Understanding and Modeling Metastasis Biology to Improve Therapeutic Strategies for Combating Osteosarcoma Progression
Open accessAbstract
Osteosarcoma is a malignant primary tumor of bone, arising from transformed progenitor cells with osteoblastic differentiation and osteoid production. While categorized as a rare tumor, most patients diagnosed with osteosarcoma are adolescents in their second decade of life and underscores the potential for life changing consequences in this vulnerable population. In the setting of localized disease, conventional treatment for osteosarcoma affords a cure rate approaching 70%; however, survival for patients suffering from metastatic disease remain disappointing with only 20% of individuals being alive past 5 years post-diagnosis. In patients with incurable disease, pulmonary metastases remain the leading cause for osteosarcoma-associated mortality; yet identifying new strategies for combating metastatic progression remains at a scientific and clinical impasse, with no significant advancements for the past four decades. While there is resonating clinical urgency for newer and more effective treatment options for managing osteosarcoma metastases, the discovery of druggable targets and development of innovative therapies for inhibiting metastatic progression will require a deeper and more detailed understanding of osteosarcoma metastasis biology. Toward the goal of illuminating the processes involved in cancer metastasis, a convergent science approach inclusive of diverse disciplines spanning the biology and physical science domains can offer novel and synergistic perspectives, inventive, and sophisticated model systems, and disruptive experimental approaches that can accelerate the discovery and characterization of key processes operative during metastatic progression. Through the lens of trans-disciplinary research, the field of comparative oncology is uniquely positioned to advance new discoveries in metastasis biology toward impactful clinical translation through the inclusion of pet dogs diagnosed with metastatic osteosarcoma. Given the spontaneous course of osteosarcoma development in the context of real-time tumor microenvironmental cues and immune mechanisms, pet dogs are distinctively valuable in translational modeling given their faithful recapitulation of metastatic disease progression as occurs in humans. Pet dogs can be leveraged for the exploration of novel therapies that exploit tumor cell vulnerabilities, perturb local microenvironmental cues, and amplify immunologic recognition. In this capacity, pet dogs can serve as valuable corroborative models for realizing the science and best clinical practices necessary for understanding and combating osteosarcoma metastases.
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Companion cell lines with enhanced lung colonization capacity have enabled study of metastasis-driving mechanisms.
“Companion cell lines with enhanced lung colonization capacity, such as SaOS2-LM7, MG63.3 and 143B 209,210,211 , have enabled the study of metastasis-driving mechanisms 50,212 .”
From Osteosarcoma (2022) · cites this paper as [212]
Genetically engineered mouse models have provided numerous insights into how osteosarcoma arises and its pathophysiology.
“Many insights into the origins 29 and pathophysiology 212 of osteosarcoma have come from mouse models engineered to develop osteosarcoma 229 .”
From Osteosarcoma (2022) · cites this paper as [212]
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Beird, H. C., Bielack, S. S., Flanagan, A. M., Gill, J., Heymann, D., Janeway, K. A., Livingston, J. A., Roberts, R. D., Strauss, S. J., & Gorlick, R. (2022) · Nature Reviews Disease Primers · doi:10.1038/s41572-022-00409-y · Cited by 660 · see citing works
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- Authors
- Fan, T. M., Roberts, R. D., & Lizardo, M. M.
- Affiliations
- University of Illinois Urbana-Champaign (US)
- The Ohio State University Comprehensive Cancer Center – Arthur G. James Cancer Hospital and Richard J. Solove Research Institute (US)
- BC Cancer Agency (CA)
- Corresponding author
- Fan, Timothy M.
- Venue
- Frontiers in Oncology
- Publisher
- Frontiers Media SA
- Published
- 2020-01-31
- Volume
- 10
- Pages
- 13-13
- ISSN
- 2234-943X (ISSN-L)
- PMC
- PMC7006476
- OpenAlex
- W3004003781
- Cited by
- 90
- References
- 283
- Citations by year
- 2026: 8 · 2025: 11 · 2024: 4 · 2023: 14 · 2022: 15 · 2021: 26 · 2020: 12
- FWCI
- 2.35
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Frontiers in Oncology (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Funders
- BC Cancer Foundation
- National Institutes of Health (NIH-R01)
- University of Illinois at Urbana-Champaign
- National Cancer Institute (R01CA120439, K08CA201638)
- Carl R. Woese Institute for Genomic Biology
- Topics
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Sarcoma Diagnosis and Treatment
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Veterinary Oncology Research
- Health Sciences › Medicine › Oncology › Cancer Cells and Metastasis
- Keywords
- osteosarcoma, metastasis biology, lung metastasis, pet dogs, comparative oncology, translational animal model, tumor microenvironment, tumor immunology, druggable targets, metastatic progression, osteogenic differentiation
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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