  It is obvious that both epigenetic and non-epigenetic actors contribute to
tumorigenesis in chondrosarcomas and more generally in other cancers. Thus, the
main altered pathways in chondrosarcomas are now well established and include
both epigenetic and non-epigenetic pathways such as the PI3K-AKT signaling,
EGFR overexpression, SPARC overexpression, c-myc overexpression, IHH/GLI1 axis,
loss of Rb function, HIF1-alpha stabilization, IDH1 mutations, hypermethylation
and SIRT1. This review aims to provide a detailed analysis of these pathways
and highlights recurrent interactions between non-epigenetic and epigenetic
actors in chondrosarcomas, raising the intriguing possibility of developing
therapeutics targeting both epigenetic and non-epigenetic actors and supporting
data from previous studies. Finally, we propose some strategies for targeting
chondrosarcomas in vivo based on properties of this tumor.
