Evidence map›Paper›PMID 37937323›Full record

SynthesisCancer reports (Hoboken, N.J.)2023

Meta-analysis of microarray data to determine gene indicators involved in the cisplatin resistance in ovarian cancer.

Somayeh Hashemi Sheikhshabani, Zeinab Amini-Farsani, Nesa Kazemifard, Parastoo Modarres, Zahra Amini-Farsani, Mir Davood Omrani, Soudeh Ghafouri-Fard

Open access · goldAbstract readMeta-Analysis
In one paragraph

Synthesis in Cancer reports (Hoboken, N.J.), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed, 1 pooled it
0.6field-weighted citation impact, top 29% 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

5 citing papers in PubMed, 1 synthesis or guideline pooled it, 4 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. 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

7 authors at 4 institutions in 2 countries.

Somayeh Hashemi SheikhshabaniStudent Research Committee, Department of Medical Genetics, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Zeinab Amini-FarsaniDepartment of Medical Genetics, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Nesa KazemifardBasic and Molecular Epidemiology of Gastrointestinal Disorders Research Center, Research Institute for Gastroenterology and Liver Diseases, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Parastoo ModarresDepartment of Cell and Molecular Biology and Microbiology, University of Isfahan, Isfahan, Iran.
Zahra Amini-FarsaniBayesian Imaging and Spatial Statistics Group, Institute for Statistics, Ludwig-Maximilians-Universität München, Munich, Germany.
Mir Davood OmraniDepartment of Medical Genetics, Shahid Beheshti University of Medical Sciences, Tehran, Iran.ORCID 0000-0002-0673-9717
Soudeh Ghafouri-FardDepartment of Medical Genetics, Shahid Beheshti University of Medical Sciences, Tehran, Iran.ORCID 0000-0002-0223-499X
Shahid Beheshti University of Medical Sciences · IRLorestan University · IRResearch Institute for Endocrine Sciences · IRUniversity of Isfahan · IR

Funding

School of Medicine, Shahid Beheshti University of Medical Sciences 1400/65258
6 · The paper itself

Abstract

backgroundSignificant miss-expressed gene indicators contributing to cisplatin resistance in ovarian cancer have not been completely understood. It seems that several regulatory genes and signaling pathways are associated with the emergence of the chemo-resistant phenotype.

aimsHere, a meta-analysis approach was adopted to assess deregulated genes involved in relapse after the first line of chemotherapy (cisplatin). METHODS AND

resultsTo do so, six ovarian cancer libraries were gathered from GEO repository. Batch effect removal and quality assessment, and boxplots and PCA were performed using SVA and ggplot2 packages in R, respectively. Cisplatin-resistant and -sensitive ovarian cancer groups were compared with find genes with significant expression changes using linear regression models in the LIMMA R package. The significance threshold for DEGs was taken as adj p-value < .05 and - 1 > logFC > 1. A total of 261 genes were identified to have significant differential expression levels in the cisplatin-resistant versus cisplatin-sensitive group. Among the 10 top up-regulated and down-regulated genes, PITX2, SNCA, and EPHA7 (up), as well as TMEM98 (down) are indirect upstream regulators of PI3K/AKT signaling pathway, contributing greatly to the development of chemo-resistance in cancer via promoting cell proliferation, survival, and cell cycle progression as well as inhibiting apoptosis. Moreover, a comprehensive assessment of DEGs revealed the dysregulation of not only membrane ion channels KCa1.1, Kv4, and CACNB4, affecting cell excitability, proliferation, and apoptosis but also cell adhesion proteins COL4A6, EPHA3, and CD9, affecting the attachment of normal cells to ECM and apoptosis, introducing good options to reverse cisplatin resistance.

conclusionOur results predict and suggest that upstream regulators of PI3K/AKT signaling pathway, ion channels, and cell adhesion proteins play important roles in cisplatin resistance development in ovarian cancer.

Indexed as

CisplatinDrug Resistance, NeoplasmOvarian NeoplasmsAntineoplastic AgentsCell Line, TumorFemaleHumansIon ChannelsMembrane ProteinsNeoplasm Recurrence, LocalPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktAntineoplastic AgentsCisplatinIon ChannelsMembrane ProteinsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTMEM98 protein, humancisplatin resistancemeta-analysisovarian cancer

Identifiers

PMID37937323
PMCPMC10728535
OpenAlexW4388494903

What OpenQuestion holds

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LicenceCC BY
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.