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Endometriosis-associated ovarian carcinoma : Differential expression of vascular endothelial growth factor and estrogen/progesterone receptors

✍ Scribed by Marcela G. del Carmen; Anne E. Smith Sehdev; Amanda Nickles Fader; Marianna L. Zahurak; Michael Richardson; John P. Fruehauf; F. J. Montz; Robert E. Bristow


Publisher
John Wiley and Sons
Year
2003
Tongue
English
Weight
193 KB
Volume
98
Category
Article
ISSN
0008-543X

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✦ Synopsis


Abstract

BACKGROUND

Multiple epidemiologic and histologic studies have suggested that ovarian endometriosis can give rise to malignant ovarian tumors, primarily those of epithelial origin. The progression of endometriosis to endometriosis‐associated ovarian carcinoma (EAOC) has not been investigated thoroughly and is poorly understood at best. Using immunohistochemical methods, we compared the differential expression patterns of various cytokines and growth factors in atypical endometriosis (AE) and EAOC.

METHODS

Using the Johns Hopkins Pathology Data Bank, tissue blocks from patients diagnosed with EAOC or AE were identified. Tissue blocks were stained for 4 markers: vascular endothelial growth factor (VEGF), Ki‐67, estrogen receptor (ER), and progesterone receptor (PR).

RESULTS

Seventeen cases of EAOC and 8 cases of AE were identified. Staining for VEGF was documented in 16 of 17 (94%) EAOC tissue blocks and in only 1 of 8 (12.5%) AE tissue blocks (P < 0.0001). Only 4 of the 17 (23%) EAOC tissue blocks exhibited positive staining for ER, compared with 8 of 8 (100%) AE tissue blocks (P = 0.0005). Positive staining for PR was noted in only 6 of 17 (35%) EAOC samples but was present in 8 of 8 (100%) AE samples (P = 0.003). Seventy percent of EAOC samples exhibited positive staining for Ki‐67, compared with 37.5% of AE samples (P = 0.19).

CONCLUSIONS

EAOC appears to be associated with overexpression of VEGF and reduced expression of both ER and PR. Variations in VEGF expression may be associated with the malignant transformation of endometriosis and may present both diagnostic and therapeutic options for the treatment of ovarian malignancies. Cancer 2003. Β© 2003 American Cancer Society.

DOI 10.1002/cncr.11714


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