ArticleOncogene2012
1q gain and CDT2 overexpression underlie an aggressive and highly proliferative form of Ewing sarcoma.
Article in Oncogene, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
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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.
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Who cites it
64 citing papers in PubMed, 114 citations in OpenAlex.
- A Practical Compass to Biological Digital Resources and Omics Integration in Ewing Sarcoma.Methods in molecular biology (Clifton, N.J.) · 2027Article
- Circulating IGF2BP3 enables risk stratification and predicts treatment response in Ewing sarcoma.Scientific reports · 2026Article
- Potential biomarkers of Ewing sarcoma identified through a Europe-wide analysis of prospectively collected samples.Scientific reports · 2026Article
- Molecular Characterization Informs Prognosis in Patients With Localized Ewing Sarcoma: A Report From the Children's Oncology Group.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2025Article
- The Puzzle of Genetic Stability and Chromosomal Copy Number Alterations for the Therapy of Ewing Sarcoma.Cancers · 2025Review
- Targeting metastasis in paediatric bone sarcomas.Molecular cancer · 2025Review
- Single-Cell RNA Sequencing of Ewing Sarcoma Tumors Demonstrates Transcriptional Heterogeneity and Clonal Evolution.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025Article
- DTL promotes the growth and migration of melanoma cells through the ERK/E2F1/BUB1 axis.Scientific reports · 2024Article
- Hypoxia-induced DTL promotes the proliferation, metastasis, and sorafenib resistance of hepatocellular carcinoma through ubiquitin-mediated degradation of SLTM and subsequent Notch pathway activation.Cell death & disease · 2024Article
- Bioinformatic Analysis of Recurrent Genomic Alterations and Corresponding Pathway Alterations in Ewing Sarcoma.Journal of personalized medicine · 2023Article
- Molecular and biologic biomarkers of Ewing sarcoma: A systematic review.Journal of bone oncology · 2023Review
- Complex/crypticGenes · 2023Article
- Somatic Copy Number Alteration in Circulating Tumor DNA for Monitoring of Pediatric Patients with Cancer.Biomedicines · 2023Article
- Systematic multi-omics cell line profiling uncovers principles of Ewing sarcoma fusion oncogene-mediated gene regulation.Cell reports · 2022Article
- Regulation of Metastasis in Ewing Sarcoma.Cancers · 2022Review
- An international working group consensus report for the prioritization of molecular biomarkers for Ewing sarcoma.NPJ precision oncology · 2022Review
- Article
- Identification of aberrantly methylated differentially expressed genes and pro-tumorigenic role of KIF2C in melanoma.Frontiers in genetics · 2022Article
- Identification of DTL as Related Biomarker and Immune Infiltration Characteristics of Nasopharyngeal Carcinoma via Comprehensive Strategies.International journal of general medicine · 2022Article
- Role of DTL in Hepatocellular Carcinoma and Its Impact on the Tumor Microenvironment.Frontiers in immunology · 2022Article
4 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
17 authors at 9 institutions in 8 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Despite extensive characterization of the role of the EWS-ETS fusions, little is known about secondary genetic alterations and their clinical contribution to Ewing sarcoma (ES). It has been demonstrated that the molecular structure of EWS-ETS lacks prognostic value. Moreover, CDKN2A deletion and TP53 mutation, despite carrying a poor prognosis, are infrequent. In this scenario identifying secondary genetic alterations with a significant prevalence could contribute to understand the molecular mechanisms underlying the most aggressive forms of ES.We screened a 67 ES tumor set for copy number alterations by array comparative genomic hybridization. 1q gain (1qG), detected in 31% of tumor samples, was found markedly associated with relapse and poor overall and disease-free survival and demonstrated a prognostic value independent of classical clinical parameters. Reanalysis of an expression dataset belonging to an independent tumor set (n=37) not only validated this finding but also led us to identify a transcriptomic profile of severe cell cycle deregulation in 1qG ES tumors. Consistently, a higher proliferation rate was detected in this tumor subset by Ki-67 immunohistochemistry. CDT2, a 1q-located candidate gene encoding a protein involved in ubiquitin ligase activity and significantly overexpressed in 1qG ES tumors, was validated in vitro and in vivo proving its major contribution to this molecular and clinical phenotype. This integrative genomic study of 105 ES tumors in overall renders the potential value of 1qG and CDT2 overexpression as prognostic biomarkers and also affords a rationale for the application of already available new therapeutic compounds selectively targeting the protein-ubiquitin machinery.
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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.