The mechanisms by which healthy cells transform into cancer cells are described in detail elsewhere (see Cancer main page; Carcinogenesis main page). The precise molecular changes that result in<unk>  are not always known, but certain types of<unk> s are associated with particular genetic mutations. Examples include: * Most cases of Ewing<unk>  are associated with a chromosomal translocation in which part of chromosome 11 fuses with part of chromosome 22. This results in the EWS gene becoming fused to other genes, including the FLI1 gene in 90% of Ewing cases and ERG gene in 5-10% of cases. These fusions result in the production of abnormal proteins, although how these abnormal proteins result in cancer is not fully known. * Dermatofibrosarcoma protuberans often is associated with a chromosomal translocation in which the COL1A1 gene becomes fused to the PDGFRB gene. This results in over-active PDGF signaling, which is thought to promote cell division and ultimately lead to tumor development. * Inflammatory myofibroblastic tumor often is associated with rearrangements of the ALK gene, and occasionally with rearrangements of the HMGA2 gene. * Giant cell tumor of soft tissue frequently is associated with a chromosomal translocation between chromosome 1 and chromosome 2, in which the CSF1 gene becomes fused with the COL6A3 gene. This results in increased CSF1 protein production, which is thought to play a role in cancer development. * Many liposarcomas are associated with duplication of part of chromosome 12, which results in extra copies of known cancer-promoting genes ("oncogenes") such as the CDK4 gene, the MDM2 gene and the HMGA2 gene.
Sarcoma
Angiosarcoma
Soft-tissue sarcoma
Hemangiosarcoma
Xanthoma
Myosarcoma
Epithelioma
Liposarcoma