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Endometrial BCL6 Overexpression in Eutopic Endometrium of Women With Endometriosis

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Abstract

The objective of this study was to examine B-cell CLL/lymphoma 6 (BCL6) expression in human eutopic endometrium across the menstrual cycle in women with and without endometriosis and to establish a cutoff for future studies. This design was a series of case-control studies in tertiary University teaching hospitals. We examined BCL6 expression by messenger RNA and immu-nohistochemically in prospectively collected samples in both the proliferative (P) and the secretory phases. BCL6 is minimally increased in the mid-secretory phase of the menstrual cycle compared to the P phase in normal patients. BCL6 protein expression was significantly higher in the secretory phase of patients with endometriosis (n = 29) versus fertile controls without endometriosis at laparoscopy (n = 20; P <.0001). Normal fertile controls (n = 28) recruited for endometrial biopsy also had low levels of secretory phase BCL6 expression compared to women with unexplained infertility (Ul; n = I 19). A receiving-operator characteristic analysis of these data revealed an area under the curve of 94% (95% confidence interval 85%-100%; P <.0001) with an HSCORE cutoff of 1.4 to differentiate cases with and without endometriosis. Using this cutoff value, BCL6 was positive in 88% of cases with Ul. Laparoscopic examination of a subset of 65 patients confirmed abnormalities in 98% of cases; 61 (93.8%) were found to have endometriosis, 3 (4.6%) with hydrosalpinx, and I (1.5%) with a normal pelvis. These data suggest that BCL6 is a promising candidate as a Single diagnostic biomarker for detection of endometriosis in women with otherwise Ul and may be associated with endometrial dysfunction, including progesterone resistance.

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Correspondence to Steven L. Young MD, PhD.

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Evans-Hoeker, E., Lessey, B.A., Jeong, J.W. et al. Endometrial BCL6 Overexpression in Eutopic Endometrium of Women With Endometriosis. Reprod. Sci. 23, 1234–1241 (2016). https://doi.org/10.1177/1933719116649711

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