This perspective article aims to raise a discussion in the field on the relevance that context might have on p53 gain-of-function mutants, assessing whether this should generally be considered a cell non-autonomous process.
         datePublished:2020-03-23T00:00:00Z
         dateModified:2020-03-23T00:00:00Z
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      headline:Context is everything: extrinsic signalling and gain-of-function p53 mutants
      description:The TP53 genomic locus is a target of mutational events in at least half of cancers. Despite several decades of study, a full consensus on the relevance of the acquisition of p53 gain-of-function missense mutants has not been reached. Depending on cancer type, type of mutations and other unidentified factors, the relevance for tumour development and progression of the oncogenic signalling directed by p53 mutants might significantly vary, leading to inconsistent observations that have fuelled a long and fierce debate in the field. Here, we discuss how interaction with the microenvironment and stressors might dictate the gain-of-function effects exerted by individual mutants. We report evidence from the most recent literature in support of the context dependency of p53 mutant biology. This perspective article aims to raise a discussion in the field on the relevance that context might have on p53 gain-of-function mutants, assessing whether this should generally be considered a cell non-autonomous process.
      datePublished:2020-03-23T00:00:00Z
      dateModified:2020-03-23T00:00:00Z
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         Cancer genetics
         Tumour-suppressor proteins
         Life Sciences
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         Cell Biology
         Stem Cells
         Apoptosis
         Cell Cycle Analysis
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      name:School of Life Sciences, University of Nottingham, Nottingham, UK
      name:Department of Experimental Medicine, TOR, University of Rome ’’Tor Vergata”, Rome, Italy
      name:Toxicology Unit, University of Cambridge, Department of Pathology, Cambridge, UK

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