Evidence map›Paper›PMID 26701206›Full record

ArticleOncotarget2016

In silico pathway analysis in cervical carcinoma reveals potential new targets for treatment.

Peter A van Dam, Pieter-Jan H H van Dam, Christian Rolfo, Marco Giallombardo, Christophe van Berckelaer, Xuan Bich Trinh, Sevilay Altintas, Manon Huizing, Kostas Papadimitriou, Wiebren A A Tjalma and 1 more

Abstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
–field-weighted citation impact
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

20 citing papers in PubMed.

  1. Article
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  12. RANK-RANKL Signaling in Cancer of the Uterine Cervix: A Review.International journal of molecular sciences · 2019
    Review
  13. Article
  14. Article
  15. Article
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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

11 authors.

Peter A van DamAntwerp University Hospital, Centre of Oncologic Research (CORE) Antwerp University, Edegem, Belgium.
Pieter-Jan H H van DamAntwerp University Hospital, Centre of Oncologic Research (CORE) Antwerp University, Edegem, Belgium.
Christian RolfoAntwerp University Hospital, Centre of Oncologic Research (CORE) Antwerp University, Edegem, Belgium.
Marco GiallombardoAntwerp University Hospital, Centre of Oncologic Research (CORE) Antwerp University, Edegem, Belgium.
Christophe van BerckelaerAntwerp University Hospital, Centre of Oncologic Research (CORE) Antwerp University, Edegem, Belgium.
Xuan Bich TrinhMultidisciplinary Oncologic Centre Antwerp (MOCA), Edegem, Belgium.
Sevilay AltintasMultidisciplinary Oncologic Centre Antwerp (MOCA), Edegem, Belgium.
Manon HuizingMultidisciplinary Oncologic Centre Antwerp (MOCA), Edegem, Belgium.
Kostas PapadimitriouMultidisciplinary Oncologic Centre Antwerp (MOCA), Edegem, Belgium.
Wiebren A A TjalmaAntwerp University Hospital, Centre of Oncologic Research (CORE) Antwerp University, Edegem, Belgium.
Steven van LaereAntwerp University Hospital, Centre of Oncologic Research (CORE) Antwerp University, Edegem, Belgium.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

An in silico pathway analysis was performed in order to improve current knowledge on the molecular drivers of cervical cancer and detect potential targets for treatment. Three publicly available Affymetrix gene expression data-sets (GSE5787, GSE7803, GSE9750) were retrieved, vouching for a total of 9 cervical cancer cell lines (CCCLs), 39 normal cervical samples, 7 CIN3 samples and 111 cervical cancer samples (CCSs). Predication analysis of microarrays was performed in the Affymetrix sets to identify cervical cancer biomarkers. To select cancer cell-specific genes the CCSs were compared to the CCCLs. Validated genes were submitted to a gene set enrichment analysis (GSEA) and Expression2Kinases (E2K). In the CCSs a total of 1,547 probe sets were identified that were overexpressed (FDR < 0.1). Comparing to CCCLs 560 probe sets (481 unique genes) had a cancer cell-specific expression profile, and 315 of these genes (65%) were validated. GSEA identified 5 cancer hallmarks enriched in CCSs (P < 0.01 and FDR < 0.25) showing that deregulation of the cell cycle is a major component of cervical cancer biology. E2K identified a protein-protein interaction (PPI) network of 162 nodes (including 20 drugable kinases) and 1626 edges. This PPI-network consists of 5 signaling modules associated with MYC signaling (Module 1), cell cycle deregulation (Module 2), TGFβ-signaling (Module 3), MAPK signaling (Module 4) and chromatin modeling (Module 5). Potential targets for treatment which could be identified were CDK1, CDK2, ABL1, ATM, AKT1, MAPK1, MAPK3 among others. The present study identified important driver pathways in cervical carcinogenesis which should be assessed for their potential therapeutic drugability.

Indexed as

Gene Expression Regulation, NeoplasticAmino Acid SequenceBiomarkers, TumorCell CycleCell Line, TumorChromatin Assembly and DisassemblyComputational BiologyComputer SimulationFemaleGene Expression ProfilingHeLa CellsHumansMAP Kinase Signaling SystemMitogen-Activated Protein KinasesOligonucleotide Array Sequence AnalysisProto-Oncogene Proteins c-mycBiomarkers, TumorMitogen-Activated Protein KinasesMYC protein, humanProto-Oncogene Proteins c-mycTransforming Growth Factor betacancercervical carcinomain silico pathway analysistreatment targets

Identifiers

PMID26701206
PMCPMC4823071

What OpenQuestion holds

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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.