The molecular docking analysis reveals the better inhibitory nature of the ACTP molecule against the colony-stimulating factor 1 (CSF1) gene which causes tenosynovial giant-cell tumor.
The biologic significance of this translocation is not clear; however, the 1p21 locus is in the region of colony stimulating factor (CSF-1), which may play a role in tumorigenesis, as has been described in pigmented villonodular synovitis and tenosynovial giant cell tumor.
We defined the CSF1 response signature by identifying genes overexpressed in tenosynovial giant cell tumor and pigmented villonodular synovitis (tumors composed predominantly of macrophages recruited in response to the overexpression of CSF1) compared with desmoid-type fibromatosis and solitary fibrous tumor.
We recently demonstrated that CSF1, the ligand of the tyrosine kinase receptor, CSF1R, can be translocated in pigmented villonodular synovitis (PVNS) and tenosynovial giant cell tumor (TGCT).