1,2), index finger in 20,3% (n=13), over the hand in 20,3% of patients (n=13), ring finger in 7,8% (n=5) and little finger in 7,8% (n=5) (Table 1). Fig. 1 Giant cell tumor of tendon sheath of thumb, preoperative aspect. Table 1 ANATOMIC LOCATION OF GCTTS. Our selleck chem Imatinib recurrence rate was 4,7% (n=3). Macroscopically the average size of tumor was 1,35 cm (min= 0,3 cm, max= 5 cm). Microscopically all tumors contained multinucleated giant cells, histiocytes and haemosiderin deposits. Five cases were single nodule within a thin capsule. In all cases we used magnifying loupe or operating microscope. In 3 patients (4,7%) we founded bone erosion, in 7 cases (10,9%) tendon involvement with flexors/extensors ratio 4:3. In these cases we made a complete excision and bone curettage.

Seven patients (10,9%) presented the involvement of neurovascular bundle; in five cases it was possible to respect the vascular axis, in the other two patients the axes were rebuilt with vein grafting. In the three recurrence cases surgical excision was difficult due to the relationship with the neurovascular structures and the layout of the surrounding soft tissues that did not allow easy exposure of the structures involved. Discussion Histologically GCTTS is composed of multinucleated giant cells, histiocytes polyhedral, fibrotic material and hemosiderin deposits (12,14,15); histological aspects such as the cellularity and mitosis does not seem to affect the prognosis of cancer (5,9,16). Jaffe was the first, in 1941, who described GCTTS as a tenosynovitis, a nonneoplastic reaction (17).

This conclusion was supported by Vogrincic et al (1997), who detected polyclonal cells in the lesion, utilizing a polymerase chain reaction based assay for methylation of the X-linked human gene (18). Cytogenetic studies, however, suggested otherwise; for example simple structural and numeric aberrations, as well as a variety of balanced chromosomal aberrations have been discovered (19). In particular, clonal structural aberrations affecting the 1p11 to 1p13 region (20) and trisomies (21)of chromosomes 5 and 7 were commonly found. Using fluorescent in situ hybridization probes, Nilsson et al detected recurrent breakpoints localized to 1p13, often partnered with 2q35 (19,20). On these results, they suggested activation of a growth promoting gene through balanced translocation as the pathogenic mechanism.

However, because similar translocations had been found in hemorrhagic and rheumatoid synovitis, there were still doubts about a neoplastic origin (3). Macrophage colony stimulating factor (CSF1) is a secreted cytokine/hematopoietic growth factor that plays an essential role in the proliferation, differentiation, and survival of monocytes, macrophages, and related cells. It is localized Anacetrapib to the 1p13 breakpoint and appears to have a major oncogenic role in GCTTS (22).