ReviewCancers2025
Advances in the Molecular Biology of Chondrosarcoma for Drug Discovery and Precision Medicine.
Review in Cancers, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed.
- Prognostic Role of TERT Mutations in Chondrosarcoma: Associations with Dedifferentiation, Survival, and IDH/TERT Co-Mutations.Cancers · 2026Article
- Molecular and Immune Mechanisms Governing Cancer Metastasis, Including Dormancy, Microenvironmental Niches, and Tumor-Specific Programs.International journal of molecular sciences · 2026Review
- Integrative biomarker and drug target discovery in osteosarcoma: traditional experimental approaches and AI-enabled insights.Frontiers in pharmacology · 2026Review
- Malignant Transformation of Musculoskeletal Lesions with Imaging-Pathology Correlation-Part 1: Bone Lesions.Diagnostics (Basel, Switzerland) · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chondrosarcomas (CSs) are generally slow-growing tumors of cartilage-producing cells, and the second most common primary bone malignancy following osteosarcoma. CSs are typically resistant to conventional chemo- and radiotherapy, and aggressive surgical resection with wide margins remains the only effective treatment option. Immunotherapies and targeted therapies in CSs have failed in clinical trials, and no prognostic biomarkers exist within the clinic. Although CSs have undergone histologic and genetic analysis, the molecular mechanisms that drive their pathogenesis and resistance are still largely unknown. A deeper understanding of the molecular biology and dysregulated pathways in CSs is essential for more efficient precision therapies. Several integrated large-scale genetic and epigenetic studies have recently been reported in CS, with several distinguished pathways holding therapeutic promise. In this review, we summarize the advances in the molecular biology of CSs, focusing on both genomic and epigenomic mechanisms as well as potential biomarkers and targets. These studies highlight several valuable clinical opportunities for earlier detection, prognostic accuracy, and therapeutic targeting that may improve patient outcomes in CSs.
Indexed as
Identifiers
What Socratic holds
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 Socratic graph.