Colony-stimulating factor-1 and its receptor do not have a role in the pathogenesis of uterine sarcomas

Objective. Several studies have demonstrated overexpression of the mononucl ear phagocytic growth factor colony-stimulating factor-1 (CSF-1) and its re ceptor (CSF-1R) in breast, ovarian, and endometrial adenocarcinomas, and th eir expression in each of these cancers is strongly correlated with poor pr ognosis. In addition to adenocarcinomas, sarcomas that are highly malignant arise at much lower frequency in the uterus. Given the common organ of ori gin and hormonal environment of the adenocarcinomas, we evaluated the poten tial role of CSF-1 and CSF-1R in the genesis of these tumors using immunohi stochemical methods. Results. Immunohistochemical analysis was performed on 19 archival uterine sarcoma samples. Affinity-purified rabbit anti-CSF-1 antiserum (R52) and hu man cross-reactive murine anti-c-fms antibody were used. In the 19 cases ev aluated for CSF-1 immunoreactivity, 42.1% had staining in less than 25% of the tumor, 36.9% had staining in 25-50% of the tumor, and only 21% had stai ning in greater than 50% of the tumor. When present, the majority of the CS F-1 immunostaining was associated with the extracellular matrix. There was variable intensity in CSF-1 expression: 52.6% had negative to mild staining , and 47.4% had moderate to strong staining. Immunostaining for the CSF-1R revealed that 52.6% of tumors had expression in less than 25% of cells, 21. 0% had expression in 25-50% of the tumor, and 26.4% had staining in greater than 50% of the tumor. There was variable intensity of CSF-1R staining. Sl ight staining was found in 31.6% of the cases, moderate staining was found in 47.4% of the tumors, and 21.0% of the cases had strong expression. There was no statistically significant correlation between CSF-1 and CSF-1R expr ession and stage, estrogen/progesterone receptor status, number of mitoses per 10 high-power fields, or disease outcome. In addition, overall expressi on and intensity of CSF-1 and CSF-1R did not predict tumor virulence or dis ease outcome. Conclusion. In contradistinction to endometrial adenocarcinomas, in which C SF-1/CSF-1R is strongly correlated with tumor progression, CSF-1 and CSF-1R overexpression does not appear to play a role in the growth and differenti ation of uterine sarcomas. (C) 1999 Academic Press.