Evidence map›Paper›PMID 12362272›Full record

ReviewOncogene2002

The p53 network in lung carcinogenesis.

Ana I Robles, Steven P Linke, Curtis C Harris

Open access · bronzeAbstract readReview
PubMed Publisher
In one paragraph

Review in Oncogene, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed, 2 pooled it
4.4field-weighted citation impact, top 5% 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

44 citing papers in PubMed, 2 syntheses or guidelines pooled it, 136 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
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  6. Review
  7. Article
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  11. Uncovering the Anti-Lung-Cancer Mechanisms of the Herbal Drug FDY2004 by Network Pharmacology.Evidence-based complementary and alternative medicine : eCAM · 2021
    Article
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  16. Review
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  18. Association ofBiomedical reports · 2015
    Article
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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

3 authors at 2 institutions in 1 country.

Ana I RoblesLaboratory of Human Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA.
Steven P Linke
Curtis C Harris
National Cancer Institute · USNational Institutes of Health · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The p53 tumor suppressor gene lies at the crossroads of multiple cellular response pathways that control a cell's fate in response to endogenous or exogenous stresses. Positive and negative regulatory loops both upstream and downstream of p53 cooperate to finely tune its functions as a transcription factor, a DNA damage sensor, and possibly, a protein-assembly scaffold. Through this plethora of activities, p53 is a major determinant of cell survival and a safeguard against genetic instability. Functional inactivation of p53 pathways through genetic and epigenetic events affecting the p53 gene itself and/or its interacting partners occur with a high frequency in lung cancer. The p53 mutational spectrum provides molecular evidence of the etiology of lung cancer and supports abundant epidemiological data indicating the role of tobacco smoke in the causation of this disease.

Indexed as

Genes, p53Cell Transformation, NeoplasticCodonHumansLung NeoplasmsMutationPolymorphism, GeneticCodon

Identifiers

PMID12362272
OpenAlexW2327358714

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.