ArticleCancer science2013
Characterization of genetic lesions in rhabdomyosarcoma using a high-density single nucleotide polymorphism array.
Article in Cancer science, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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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.
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Who cites it
25 citing papers in PubMed.
- Aneuploidy of chromosome 8 promotes the mesenchymal lineage during cell fate transitions.Science advances · 2026Article
- The Emerging Role and Clinical Significance of PI3K-Akt-mTOR in Rhabdomyosarcoma.Biomolecules · 2025Review
- CRISPR-Cas9-Mediated Bioluminescent Tagging of Endogenous Proteins by Fluorescent Protein-Assisted Cell Sorting.Methods in molecular biology (Clifton, N.J.) · 2024Article
- Article
- Myogenetic Oligodeoxynucleotides as Anti-Nucleolin Aptamers Inhibit the Growth of Embryonal Rhabdomyosarcoma Cells.Biomedicines · 2022Article
- MCKAT: a multi-dimensional copy number variant kernel association test.BMC bioinformatics · 2021Article
- SMCKAT, a Sequential Multi-Dimensional CNV Kernel-Based Association Test.Life (Basel, Switzerland) · 2021Article
- Review
- Article
- The Role of Glypicans in Cancer Progression and Therapy.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2020Review
- Single-cell lineage analysis reveals genetic and epigenetic interplay in glioblastoma drug resistance.Genome biology · 2020Article
- Soft Tissue Special Issue: Skeletal Muscle Tumors: A Clinicopathological Review.Head and neck pathology · 2020Review
- Focal adhesion kinase (FAK) phosphorylation is a key regulator of embryonal rhabdomyosarcoma (ERMS) cell viability and migration.Journal of cancer research and clinical oncology · 2019Article
- Integration of genomic copy number variations and chemotherapy-response biomarkers in pediatric sarcoma.BMC medical genomics · 2019Article
- Anaplastic Lymphoma Kinase (ALK) Receptor Tyrosine Kinase: A Catalytic Receptor with Many Faces.International journal of molecular sciences · 2018Review
- Glypicans as Cancer Therapeutic Targets.Trends in cancer · 2018Review
- Targeting Anaplastic Lymphoma Kinase (ALK) in Rhabdomyosarcoma (RMS) with the Second-Generation ALK Inhibitor Ceritinib.Targeted oncology · 2017Article
- The role of anaplastic lymphoma kinase in pediatric cancers.Cancer science · 2017Review
- Primary cardiac rhabdomyosarcoma developed after receiving radiotherapy for left breast cancer 18 years prior.Journal of cardiology cases · 2017Article
- Article
Corrections and comments
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Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rhabdomyosarcoma (RMS) is a common solid tumor in childhood divided into two histological subtypes, embryonal (ERMS) and alveolar (ARMS). The ARMS subtype shows aggressive clinical behavior with poor prognosis, while the ERMS subtype has a more favorable outcome. Because of the rarity, diagnostic diversity and heterogeneity of this tumor, its etiology remains to be completely elucidated. Thus, to identify genetic alterations associated with RMS development, we performed single nucleotide polymorphism array analyses of 55 RMS samples including eight RMS-derived cell lines. The ERMS subtype was characterized by hyperploidy, significantly associated with gains of chromosomes 2, 8 and 12, whereas the majority of ARMS cases exhibited near-diploid copy number profiles. Loss of heterozygosity of 15q was detected in 45.5% of ARMS that had been unrecognized in RMS to date. Novel amplifications were also detected, including IRS2 locus in two fusion-positive tumors, and KRAS or NRAS loci in three ERMS cases. Of note, gain of 13q was significantly associated with good patient outcome in ERMS. We also identified possible application of an ALK inhibitor to RMS, as ALK amplification and frequent expression of ALK were detected in our RMS cohort. These findings enhance our understanding of the genetic mechanisms underlying RMS pathogenesis and support further studies for therapeutic development of RMS.
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