ArticleNPJ precision oncology2025
Targeting high-risk MYC-overexpressed osteosarcoma with an Aurora kinase inhibitor:--results from a pilot umbrella trial.
Article in NPJ precision oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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
4 citing papers in PubMed, 1 synthesis or guideline pooled it.
- From mechanism to therapy: advances in macrophage polarisation and targeted intervention in osteosarcoma.Frontiers in immunology · 2026Pooled it
- Osteosarcoma Across the Age Spectrum: Why Outcomes Diverge and Trials Must Adapt.Journal of clinical medicine · 2026Review
- Understanding and Overcoming Osteosarcoma Heterogeneity.Biomolecules · 2026Review
- Comparative Molecular Insights and Computational Modeling of Multiple Myeloma and Osteosarcoma.International journal of molecular sciences · 2026Review
Corrections and comments
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Authors and funding
19 authors.
Funding
Abstract
Osteosarcoma is a highly heterogeneous cancer, and molecular subtyping has the potential to increase diagnostic precision and facilitate targeted therapies. In our previous study, we classified osteosarcoma into four distinct subtypes. Here, we conducted a genomic subtype-guided pilot umbrella trial (ChiCTR2000036618, 2020/08/24) to evaluate the efficacy and safety of multiple precision therapies. Nineteen patients with refractory metastatic osteosarcoma were enrolled and stratified using whole-exome sequencing (WES) and immunohistochemistry (IHC). Patients were assigned to three arms: (A) PD-1 antibody plus gemcitabine and docetaxel; (B) PARP inhibitor combined with temozolomide; or (C) tinengotinib (TT-00420), a small-molecule aurora kinase inhibitor currently in clinical trials. The median progression-free survival and overall survival were 50 days (95% CI: 33-89) and 149 days (95% CI: 90-185). Tinengotinib has shown promising efficacy in our preclinical studies, suggesting its potential for clinical use, particularly in combination with immunotherapy. Additionally, we found that patients with MYC amplification presented increased tumor purity and ploidy, homologous recombination deficiency scores, and an immunosuppressive microenvironment. This study demonstrated the feasibility of using genomic molecular subtyping to guide the precise treatment of osteosarcoma. We also revealed that the abnormal genomic and transcriptomic profiles caused by MYC amplification could be suppressed by tinengotinib.
Identifiers
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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.