目的 研究c-myc、cyclinE在子宫内膜息肉中的表达情况，进一步从分子水平阐明子宫内膜息肉的发病机制。方法 绝经前子宫内膜息肉组织64例作为息肉组，同时选择同一患者宫腔内远离息肉组织的正常内膜64例作为对照组1，绝经前宫腔镜下取环的正常子宫内膜及行子宫纵隔宫腔镜电切术的正常子宫内膜64例作为对照组2。采用免疫组织化学法检测c-myc、cyclinE在各组腺体和间质的表达情况并进行比较。结果 c-myc在息肉组腺体、间质中表达的阳性率分别为76.6%、71.9%，同样cyclinE在腺体、间质中表达的阳性率分别为81.3%、75.0%，这些率均高于对照组，差异有统计学意义（P＜0.01）。c-myc和cyclinE在子宫内膜息肉腺体和间质中的表达均呈正相关（r=0.585，P＜0.01；r=0.522，P＜0.01）。结论 c-myc、cyclinE在绝经前子宫内膜息肉的腺体和间质中的过度表达可能是子宫内膜息肉发生、发展的原因。
Abstract
Objective To investigate the expression of c-myc and cyclinE in endometrial polyps, and to clarify the pathogenesis of endometrial polyps in molecular level. Methods 64 patients with premenopausal endometrial polyps were recruited as polyps group. At the same time, from the same 64 patients’ endometium, far from endometrial polyps, normal endomentrial tissues were taken as control group 1. And, from other 64 premenopausa patients, who underwent hysteroscopic removal of contraceptive ring or hysteroscopic resection of uterine septum, normal endometrial tissues were taken as control group 2. Immunohistochemistrical Methods were used to detect c-myc、cyclinE expression and to compare in each group of glands and stroma. Results The positive rates of expression of c-myc in glands and stroma in polyps group were 76.6% and 71.9%, respectively. And the positive rates of expression of cyclinE in glands and stroma were 81.3% and 75.0%, respectively. These rates were higher than those in the control groups and the difference was statistically significant（P＜0.01）. The expression of c-myc and cyclinE in glands and stroma in endometrial polyps was positively correlated（r=0.585，P＜0.01；r=0.522，P＜0.01）. Conclusions Excessive expression of c - myc and cyclinE in premenopausal endometrial polyps of the glands and stroma may be the cause of occurrence and development of endometrial polyps.
关键词
子宫内膜息肉 /
c-myc /
cyclinE
Key words
Endometrial polyps /
c-myc /
cyclinE
{{custom_sec.title}}
{{custom_sec.title}}
{{custom_sec.content}}
参考文献
［1］ Anastasiadis P G, Koutlaki N G, Skaphida P G, et al. Endometrial polyps: prevalence, detection, and malignant potential in women with abnormal uterine bleeding ［J］. Eur J Gnaecol Oncol, 2000, 21(2) : 180-183.
［2］ Bakour S H, Gupta J K, Khan K S. Risk factors associated with endometrial polyps in abnormal uterine bleeding ［J ］. Int J Gynaecol Obstet, 2002, 76(2): 165-168.
［3］ Taylor L J, Jackson T L, Reid J G, et al. The differential expression of oestrogen receptors, progesterone receptors, Bcl-2 and Ki67 in endometrial polyps［J］. BJOG, 2003, 110(9): 794-798.
［4］ Mittal K, Schwartz L, Goswami S, et al. Estrogen and progesterone receptor expression in endometrial polyps［J］. Int J Gynecol Patho, 1996, 15( 4): 345-348 .
［5］ Gul A, Ugur M, Iskender C, et al. Immunohistochemical expression of estrogen and progesterone receptor in endometrial polyps and its relationship tocl-inical parameters ［J］. Arch Gynecol Obstet，2010，281(3): 479-483.
［6］ S rlie T, Wang Y, Xiao C, et al. Distinct molecular mechanisms underlying clinically relevant subtypes of breast cancer: gene expression analyses across three different platforms［J］. BMC Genomics, 2006, 7:127.
［7］ Cheng P C, Chang H K, Chen S H. Quantitative nanoproteomics for protein complexes (QNanoPX) related to estrogen transcriptional action［J］. Mol Cell Proteomics，2010, 9(2): 209-224.
［8］ Guo P, Dong X Y, Zhao K W, et al. Estrogen-induced interaction between KLF5 and estrogen receptor (ER) suppresses the function of ER in ER-positive breast cancer cells ［J］. Int J Cancer, 2010, 126(1): 81-89.
［9］ Rosenberg E, Demopoulos R I, Zeleniuch-Jacquotte A, et al. Expression of cell cycle regulators p57 (kip2), cyclinD1, and cyclinE in epithelial ovarian tumors and survival［J］. Hum Pathol，2001, 32(8): 808-813.
［10］ Farley J, Smith L M, Darcy K M, et al. CyclinE expression is a significant predictor of survival in advanced, suboptimally debulked ovarian epithelial cancers: a Gynecologic Oncology Group study ［J］. Cancer Res, 2003, 63(6): 1235-1241.
［11］ O’Hagan R C, Ohh M, David G, et al. Myc-enhanced expression of cul1 promotes ubiquitin-dependent proteolysis and cell cycleprogression ［J］. Genes Dev, 2000, 14(17): 2185-2191.
［12］ Yang W, Shen J, Wu M, et al. Repression of transcription of the p27(Kip1) cyclin-dependent kinase inhibitor gene by c-Myc［J］. Oncogene, 2001, 20(14): 1688-1702.
［13］ Jiang X L, Cui H F. Analysis of 10218 ulcerative colitis cases in China ［J］. World J Gastroenterol, 2002, 8(1): 158-161.
PDF(1149 KB)
