ArticleCancer cell2014
Notch activation as a driver of osteogenic sarcoma.
Article in Cancer cell, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.
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.
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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.
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Who cites it
81 citing papers in PubMed, 134 citations in OpenAlex.
- An immunocompetent, multifluorescent resource for real-time analysis of osteosarcoma progression, metastasis, and response to therapy.Science advances · 2026Article
- Skeletal stem cell lineages in osteosarcoma and bone metastasis.Journal of bone and mineral metabolism · 2026Review
- Mouse Models of Osteosarcoma: Unraveling Disease Mechanisms and Accelerating Drug Discovery and Development.Cancer reports (Hoboken, N.J.) · 2025Review
- Emerging roles and therapeutic potential of non-coding RNA in osteosarcoma: a review.Medical oncology (Northwood, London, England) · 2025Review
- Targeting developmental vulnerabilities in childhood sarcomas.Cancer metastasis reviews · 2025Review
- Molecular and Glycosylation Pathways in Osteosarcoma: Tumor Microenvironment and Emerging Strategies Toward Personalized Oncology.Current issues in molecular biology · 2025Review
- Review
- Clinical, pathologic and molecular findings in 2 Rottweiler littermates with appendicular osteosarcoma.Research square · 2024Article
- Hdac1 and Hdac2 positively regulate Notch1 gain-of-function pathogenic signaling in committed osteoblasts of male mice.Birth defects research · 2024Article
- Emerging roles of long non-coding RNAs in osteosarcoma.Frontiers in molecular biosciences · 2024Review
- Oncogenic signaling-mediated regulation of chromatin during tumorigenesis.Cancer metastasis reviews · 2023Review
- Signal Pathways and microRNAs in Osteosarcoma Growth and the Dual Role of Mesenchymal Stem Cells in Oncogenesis.International journal of molecular sciences · 2023Review
- The Intricate Notch Signaling Dynamics in Therapeutic Realms of Cancer.ACS pharmacology & translational science · 2023Review
- Self-Renewal and Pluripotency in Osteosarcoma Stem Cells' Chemoresistance: Notch, Hedgehog, and Wnt/β-Catenin Interplay with Embryonic Markers.International journal of molecular sciences · 2023Review
- Protein kinase CK2 phosphorylates a conserved motif in the Notch effector E(spl)-Mγ.Molecular and cellular biochemistry · 2023Article
- NOTCH Signaling in Osteosarcoma.Current issues in molecular biology · 2023Review
- Cellular dynamics of distinct skeletal cells and the development of osteosarcoma.Frontiers in endocrinology · 2023Review
- Multi-omics analysis identifies osteosarcoma subtypes with distinct prognosis indicating stratified treatment.Nature communications · 2022Article
- Regulation of Molecular Targets in Osteosarcoma Treatment.International journal of molecular sciences · 2022Review
- Nanoengineering a metal-organic framework for osteosarcoma chemo-immunotherapy by modulating indoleamine-2,3-dioxygenase and myeloid-derived suppressor cells.Journal of experimental & clinical cancer research : CR · 2022Article
21 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
12 authors at 1 institution in 1 country.
Funding
Abstract
Osteogenic sarcoma (OS) is a deadly skeletal malignancy whose cause is unknown. We report here a mouse model of OS based on conditional expression of the intracellular domain of Notch1 (NICD). Expression of the NICD in immature osteoblasts was sufficient to drive the formation of bone tumors, including OS, with complete penetrance. These tumors display features of human OS; namely, histopathology, cytogenetic complexity, and metastatic potential. We show that Notch activation combined with loss of p53 synergistically accelerates OS development in mice, although p53-driven OS is not Rbpj dependent, which demonstrates a dual dominance of the Notch oncogene and p53 mutation in the development of OS. Using this model, we also reveal the osteoblasts as the potential sources of OS.
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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.