ReviewOncology letters2020
Biology and pathogenesis of human osteosarcoma.
Review in Oncology letters, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers, 1 of them a synthesis that pooled it.
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
87 citing papers in PubMed, 1 synthesis or guideline pooled it, 108 citations in OpenAlex.
- Risk factors for pulmonary metastases in osteosarcoma: a systematic review and meta-analysis.BMC cancer · 2026Pooled it
- Osteosarcoma Across the Age Spectrum: Why Outcomes Diverge and Trials Must Adapt.Journal of clinical medicine · 2026Review
- Next-generation osteosarcoma models for precision medicine.Communications biology · 2026Review
- Network pharmacology reveals thatGenes & diseases · 2026Article
- GPRC5B Identified by m5C meRIP-Seq Suppresses Apoptosis in Osteosarcoma Through NSUN2-Mediated RNA Methylation.Cancer science · 2026Article
- Exposure to nitrosatable drugs during pregnancy and childhood cancer: A cohort study in Taiwan.International journal of cancer · 2026Article
- Deciphering lncRNA and circRNA control of autophagy in osteosarcoma mechanisms and clinical translation.Discover oncology · 2026Review
- Single-Cell Transcriptomic Analysis Suggests That JUN May Regulate BAMBI to Promote Osteosarcoma Cell Migration and Invasion.Human mutation · 2026Article
- Decoding osteosarcoma from heterogeneity to precision therapy.Discover oncology · 2025Review
- Exploring Emerging Therapeutic Targets in Osteosarcoma by Revisiting the Immune and Cancer-Intrinsic Hallmarks of Cancer.Cancers · 2025Review
- Review
- Therapeutic Targeting of BET Proteins in Sarcoma.Molecular cancer therapeutics · 2025Review
- CAFs exosomal miR-21-5p suppresses ferroptosis and promotes proliferation and migration in osteosarcoma.Cancer cell international · 2025Article
- Epigenetic Modifications in Osteosarcoma: Mechanisms and Therapeutic Strategies.Life (Basel, Switzerland) · 2025Review
- Comparison of Differentially Expressed Genes in Human and Canine Osteosarcoma.Life (Basel, Switzerland) · 2025Article
- Androgen-induced AR-BRD4 transcriptional regulatory complex promotes malignant proliferation of osteosarcoma cells.Cell death discovery · 2025Article
- Piperazine-Derived Bisphosphonate-Based Ionizable Lipid Nanoparticles Enhance mRNA Delivery to the Bone Microenvironment.Angewandte Chemie (International ed. in English) · 2025Article
- COL12A1 Promotes Osteosarcoma Progression via the FAK/PI3K/AKT/mTOR Pathway.Current molecular medicine · 2025Article
- Involvement ofFrontiers in oncology · 2025Review
- Development and pan-cancer validation of an epigenetics-based random survival forest model for prognosis prediction and drug response in OS.Frontiers in pharmacology · 2025Article
27 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Osteosarcoma (OS) is a bone tumor of mesenchymal origin, most frequently occurring during the rapid growth phase of long bones, and usually located in the epiphyseal growth plates of the femur or the tibia. Its most common feature is genome disorganization, aneuploidy with chromosomal alterations, deregulation of tumor suppressor genes and of the cell cycle, and an absence of DNA repair. This suggests the involvement of surveillance failures, DNA repair or apoptosis control during osteogenesis, allowing the survival of cells which have undergone alterations during differentiation. Epigenetic events, including DNA methylation, histone modifications, nucleosome remodeling and expression of non-coding RNAs have been identified as possible risk factors for the tumor. It has been reported that p53 target genes or those genes that have their activity modulated by p53, in addition to other tumor suppressor genes, are silenced in OS-derived cell lines by hypermethylation of their promoters. In osteogenesis, osteoblasts are formed from pluripotent mesenchymal cells, with potential for self-renewal, proliferation and differentiation into various cell types. This involves complex signaling pathways and multiple factors. Any disturbance in this process can cause deregulation of the differentiation and proliferation of these cells, leading to the malignant phenotype. Therefore, the origin of OS seems to be multifactorial, involving the deregulation of differentiation of mesenchymal cells and tumor suppressor genes, activation of oncogenes, epigenetic events and the production of cytokines.
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Identifiers
What OpenQuestion 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 OpenQuestion graph.