Evidence map›Paper›PMID 17054779›Full record

ArticleBMC genomics2006

Gene expressions and copy numbers associated with metastatic phenotypes of uterine cervical cancer.

Heidi Lyng, Runar S Brøvig, Debbie H Svendsrud, Ruth Holm, Olav Kaalhus, Kjetil Knutstad, Halldis Oksefjell, Kolbein Sundfør, Gunnar B Kristensen, Trond Stokke

Open access · goldAbstract readComparative Study
In one paragraph

Article in BMC genomics, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
81citing papers in PubMed, 3 pooled it
3.1field-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

81 citing papers in PubMed, 3 syntheses or guidelines pooled it, 157 citations in OpenAlex.

  1. Pooled it
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  6. Mitochondrial Ribosomal Proteins and Cancer.Medicina (Kaunas, Lithuania) · 2025
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21 more citing papers are in PubMed but not listed here.

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 2 institutions in 1 country.

Heidi LyngDepartment of Radiation Biology, Health Enterprise Rikshospitalet--Radiumhospitalet, Oslo, Norway. heidi.lyng@rr-research.no
Runar S Brøvig
Debbie H Svendsrud
Ruth Holm
Olav Kaalhus
Kjetil Knutstad
Halldis Oksefjell
Kolbein Sundfør
Gunnar B Kristensen
Trond Stokke
Med-Storm Innovation (Norway) · NOUniversity of Oslo · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundA better understanding of the development of metastatic disease and the identification of molecular markers for cancer spread would be useful for the design of improved treatment strategies. This study was conducted to identify gene expressions associated with metastatic phenotypes of locally advanced cervical carcinomas and investigate whether gains or losses of these genes could play a role in regulation of the transcripts. Gene expressions and copy number changes were determined in primary tumors from 29 patients with and 19 without diagnosed lymph node metastases by use of cDNA and genomic microarray techniques, respectively.

resultsThirty-one genes that differed in expression between the node positive and negative tumors were identified. Expressions of eight of these genes (MRPL11, CKS2, PDK2, MRPS23, MSN, TBX3, KLF3, LSM3) correlated with progression free survival in univariate analysis and were therefore more strongly associated with metastatic phenotypes than the others. Immunohistochemistry data of CKS2 and MSN showed similar relationships to survival. The prognostic genes clustered into two groups, suggesting two major metastatic phenotypes. One group was associated with rapid proliferation, oxidative phosphorylation, invasiveness, and tumor size (MRPS23, MRPL11, CKS2, LSM3, TBX3, MSN) and another with hypoxia tolerance, anaerobic metabolism, and high lactate content (PDK2, KLF3). Multivariate analysis identified tumor volume and PDK2 expression as independent prognostic variables. Gene copy number changes of the differentially expressed genes were not frequent, but correlated with the expression level for seven genes, including MRPS23, MSN, and LSM3.

conclusionGene expressions associated with known metastatic phenotypes of cervical cancers were identified. Our findings may indicate molecular mechanisms underlying development of these phenotypes and be useful as markers of cancer spread. Gains or losses of the genes may be involved in development of the metastatic phenotypes in some cases, but other mechanisms for transcriptional regulation are probably important in the majority of tumors.

Indexed as

Gene Expression Profiling3-Phosphoinositide-Dependent Protein KinasesAnalysis of VarianceCarcinoma, Squamous CellCarrier ProteinsCDC2-CDC28 KinasesCell Cycle ProteinsCluster AnalysisFemaleGene DosageGene Expression Regulation, NeoplasticHumansImmunohistochemistryKruppel-Like Transcription FactorsLymphatic MetastasisMicrofilament Proteins3-Phosphoinositide-Dependent Protein KinasesCarrier ProteinsCDC2-CDC28 KinasesCell Cycle ProteinsCKS2 protein, humanKLF3 protein, humanKruppel-Like Transcription FactorsMicrofilament ProteinsmoesinProtein KinasesProtein Serine-Threonine Kinasesribosomal protein L11Ribosomal ProteinsT-Box Domain ProteinsTBX3 protein, human

Identifiers

PMID17054779
PMCPMC1626467
OpenAlexW2170540646

What OpenQuestion holds

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LicenceCC BY
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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.