Evidence map›Paper›PMID 12746555›Full record

ReviewMolecular biotechnology2003

Clinical implication of p53 mutation in lung cancer.

Barbara G Campling, Wafik S El-Deiry

Abstract readReview
PubMed Publisher
In one paragraph

Review in Molecular biotechnology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

23 citing papers in PubMed, 63 citations in OpenAlex.

  1. The therapeutic potential of RNA m(6)A in lung cancer.Cell communication and signaling : CCS · 2024
    Review
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  14. [P53 family proteins provide new insights into lung carcinogenesis and clinical treatment].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2013
    Review
  15. Article
  16. Allele specific gain-of-function activity of p53 mutants in lung cancer cells.Biochemical and biophysical research communications · 2012
    Article
  17. 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

2 authors at 1 institution in 1 country.

Barbara G CamplingUniversity of Pennsylvania, School of Medicine, Clinical Research Buiding 437A, 415 Curie Blvd, Philadelphia, PA 19104, USA.
Wafik S El-Deiry
University of Pennsylvania · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lung cancer development involves multiple genetic abnormalities leading to malignant transformation of the bronchial epithelial cells, followed by invasion and metastasis. One of the most common changes is mutation of the p53 tumor suppressor gene. The frequency of p53 alterations in lung cancer is highest in small cell and squamous cell carcinomas. A genetic "signature" of the type of p53 mutations has been associated with carcinogens in cigarette smoke. The majority of clinical studies suggest that lung cancers with p53 alterations carry a worse prognosis, and may be relatively more resistant to chemotherapy and radiation. An understanding of the role of p53 in human lung cancer may lead to more rational targeted approaches for treating this disease. P53 gene replacement is currently under clinical investigation but clearly more effective means of gene deliver to the tumor cells are required. Novel approaches to lung cancer therapy are needed to improve the observed poor patient survival despite current therapies.

Indexed as

AnimalsGene Expression Regulation, NeoplasticGenes, p53Genetic Predisposition to DiseaseHumansLung NeoplasmsMutationSmokingTumor Suppressor Protein p53Tumor Suppressor Protein p53

Identifiers

PMID12746555
OpenAlexW1984166331

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.