Evidence map›Paper›PMID 17693665›Full record

ReviewCarcinogenesis2007

Genetic pathways and mutation profiles of human cancers: site- and exposure-specific patterns.

I A Lea, M A Jackson, X Li, S Bailey, S D Peddada, J K Dunnick

Open access · greenAbstract readReview
In one paragraph

Review in Carcinogenesis, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed, 6 pooled it
3.5field-weighted citation impact, top 7% 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

57 citing papers in PubMed, 6 syntheses or guidelines pooled it, 119 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
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  5. TP53 Arg72Pro polymorphism and endometrial cancer risk: a meta-analysis.Medical oncology (Northwood, London, England) · 2011
    Pooled it
  6. Pooled it
  7. Trial
  8. Article
  9. Article
  10. Review
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  13. Pulmonary metastasectomy in colorectal carcinoma.Journal of thoracic disease · 2021
    Review
  14. Review
  15. Review
  16. Observational
  17. Article
  18. Review
  19. DRP1 Promotes BRAFFrontiers in oncology · 2020
    Article
  20. Article
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

6 authors at 2 institutions in 1 country.

I A LeaIntegrated Laboratory Systems, Inc., Research Triangle Park, NC 27709, USA. ilea@ils-inc.com
M A Jackson
X Li
S Bailey
S D Peddada
J K Dunnick
National Institute of Environmental Health Sciences · USIntegrated Laboratory Systems, Inc. · US

Funding

NIEHS STATISTICAL CONSULTING SERVICEZ01ES045005 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI PEDDADA, SHYAMAL · 1997 to 2008
$741k
Intramural NIH HHS Z99 ES999999NIEHS NIH HHS N43 ES015477
6 · The paper itself

Abstract

Cancer is a complex disease that involves the accumulation of both genetic and epigenetic alterations of numerous genes. Data in the Genetic Alterations in Cancer database for gene mutations and allelic loss [loss of heterozygosity (LOH)] in human tumors (e.g. lung, oral, esophagus, stomach and colon/rectum) were reviewed. Results for the genes and pathways implicated in tumor development at these sites are presented. Mutation incidence, spectra and codon specificity are described for lung, larynx and oral tumors. LOH occurred more frequently than gene mutations in tumors from all sites examined. The cell cycle gene, TP53 (all sites), and cell signaling gene, APC (colorectal and gastric cancers), were the only genes with similar incidences of LOH and mutation. Alterations of one or more cell cycle and cell signaling genes were reported for tumors from each site. Site-specific activation was apparent in the cell signaling mitogen-activated protein kinase oncogenes (KRAS in lung, HRAS in oral cancers and BRAF in esophageal and colorectal cancers). Analysis of genetic changes in lung tumors showed that the incidence of mutations in the TP53 and KRAS genes and the incidence of LOH in the FHIT gene were significantly greater in smokers versus non-smokers (P < 0.01). In lung and oral cancers, the TP53 GC --> TA transversion frequency increased with tobacco smoke exposure (P < 0.05). Furthermore, the TP53 mutational hot spots for lung and laryngeal cancers from smokers included codons 157, 245 and 273, whereas for oral tumors included codons 280 and 281.

Indexed as

Gene Expression Regulation, NeoplasticMutationCell CycleColorectal NeoplasmsEsophageal NeoplasmsFrameshift MutationHumansLoss of HeterozygosityLung NeoplasmsNeoplasmsPoint MutationSignal TransductionStomach Neoplasms

Identifiers

PMID17693665
PMCPMC2131731
OpenAlexW2105309532

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.