Evidence map›Paper›PMID 12037679›Full record

ArticleOncogene2002

The focal adhesion kinase (P125FAK) is constitutively active in human malignant melanoma.

Orlie Kahana, Michael Micksche, Isaac P Witz, Ilana Yron

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

29 citing papers in PubMed, 73 citations in OpenAlex.

  1. Anoikis: To Die or Not to Die?International journal of molecular sciences · 2026
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  19. Focal adhesion kinase as a cancer therapy target.Anti-cancer agents in medicinal chemistry · 2010
    Review
  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 2 institutions in 2 countries.

Orlie KahanaThe Department of Cell Research and Immunology, Tel Aviv, Israel.
Michael Micksche
Isaac P Witz
Ilana Yron
Tel Aviv University · ILUniversity of Vienna · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Malignant melanoma cells show high aggressiveness and metastatic potential. Tumor cells as they become more metastatic, gradually lose their dependence on both adhesion and serum. Thus, in the process of tumor progression cells undergo series of changes that allow them to adapt to different tissue milieu. This implies that during this process, points on the integrin pathway may become constitutively activated. In the present study we investigated the possible role of FAK, being one of the key members of the integrin-signaling pathway, in the multistep progression towards a malignant phenotype in human melanoma. In our study we show that in melanoma cells there is neither an increase in the amount of FAK nor in its phosphorylation capacity, but rather in its levels of constitutive activation. Indeed, in all melanoma cells tested and not in nevus and neuroblastoma cells, we observed various degrees of constitutive activation of FAK. Our results also suggest that FAK constitutive activation is regulated at least in part by the cytoskeleton, implying that steps along the integrin signaling pathway involving FAK could be among the oncogenic mechanisms that operate in melanoma and may account for the highly aggressive, anchorage independent phenotype of this tumor.

Indexed as

Cell AdhesionEnzyme ActivationFibronectinsFlow CytometryFocal Adhesion Kinase 1Focal Adhesion Protein-Tyrosine KinasesHumansIntegrinsMelanomaNeoplasm MetastasisNeuroblastomaNevus, PigmentedPhosphorylationPrecipitin TestsProtein-Tyrosine KinasesSignal TransductionFibronectinsFocal Adhesion Kinase 1Focal Adhesion Protein-Tyrosine KinasesIntegrinsProtein-Tyrosine KinasesPTK2 protein, human

Identifiers

PMID12037679
OpenAlexW1979741100

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.