The activated macrophage colony-stimulating factor (CSF-1) receptor as a predictor of poor outcome in advanced epithelial ovarian carcinoma

Objective. We have previously shown that the macrophage colony-stimulating factor receptor (CSF-1R) and its ligand, CSF-1, together predict poor progn osis in epithelial ovarian carcinoma. The activated or phosphorylated form of CSF-1R (CSF-1Rphos) has been associated with enhanced invasive and metas tatic potential. Our goal is to correlate CSF-1Rphos with known prognostic factors and to determine its role in predicting outcome in advanced ovarian cancer. Methods. One hundred forty-two primary and forty-seven metastatic epithelia l ovarian tumors from 98 patients were immunohistochemically stained using antibodies PY809 and PY723 against their respective tyrosine residues assoc iated with local invasiveness and metastasis. chi (2) analysis was used to correlate CSF-1Rphos staining and previously studied prognosticators within each group. Kaplan-Meier curves of survival were compared using the log-ra nk test with significance of P < 0.05. Results. Forty-seven and nine-tenths percent (68/142) of primary tumors and forty-eight and nine-tenths percent (23/47) of metastatic tumors stained p ositive for PY809 and PY723, respectively. The PY809+ group was strongly as sociated with CSF-1R (P = 0.015) as was the PY723 + group (P = 0.025) in it s respective subset. CSF-1Rphos by itself was not a predictor of survival o r disease-free interval (DFI) in either the primary or metastatic group. Ho wever, when combined with CSF-1R in the metastatic group, the two together predicted worse survival (P = 0.007) and decreased DFI (P = 0.011). Conclusions, Phosphorylated tyrosine kinase receptors are detectable in a s ignificant number of ovarian tumors, Staining strongly correlates with CSF- 1R. PY723+ metastases coexpressing CSF-1R portend a highly significant decr ease in survival and increased risk of recurrence which may serve to identi fy high-risk ovarian cancer patients. (C) 2001 Academic Press.