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Epigenetic Abnormalities in Chondrosarcoma

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MDPI
DOI: 10.3390/ijms24054539

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chondrosarcoma; epigenetic mechanisms; targeted therapy

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In recent years, there has been significant progress in understanding the role of epigenetic mechanisms in tumor pathology. Various modifications to DNA and histones can impact gene expression and contribute to the development of tumors. MicroRNAs also play a role in regulating gene expression at a post-transcriptional level. This review focuses on the specific case of chondrosarcoma, a rare bone tumor, and summarizes the current understanding of how epigenetic alterations contribute to its pathogenesis and potential therapeutic approaches that target these modifications.
In recent years, our understanding of the epigenetic mechanisms involved in tumor pathology has improved greatly. DNA and histone modifications, such as methylation, demethylation, acetylation, and deacetylation, can lead to the up-regulation of oncogenic genes, as well as the suppression of tumor suppressor genes. Gene expression can also be modified on a post-transcriptional level by microRNAs that contribute to carcinogenesis. The role of these modifications has been already described in many tumors, e.g., colorectal, breast, and prostate cancers. These mechanisms have also begun to be investigated in less common tumors, such as sarcomas. Chondrosarcoma (CS) is a rare type of tumor that belongs to sarcomas and is the second most common malignant bone tumor after osteosarcoma. Due to unknown pathogenesis and resistance to chemo- and radiotherapies of these tumors, there is a need to develop new potential therapies against CS. In this review, we summarize current knowledge on the influence of epigenetic alterations in the pathogenesis of CS by discussing potential candidates for future therapies. We also emphasize ongoing clinical trials that use drugs targeting epigenetic modifications in CS treatment.

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