Osteosarcomagenesis: Modeling Cancer Initiation in the Mouse
Open accessAbstract
Osteosarcoma remains a deadly malignancy afflicting adolescents and young adults. The lack of a precursor and the panoply of genetic aberrations present in identified osteosarcomas makes study of its initiation difficult. A number of candidate hypotheses have been tested in the mouse, a species with a higher background incidence of osteosarcoma. Chemical carcinogens, external beam radiation, and bone-seeking heavy metal radioisotopes have all proven to be osteosarcomagenic in wild-type mice. A number of oncogenes, introduced via integrating viruses or aberrantly activated from heritable genetic loci, participate in and can individually drive osteosarcomagenesis. Germline and conditional gene ablations in the form of some but not all aneuploidy-inducing genes, conventional tumor suppressors, and factors that function normally in mesenchymal differentiation have also proven osteosarcomagenic, especially in combinations that silence the Rb1 and p53 pathways. This paper reviews the rich history of mouse models of osteosarcomagenesis, what they have taught us about the human disease, and what future mouse experiments yet promise to teach.
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Epidemiological observations support the interpretation that osteosarcoma arises most frequently within the metaphyses of long bones during peak linear growth, suggesting that rapidly proliferating bone-producing and cartilage-producing cells are susceptible to transformation.
“Epidemiological observations support this interpretation as tumours were found to arise most frequently within the metaphyses of long bones in children, adolescents and young adults during times of peak linear growth, suggesting that the bone-producing and cartilage-producing cells that proliferate rapidly during those growth spurts are those susceptible to the transformation giving rise to osteos”
From Osteosarcoma (2022) · cites this paper as [29]
Genetically engineered mouse models have been most successful when introducing TP53 and other mutations using promoters for genes activated along the path from mesenchymal stem cells to osteoblasts.
“Similarly, genetically engineered mouse models have been most successful when introducing TP53 and other mutations using promoters for genes activated along the path that leads from mesenchymal stem cells to osteoblasts 29 .”
From Osteosarcoma (2022) · cites this paper as [29]
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 [29]
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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
Roberts, R. D., Lizardo, M. M., Reed, D. R., Hingorani, P., Glover, J., Allen‐Rhoades, W., Fan, T., Khanna, C., Sweet‐Cordero, E. A., Cash, T., et al. (2019) · Cancer · doi:10.1002/cncr.32351 · Cited by 127 · see citing works
At-Risk Populations for Osteosarcoma: The Syndromes and Beyond
Calvert, G. T., Randall, R. L., Jones, K. B., Cannon-Albright, L., Lessnick, S., & Schiffman, J. D. (2012) · Sarcoma · doi:10.1155/2012/152382 · Cited by 90 · see citing works
Self-citationFan, T. M., Roberts, R. D., & Lizardo, M. M. (2020) · Frontiers in Oncology · doi:10.3389/fonc.2020.00013 · Cited by 90 · see citing works
Du, L., Han, X.-G., Tu, B., Wang, M.-Q., Qiao, H., Zhang, S.-H., Fan, Q.-M., & Tang, T.-T. (2018) · Cell Death & Disease · doi:10.1038/s41419-018-0745-0 · Cited by 70 · see citing works
- Authors
- Jones, K. B.
- Affiliations
- University of Utah (US)
- Corresponding author
- Jones, Kevin B.
- ORCID
- Jones, Kevin B.
- Venue
- Sarcoma
- Publisher
- Wiley
- Published
- 2011
- Volume
- 2011
- Pages
- 1-10
- ISSN
- 1357-714X (ISSN-L)
- 1369-1643
- PMC
- PMC3043296
- OpenAlex
- W2023269839
- Cited by
- 40
- References
- 95
- Citations by year
- 2024: 2 · 2023: 1 · 2022: 3 · 2021: 1 · 2020: 3 · 2019: 3 · 2018: 4 · 2017: 2 · 2016: 7 · 2015: 2 · 2014: 4 · 2013: 2 · 2012: 5
- FWCI
- 3.27
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Locations
- Sarcoma (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Institutes of Health (K08CA138764)
- Huntsman Cancer Institute Nuclear Control Program (K08CA138764)
- Huntsman Cancer Foundation (K08CA138764)
- University of Utah (K08CA138764)
- Topics
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Sarcoma Diagnosis and Treatment
- Health Sciences › Medicine › Rheumatology › Bone Tumor Diagnosis and Treatments
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Keywords
- osteosarcoma, tumor initiation, mouse model, chemical carcinogens, radiation-induced sarcoma, oncogenes, tumor suppressor, mesenchymal differentiation, p53 pathway, gene ablation
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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