Abstract
Chondrosarcomas are the second most common primary bone malignancy. Chondrosarcomas are characterized by the production of cartilaginous matrix and are generally resistant to radiation and chemotherapy and the outcomes are overall poor. Hence, there is strong interest in determining mechanisms of cancer aggressiveness and therapeutic resistance in chondrosarcomas. There are metabolic alterations in chondrosarcoma that are linked to the epigenetic state and tumor microenvironment that drive treatment resistance. This review focuses on metabolic changes in chondrosarcoma, and the relationship between signaling via isocitrate dehydrogenase 1 and 2 (IDH1 and IDH2), hedgehog, PI3K-mTOR-AKT, and SRC, as well as histone acetylation and angiogenesis. Also, potential treatment strategies targeting metabolism will be discussed including potential synergy with immunotherapies.
Highlights
Chondrosarcomas encompass a heterogeneous group of malignant cartilaginous matrix- producing tumors of the bone and are the second most common primary bone malignancy in humans, representing 25% of bone neoplasms [1]
Histological grading and staging of chondrosarcomas are the most important factors to aid in prognostication. 85% of chondrosarcomas are histologically classified as conventional chondrosarcomas and can be subcategorized as central or peripherally located [1,2,3]
Dedifferentiated chondrosarcomas are known to have tumor lymphocyte infiltration that correlates with PD-L1 expression and HLA expression, which suggest that these tumors might be sensitive to anticancer immunotherapy [78]
Summary
Ida Micaily 1, Megan Roche 1, Mohammad Y. Ibrahim 2, Ubaldo Martinez-Outschoorn 1 and Atrayee Basu Mallick 1*. Reviewed by: Cinzia Domenicotti, Università di Genova, Italy Maria Elena Pisanu, National Institute of Health (ISS), Italy. Specialty section: This article was submitted to Cancer Metabolism, a section of the journal
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