ArticleCancer research2023
Subclonal Somatic Copy-Number Alterations Emerge and Dominate in Recurrent Osteosarcoma.
Article in Cancer research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
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Who cites it
21 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.
- Biological Sample Collection to Advance Research and Treatment: A Fight Osteosarcoma Through European Research and Euro Ewing Consortium Statement.Clinical cancer research : an official journal of the American Association for Cancer Research · 2024Guideline
- Unraveling the lexicon of complex mutational phenomena in human cancers.Nature cancer · 2026Review
- Genomic landscape and tumor immune microenvironment of osteosarcoma: Bridging mechanistic insights to precision therapeutics.Bone reports · 2026Review
- Extracellular vesicles in osteosarcoma: bridging resistance, immunity, and clinical translation.Journal of bone oncology · 2026Review
- Long-read sequencing of single cell-derived melanoma sublines reveals divergent and parallel genomic and epigenomic evolutionary trajectories.Nature communications · 2026Article
- Understanding and Overcoming Osteosarcoma Heterogeneity.Biomolecules · 2026Review
- Radiobiotherapy in Osteosarcoma: A State-Based Educational Framework for Strategy Selection and Trial Design.Current oncology (Toronto, Ont.) · 2026Review
- An international framework for clinical translation of molecular classifiers in osteosarcoma.NPJ precision oncology · 2026Article
- Single-Cell RNA Analysis of Murine Osteosarcoma Uncovers Skp2 Function in Metastasis, Genomic Instability, and Immune Activation and Reveals Additional Target Pathways.Cancer research communications · 2026Article
- Emerging research themes in drug resistance in osteosarcoma: a 25-year bibliometric and visualized analysis.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Dynamic immune state transitions and metastatic niche remodelling drive osteosarcoma evolution as a barrier-restricted immune-cold ecosystem.Frontiers in immunology · 2026Review
- Satellite DNA fragility accompanies complex genome rearrangements and ecDNA oncogene amplification in canine osteosarcomas.bioRxiv : the preprint server for biology · 2025Article
- Long-read sequencing of single cell-derived melanoma subclones reveals divergent and parallel genomic and epigenomic evolutionary trajectories.bioRxiv : the preprint server for biology · 2025Article
- Elucidation of novel diagnostic biomarkers and therapeutic targets in colorectal carcinoma: an integrative approach leveraging multi-omics, computational biology, and single-cell sequencing technologies.Mammalian genome : official journal of the International Mammalian Genome Society · 2025Article
- Whole‑exome evolutionary profiling of osteosarcoma uncovers metastasis‑related driver mutations and generates an independently validated predictive classifier.Journal of translational medicine · 2025Article
- Age-related genomic alterations and chemotherapy sensitivity in osteosarcoma: insights from cancer genome profiling analyses.International journal of clinical oncology · 2025Article
- Bayesian unsupervised clustering identifies clinically relevant osteosarcoma subtypes.Briefings in bioinformatics · 2024Article
- The Interplay Between theInternational journal of molecular sciences · 2024Review
- Pediatric Leukemia Roadmaps Are a Guide for Positive Metastatic Bone Sarcoma Trials.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2024Article
- Establishment and characterization of DPC-X4: a novel mixed-type ampullary cancer cell line.Human cell · 2024Article
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Authors and funding
30 authors at 3 institutions in 2 countries.
Funding
Abstract
Multiple large-scale genomic profiling efforts have been undertaken in osteosarcoma to define the genomic drivers of tumorigenesis, therapeutic response, and disease recurrence. The spatial and temporal intratumor heterogeneity could also play a role in promoting tumor growth and treatment resistance. We conducted longitudinal whole-genome sequencing of 37 tumor samples from 8 patients with relapsed or refractory osteosarcoma. Each patient had at least one sample from a primary site and a metastatic or relapse site. Subclonal copy-number alterations were identified in all patients except one. In 5 patients, subclones from the primary tumor emerged and dominated at subsequent relapses. MYC gain/amplification was enriched in the treatment-resistant clones in 6 of 7 patients with multiple clones. Amplifications in other potential driver genes, such as CCNE1, RAD21, VEGFA, and IGF1R, were also observed in the resistant copy-number clones. A chromosomal duplication timing analysis revealed that complex genomic rearrangements typically occurred prior to diagnosis, supporting a macroevolutionary model of evolution, where a large number of genomic aberrations are acquired over a short period of time followed by clonal selection, as opposed to ongoing evolution. A mutational signature analysis of recurrent tumors revealed that homologous repair deficiency (HRD)-related SBS3 increases at each time point in patients with recurrent disease, suggesting that HRD continues to be an active mutagenic process after diagnosis. Overall, by examining the clonal relationships between temporally and spatially separated samples from patients with relapsed/refractory osteosarcoma, this study sheds light on the intratumor heterogeneity and potential drivers of treatment resistance in this disease. SIGNIFICANCE: The chemoresistant population in recurrent osteosarcoma is subclonal at diagnosis, emerges at the time of primary resection due to selective pressure from neoadjuvant chemotherapy, and is characterized by unique oncogenic amplifications.
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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.