Expression of survivin in extrapelvic endometriosis and in normal endometrium

Abstract

Endometriosis in cicatrix after cesarean section represents the only localization of endometriotic implant which etiology is unknown. Survivin is a new inhibitor of apoptosis (IAP) expressed during development and in human malignancy, but its expression has not been reported in normal adult tissues or benign disease. Recently, survivin mRNA expression levels in endometriotic implants were significantly higher than those in normal endometrium. In this study, we examined survivin expression in extrapelvic endometriosis and normal endometrium by immunohistochemical stain. Retrospective study The study was enrolled 49 patients. The study group was 15 patients with extrapelvic endometriosis and the control group was 34 patients (19 proliferative phase, 15 secretory phase) without endometriosis who underwent hysterectomy with myoma. Expression of Survivin was immunohistochemically investigated in extrapelvic endometriosis. For immunohistochemical staining, survivin used polyclonal rabbit antihuman antibody (Surv 11; Alfa Diagnostic International, San Antonio, TX, USA) The extensity was scored as 0=<5%; 1=5–25%; 2=25–50%; 3=50–75%; and 4=>75%. The intensity was scored as 1+(weak), 2+(moderate), or 3+ (intense). The score of immunohistochemical staining was evaluated semi quantitative method modified by Sinicrope and Lu. Statistical analyses were carried out using one-way ANOVA with Turkey test. P<0.05 was considered to be statistically significant. Survivin was expressed in glandular epithelial cells and stromal cells with extrapelvic endometriosis. Staining of survivin was located to cytoplasm and nucleus in both groups. In normal endometrium, cytoplasmic expression of survivin in glandular epithelial cells (proliferative phase; 3.32± 1.97 vs. secretory phase; 0.60 ± 1.68, p<0.05) and stromal cells (proliferative phase; 2.05 ± 2.01 vs. secretory phase; 0.40 ± 1.06, p<0.05) varied marked during menstrual cycle. In nuclear expression in glandular epithelial cells and stromal cells, no statistically significant cyclic variation were observed throuthout the cycle. In extrapelvic endometriosis, survivin expression in glandular epithelium ( nucleus; 6.40 ± 2.53, cytoplasm; 3.33 ± 2.77) was stronger than normal endometrium ( proliferative phases: nucleus; 5.47 ± 2.39, cytoplasm; 3.32 ± 1.97, secretory phase: nucleus; 6.39 ± 2.50, cytoplasm; 0.60 ± 1.68). But only cytoplasm of glandular epithelial cells in extrapelvic endometriosis (3.33 ± 2.77) showed statistically significant in comparison with secretory phases ( 0.60 ± 1.68) in normal endometrium. The expression of nucleus in stromal cells with extrapelvic endometriosis ( 6.40± 2.53) was stronger than during proliferative phase (4.74 ± 2.23) and secretory phase ( 4.73 ± 2.78) but was not significant. In extrapelvic endometriosis, survivin expression was stronger than normal endometrium except cytoplasm of stromal cells. Our findings suggest that increased survivin expression may contribute to survival of extrapelvic implants. Moreover, the antiapoptosis function of survivin may play an important role in the endometriotic implant growth promotion.