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- Title
Expression of the macrophage colony-stimulating factor and its receptor in gynecologic malignancies.
- Authors
Baiocchi, Gabriela; Talpaz, Moshe; Gutterman, Jordan U.; Kurzrock, Razelle; Kavanagh, John J.; Wharton, J. Taylor; Baiocchi, G; Kavanagh, J J; Talpaz, M; Wharton, J T; Gutterman, J U; Kurzrock, R
- Abstract
Recently, hematopoietic growth factors have been implicated in protean nonhematopoietic processes. In the current study, expression of macrophage colony-stimulating factor (M-CSF) and its receptor (the c-fms proto-oncogene) was investigated in 42 samples of gynecologic tissues. There were 15 samples of normal ovarian and uterine tissue or benign conditions of these organs; 11 samples of primary ovarian cancer tissue; seven samples of metastatic ovarian cancer tissue; and nine samples of primary endometrial cancer tissue. Steady state transcript levels were assessed by Northern Blot analysis. Macrophage colony-stimulating factor (M-CSF) expression was not observed in any of the specimens of benign abnormalities or of normal organs; c-fms expression was detected in two of 15 (13%) of these specimens, albeit at very low levels. In contrast, 14 (78%) of 18 ovarian tumor specimens, and five (55%) of nine endometrial tumor specimens expressed M-CSF. Similarly, 16 (89%) of 18 ovarian tumor specimens and six (67%) of nine endometrial tumor specimens expressed c-fms. Most positive malignant tissues (19 [86%] of 22) showed coexpression of M-CSF and c-fms. Of interest, M-CSF and c-fms mRNA were detected in tumor, but not in adjacent normal tissue. Furthermore, M-CSF and c-fms transcripts were produced by all metastatic tumors, including two cases in which the corresponding primary tumor from the same patient was negative. Because M-CSF mediates its effects by binding to its receptor, the increased levels of both these gene products in gynecologic malignancies suggest that an interaction between M-CSF and c-fms may participate in the development of ovarian and endometrial carcinomas and especially in progression to the metastatic state.
- Publication
Cancer (0008543X), 1991, Vol 67, Issue 4, p990
- ISSN
0008-543X
- Publication type
journal article
- DOI
10.1002/1097-0142(19910215)67:4<990::AID-CNCR2820670422>3.0.CO;2-8