Evidence map›Paper›PMID 15287022›Full record

ArticleGenes, chromosomes & cancer2004

Mutational activation of the MAP3K8 protooncogene in lung cancer.

Adam Michael Clark, Steven H Reynolds, Marshall Anderson, Jonathan S Wiest

Abstract read
In one paragraph

Article in Genes, chromosomes & cancer, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
0.2field-weighted citation impact, top 46% 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

27 citing papers in PubMed, 50 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Epigenetic Regulation of MAP3K8 in EBV-Associated Gastric Carcinoma.International journal of molecular sciences · 2023
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. A Review of the Molecular Pathways Involved in Resistance to BRAF Inhibitors in Patients with Advanced-Stage Melanoma.Medical science monitor : international medical journal of experimental and clinical research · 2020
    Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Expansion of the RASopathies.Current genetic medicine reports · 2016
    Article
  18. Article
  19. Uncovering and dissecting the genotoxicity of self-inactivating lentiviral vectors in vivo.Molecular therapy : the journal of the American Society of Gene Therapy · 2014
    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

4 authors at 3 institutions in 1 country.

Adam Michael ClarkLaboratory of Cellular Carcinogenesis and Tumor Promotion, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland 20892, USA.
Steven H Reynolds
Marshall Anderson
Jonathan S Wiest
National Cancer Institute · USNational Institute for Occupational Safety and Health · USUniversity of Cincinnati Medical Center · US

Funding

ENVIRONMETAL CARCINOGENESIS AND MUTAGENESIST32ES007250 · NIEHS · UNIVERSITY OF CINCINNATI · PI MILLER, WILLIAM E · 1988 to 2024
$11.9M
Genetic Alterations in Lung CancerZIABC010448 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI WIEST, JONATHAN SCOTT · 2009 to 2014
$1.4M
Intramural NIH HHS ZIA BC010448NIEHS NIH HHS 5 T32 ES07250NIEHS NIH HHS T32 ES007250
6 · The paper itself

Abstract

The MAP3K8 protooncogene (Cot/Tpl-2) activates the MAP kinase, SAP kinase, and NF-kappaB signaling pathways. MAP3K8 mutations occur in the rat homologue, but activating mutations have yet to be identified in primary human tumors. We have identified MAP3K8 as a transforming gene from a human lung adenocarcinoma and characterized a 3' end mutation in the cDNA. In addition, we confirmed that the mutation occurs in the original lung tumor, and we screened a series of lung cancer cell lines to determine whether the MAP3K8 mutation is a common occurrence in lung tumorigenesis. The oncogene was isolated and identified with the NIH3T3 nude mouse tumorigenicity assay and cDNA library screening. The gene was analyzed by polymerase chain reaction (PCR), single-strand conformational polymorphism (SSCP), and 3'RACE for mutations. The mutation was localized to MAP3K8 exon 8 and confirmed in the primary tumor DNA. Both wild-type and mutant MAP3K8 cDNAs transformed NIH3T3 cells, but the transforming activity of the mutant was much greater than that of the wild type. PCR-SSCP screening of cell line cDNAs identified one silent polymorphism in cell line SK-LU-1. Although we were unable to find additional activating mutations, these data support a role for MAP3K8 activity in cellular transformation, but suggest that mutational activation of the gene is a rare event in lung cancer.

Indexed as

AdenocarcinomaAmino Acid SequenceAnimalsBase SequenceDNA PrimersGene Expression Regulation, NeoplasticHumansLung NeoplasmsMAP Kinase Kinase KinasesMiceMice, NudeMolecular Sequence DataMutationPolymerase Chain ReactionPolymorphism, Single-Stranded ConformationalProto-Oncogene ProteinsDNA PrimersMAP3K8 protein, humanMAP Kinase Kinase KinasesProto-Oncogene Proteins

Identifiers

PMID15287022
PMCPMC3459321
OpenAlexW2032261877

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.