Evidence map›Paper›PMID 24381013›Full record

ArticleCarcinogenesis2014

Understanding the non-canonical pathways involved in p53-mediated tumor suppression.

Kayla M Hager, Wei Gu

Open access · bronzeAbstract read
In one paragraph

Article in Carcinogenesis, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
2.5field-weighted citation impact, top 10% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

38 citing papers in PubMed, 72 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Kayla M HagerDepartment of Pathology and Cell Biology, Institute for Cancer Genetics and.
Wei Gu
Cancer Genetics (United States) · US

Funding

PW1--A mediator of cell survival by NFKB and cell death by p53P01CA080058 · NCI · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI AARONSON, STUART A · 2000 to 2016
$20.2M
Regulation of Mdmx stability and subcellular localization by ubiquitinationR01CA166294 · NCI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI GU, WEI · 2012 to 2016
$1.5M
NCI NIH HHS 5R01 CA166294NCI NIH HHS P01 CA080058NCI NIH HHS P01CA080058NCI NIH HHS R01 CA166294
6 · The paper itself

Abstract

In the last three decades since the discovery of p53, it has become increasingly apparent that p53 plays a very important role in tumor suppression. Previously, it was thought that the tumor suppressive functions lied solely in the canonical p53-mediated apoptosis, cell cycle arrest and senescence. However, more recent research has shown that anti-oncogenic activity of p53 can still occur in the absence of these downstream functions. These results suggest that more non-canonical roles of p53 may have a much larger impact on other p53-regulated programs then initially anticipated. Recently, the non-canonical activities of p53 such as cell metabolism, autophagy and necrosis have been the subject of intense study. p53 affects many aspects of cellular metabolism including catabolism, anabolism and reactive oxygen species levels. p53 has a dual role in autophagy regulation. Initiation of autophagy occurs through direct transcription of pro-autophagy genes and inhibition transpires through a transcription-independent mechanism. The role of p53 in these cellular processes is quite complex and evidence suggests that p53 can play both a pro- and anti-oncogenic role in these non-conical pathways. Despite of more than 60,000 publications on p53 in the literature, the mechanisms for p53-mediated tumor suppression apparently needs to be further elucidated.

Indexed as

Genes, p53Genes, Tumor SuppressorAutophagyHumansNeoplasms

Identifiers

PMID24381013
PMCPMC3977149
OpenAlexW2119823095

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.