Neoplastic lesions
TGCT is a reactive, inflammatory neoplasm, although originally it was regarded as a nontumoral process.1,3,4
Molecular pathogenesis
As explained above, pathogenesis of TGCT is believed to start when a small number of neoplastic cells that arise from the lining of the synovium overexpress a growth factor called CSF-1. In most patients, CSF-1 overexpression is reported as a result of a genetic translocation.1,2
Tumor landscape
Typically, TGCT tumors are composed of a small number of these neoplastic cells (2% to 16%) and a high number of CSF-1R–expressing myeloid-lineage cells, including monocytes and macrophages, recruited through CSF-1 signaling.1,3
CSF-1 and TGCT formation and progression
Autocrine stimulation
CSF-1 may activate CSF-1R in cells within
the tumor, resulting in the proliferation of neoplastic cells.1
Paracrine effect
CSF-1 may recruit CSF-1R–expressing myeloid-lineage cells that comprise
the majority of the tumor mass.1
TGCT morbidity
CSF-1 overexpression may also contribute
to the inflammation and osteochondral destruction seen in some cases of tenosynovial giant cell tumor (TGCT)
within the affected joint.2,5
References