Trial reportPloS one2014
Analysis of molecular cytogenetic alteration in rhabdomyosarcoma by array comparative genomic hybridization.
Trial report in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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.
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.
Who cites it
16 citing papers in PubMed, 29 citations in OpenAlex.
- Novel Genomic Biomarkers Improve Post-Hematopoietic Cell Transplantation Relapse Risk Stratification for Patients With Myelodysplastic Syndromes.JCO precision oncology · 2026Article
- GEFT inhibits the GSDM-mediated proptosis signalling pathway, promoting the progression and drug resistance of rhabdomyosarcoma.Cell death & disease · 2024Article
- Lnc-PSMA8-1 activated by GEFT promotes rhabdomyosarcoma progression via upregulation of mTOR expression by sponging miR-144-3p.BMC cancer · 2024Article
- Soft Tissue Special Issue: Skeletal Muscle Tumors: A Clinicopathological Review.Head and neck pathology · 2020Review
- MicroRNA-29 family inhibits rhabdomyosarcoma formation and progression by regulating GEFT function.American journal of translational research · 2020Article
- Article
- MiRNAs as Players in Rhabdomyosarcoma Development.International journal of molecular sciences · 2019Review
- Alveolar rhabdomyosarcoma with unusual cytogenetic findings: one more case and review of the literature.Oxford medical case reports · 2019Article
- Review
- Integration of genomic copy number variations and chemotherapy-response biomarkers in pediatric sarcoma.BMC medical genomics · 2019Article
- MicroRNA-874 functions as a tumor suppressor in rhabdomyosarcoma by directly targeting GEFT.American journal of cancer research · 2019Article
- Role of GLI Transcription Factors in Pathogenesis and Their Potential as New Therapeutic Targets.International journal of molecular sciences · 2018Review
- Safety markers for rhabdomyosarcoma cells using anOncology letters · 2018Article
- c-MET expression potentially contributes to the poor prognosis of rhabdomyosarcoma.International journal of clinical and experimental pathology · 2018Article
- Integrated genetic and epigenetic analysis defines novel molecular subgroups in rhabdomyosarcoma.Nature communications · 2015Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rhabdomyosarcoma (RMS) is the most common pediatric soft tissue sarcoma with poor prognosis. The genetic etiology of RMS remains largely unclear underlying its development and progression. To reveal novel genes more precisely and new therapeutic targets associated with RMS, we used high-resolution array comparative genomic hybridization (aCGH) to explore tumor-associated copy number variations (CNVs) and genes in RMS. We confirmed several important genes by quantitative real-time polymerase chain reaction (QRT-PCR). We then performed bioinformatics-based functional enrichment analysis for genes located in the genomic regions with CNVs. In addition, we identified miRNAs located in the corresponding amplification and deletion regions and performed miRNA functional enrichment analysis. aCGH analyses revealed that all RMS showed specific gains and losses. The amplification regions were 12q13.12, 12q13.3, and 12q13.3-q14.1. The deletion regions were 1p21.1, 2q14.1, 5q13.2, 9p12, and 9q12. The recurrent regions with gains were 12q13.3, 12q13.3-q14.1, 12q14.1, and 17q25.1. The recurrent regions with losses were 9p12-p11.2, 10q11.21-q11.22, 14q32.33, 16p11.2, and 22q11.1. The mean mRNA level of GLI1 in RMS was 6.61-fold higher than that in controls (p = 0.0477) by QRT-PCR. Meanwhile, the mean mRNA level of GEFT in RMS samples was 3.92-fold higher than that in controls (p = 0.0354). Bioinformatic analysis showed that genes were enriched in functions such as immunoglobulin domain, induction of apoptosis, and defensin. Proto-oncogene functions were involved in alveolar RMS. miRNAs that located in the amplified regions in RMS tend to be enriched in oncogenic activity (miR-24 and miR-27a). In conclusion, this study identified a number of CNVs in RMS and functional analyses showed enrichment for genes and miRNAs located in these CNVs regions. These findings may potentially help the identification of novel biomarkers and/or drug targets implicated in diagnosis of and targeted therapy for RMS.
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Registered trials
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.