Evidence map›Paper›PMID 12937139›Full record

ArticleThe American journal of pathology2003

Combined array comparative genomic hybridization and tissue microarray analysis suggest PAK1 at 11q13.5-q14 as a critical oncogene target in ovarian carcinoma.

Peter Schraml, Georg Schwerdtfeger, Felix Burkhalter, Anna Raggi, Dietmar Schmidt, Teresa Ruffalo, Walter King, Kim Wilber, Michael J Mihatsch, Holger Moch

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
9.9field-weighted citation impact, top 1% 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, 178 citations in OpenAlex.

  1. Trial
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  5. P2YCancers · 2022
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  7. Cancers · 2019
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  14. Review
  15. Review
  16. Pak and Rac GTPases promote oncogenic KIT-induced neoplasms.The Journal of clinical investigation · 2013
    Article
  17. Article
  18. PAK1-dependent MAPK pathway activation is required for colorectal cancer cell proliferation.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2012
    Article
  19. Article
  20. Pak1/LIMK1/Cofilin Pathway Contributes to Tumor Migration and Invasion in Human Non-Small Cell Lung Carcinomas and Cell Lines.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2012
    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

10 authors at 3 institutions in 3 countries.

Peter SchramlInstitute of Pathology, University Hospital, University of Basel, Schönbeinstrasse 40, 4031 Basel, Switzerland. peter.schraml@unibas.ch
Georg Schwerdtfeger
Felix Burkhalter
Anna Raggi
Dietmar Schmidt
Teresa Ruffalo
Walter King
Kim Wilber
Michael J Mihatsch
Holger Moch
University of Basel · CHDowners Grove Public Library · USUniversity of Mannheim · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Amplification of chromosomal regions leads to an increase of DNA copy numbers and expression of oncogenes in many human tumors. The identification of tumor-specific oncogene targets has potential diagnostic and therapeutic implications. To identify distinct spectra of oncogenic alterations in ovarian carcinoma, metaphase comparative genomic hybridization (mCGH), array CGH (aCGH), and ovarian tumor tissue microarrays were used in this study. Twenty-six primary ovarian carcinomas and three ovarian carcinoma cell lines were analyzed by mCGH. Frequent chromosomal overrepresentation was observed on 2q (31%), 3q (38%), 5p (38%), 8q (52%), 11q (21%), 12p (21%), 17q (21%), and 20q (52%). The role of oncogenes residing in gained chromosomal loci was determined by aCGH with 59 genetic loci commonly amplified in human tumors. DNA copy number gains were most frequently observed for PIK3CA on 3q (66%), PAK1 on 11q (59%), KRAS2 on 12p (55%), and STK15 on 20q (55%). The 11q13-q14 amplicon, represented by six oncogenes (CCND1, FGF4, FGF3, EMS1, GARP, and PAK1) revealed preferential gene copy number gains of PAK1, which is located at 11q13.5-q14. Amplification and protein expression status of both PAK1 and CCND1 were further examined by fluorescence in situ hybridization and immunohistochemistry using a tissue microarray consisting of 268 primary ovarian tumors. PAK1 copy number gains were observed in 30% of the ovarian carcinomas and PAK1 protein was expressed in 85% of the tumors. PAK1 gains were associated with high grade (P < 0.05). In contrast, CCND1 gene alterations and protein expression were less frequent (10.6% and 25%, respectively), suggesting that the critical oncogene target of amplicon 11q13-14 lies distal to CCND1. This study demonstrates that aCGH facilitates further characterization of oncogene candidates residing in amplicons defined by mCGH.

Indexed as

CarcinomaChromosome MappingChromosomes, Human, Pair 11Cyclin D1FemaleHumansImmunohistochemistryIn Situ Hybridization, FluorescenceMetaphaseNucleic Acid HybridizationOligonucleotide Array Sequence AnalysisOvarian Neoplasmsp21-Activated KinasesProtein Serine-Threonine KinasesTumor Cells, CulturedCyclin D1p21-Activated KinasesPAK1 protein, humanProtein Serine-Threonine Kinases

Identifiers

PMID12937139
PMCPMC1868266
OpenAlexW2019729084

What OpenQuestion holds

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Registered trials

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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.