MMP-7、PTEN在子宫内膜增生症及内膜样腺癌中的表达

目的研究基质金属蛋白酶-7(MMP-7)和抑癌基因(PTEN)在子宫内膜增生症至子宫内膜样腺癌组织中的异常表达及变化规律,探讨其作为子宫内膜早期癌变及浸润、转移的生物学标志的可能性。方法应用免疫组化S-P法检测15例正常增生期子宫内膜组织、40例子宫内膜增生症组织、38例子宫内膜样腺癌组织中MMP-7、PTEN的表达。结果在正常增生期子宫内膜,子宫内膜简单型、复杂型、不典型增生及子宫内膜样腺癌,MMP-7的阳性表达率呈递增趋势,PTEN呈递减趋势。等级相关分析结果显示:MMP-7、PTEN表达异常与癌组织学分级均显著相关(r分别为0.410和-0.569,P均<0.01)。除不典型增生外,正常增生期子宫内膜、子宫内膜简单型、复杂型增生与子宫内膜样腺癌组织中的MMP-7、PTEN表达差异有显著性。正常增生期子宫内膜、子宫内膜简单型增生与不典型增生比较,MMP-7、PTEN表达差异显著;在内膜样腺癌中,MMP-7与PTEN表达呈负相关(r=-0.392,P<0.01);MMP-7与肿瘤浸润深度呈正相关(r=0.389,P<0.05);PTEN蛋白表达与子宫内膜样腺癌的临床分期、组织学分级无关(P>0.05),与肌层浸润呈负相关(P<0.05)。结论MMP-7、PTEN蛋白在子宫内膜增生症至子宫内膜样腺癌组织中表达异常,两者可能成为子宫内膜组织早期癌变和预测生物学行为的重要分子标记物。     

PTEN、Ki-67与β-cat、MMP-7在Ⅰ型子宫内膜癌组织中的表达及意义

目的 探讨抑癌基因PTEN、增殖细胞核抗原Ki-67、β-连环素(P-Cat)及基质金属蛋白酶-7(MMP-7)在Ⅰ型子宫内膜癌发生、发展中的作用.方法 采用免疫组化SP法检测20份正常子宫内膜、69份单纯性增生、65份复杂性增生、57份非典型增生和82份Ⅰ型子宫内膜癌组织中PTEN、Ki-67与β-Cat、MMP-7表达并分析其与临床病 理参数的关系.结果 正常子宫内膜、单纯性增生、复杂性增生、非典型增生和Ⅰ型子宫内膜癌组织中PTEN蛋白阳性表达率依次降低,而Ki-67、β-Cat、MMP-7阳性表达率依次升高,子宫内膜癌和非典型增生组织中PTEN、MMP-7阳性表达率明显低于复杂性增生组织(P均＜0.05),内膜癌组织中Ki-67的阳性表达率明显高于非典型增生、复杂性增生组织(P均＜0.05),β-Cat 的异常表达率显著高于正常子宫内膜(P＜0.05).PTEN、Ki-67、β-Cat阳性率与临床分期和组织学分级有关,MMP-7阳性率仅与肌层浸润程度有关.内膜癌中PTEN蛋白表达与Ki-67、β-Cat呈负相关(P均＜0.05),β-Cat砒蛋白表达与MMP-7呈正相关(P＜0.05).结论 PTEN、Ki-67和β-Cat、MMP-7蛋白均参与了子宫内膜癌的发生、发展,有可能成为子宫内膜组织早期癌变的有用标记物.     

子宫内膜样腺癌组织中TFF3、ER、PR的表达及意义

目的探讨子宫内膜样腺癌（EC）组织中三叶因子3（TFF3）、雌激素受体（ER）及孕激素受体（PR）的表达及意义。方法采用免疫组化sP法检测15例良性子宫肌瘤组织、20例子宫内膜不典型增生组织、42例Ec组织中的TFF3、ER和PR,分析TFF3、ER、PR表达与Ec临床病理参数的关系及其相关性。结果TFF3在良性子宫肌瘤组织中的阳性表达率为20．0％,不典型增生组织中为45．0％,EC组织中为66．7％,不同组织间比较P均〈0．01;TFF3蛋白表达与EC的组织学分级和病理分期有关（P均〈0．05）,与浸润程度和淋巴结转移无关。ER在良性子宫肌瘤组织中的阳性表达率为93．3％,不典型增生组织中为70．O％,EC组织中为54．8％,不同组织间比较P均〈0．05;ER阳性表达与Ec的组织学分级相关（P〈0．05）,与分期、淋巴结转移和浸润程度无关。PR在良性子宫肌瘤组织中阳性表达率为86．7％,不典型增生组织中为75．0％,EC组织中为59．5％,不同组织间比较P〉0．05;PR表达与EC的组织学分级相关（P〈0．05）,与分期、淋巴结转移和浸润程度无关。Ec组织中TFF3表达与ER、PR均呈正相关（r=0．002、0．004,P均〈0．01）。结论Ec组织中TFF3表达明显升高,ER表达明显下降;TFF3、ER、PR对EC的发生、发展及预后可能起重要作用。     

不同病理类型子宫内膜组织中β-catenin、YAP-1、Survivin 表达观察

目的观察不同病理类型子宫内膜组织中β-链蛋白(β-catenin)、Yes相关蛋白1(YAP-1)和生存素(Survivin)的表达变化,并探讨三者与子宫内膜样腺癌发病的关系。方法采用免疫组化法分别检测增殖期、单纯性增生、复杂性增生子宫内膜组织及子宫内膜样腺癌组织中的β-catenin、YAP-1、Survivin。结果β-catenin、YAP-1、Survivin在增殖期、单纯性增生、复杂性增生子宫内膜组织及子宫内膜样腺癌组织中的阳性表达依次增多(P均<0.05);β-catenin在高分化、中分化、低分化子宫内膜样腺癌组织中的阳性表达依次减少(P均<0.05)。子宫内膜样腺癌组织中β-catenin与YAP-1、YAP-1与Survivin阳性表达均呈正相关关系(r分别为0.378、0.700,P均<0.05)。结论子宫内膜样腺癌组织中β-catenin、YAP-1、Survivin阳性表达增高,三者可能协同参与了子宫内膜样腺癌的发病。     

老年子宫内膜癌组织中ER、PR的表达及临床意义

目的 探讨老年子宫内膜癌雌激素受体(ER)、孕激素受体(PR)的表达以及临床意义.方法 选取老年子宫内膜癌患者43例(实验组),32例正常子宫内膜组织(对照组),采用免疫组化法检测两组人群中ER、PR的表达水平,结合临床病理资料进行相关分析.结果 (1)老年子宫内膜癌组织中ER和PR表达较对照组低(P＜0.05).(2)在老年子宫内膜癌组织中,随临床病理分期、组织学分级的升高和肌层浸润的加深,ER、PR的表达水平下降,差异均有统计学意义(P＜0.05).结论 ER、PR的检测反映了子宫内膜癌的生物学行为和预后,有助于指导其治疗.     

子宫内膜腺癌DNA结合抑制因子-1的表达及与雌激素受体(ER)α的相关性

目的 探讨DNA结合抑制因子-1(Id-1)在子宫内膜腺癌组织中的表达状态及与雌激素受体(ER)α之间的关系.方法 免疫组化法检测56例子宫内膜腺癌、18例子宫内膜不典型增生、20例正常子宫内膜组织中Id-1及ERα蛋白表达.结果 在正常子宫内膜组织、子宫内膜不典型增生及子宫内膜癌中Id-1表达逐渐增强(P＜0.05),ERα表达则逐渐减少(P＜0.05).Id-1蛋白阳性表达与组织分化程度及浸润肌层深度、手术病理分期有关(P＜0.05).ERα阳性表达与浸润肌层深度有关(P＜0.05).Id-1高表达患者的5年生存率低,但两组生存率差别无显著性意义(P＞0.05).Id-1与ERα表达之间呈正相关(r=0.284,P =0.034 ).结论 Id-1在子宫内膜癌中存在着过表达,并且可能与ERα协同参与了子宫内膜腺癌的发生发展.     

HOXA-11基因与女性生殖调节的研究

检测41例不明原因不孕患者（不孕组）及28例正常未孕者（对照组）子宫内膜组织中H0xA-11基因mRNA及雌激素受体（ER）、孕激素受体（PR）蛋白的表达,并通过组织学区分子宫内膜标本期别。结果不孕组中晚分泌期子宫内膜间质细胞中HOXA-11基因阳性表达率明显高于增生期,P＜0．05;HOXA-11基因在增生期及分泌期上皮细胞、间质细胞中表达率均明显高于不孕组,P均〈0．05。对照组分泌期子宫内膜腺上皮细胞中ER、PR阳性表达率明显低于间质细胞,P＜0．05;ER、PR在正常增生期子宫内膜腺上皮细胞中阳性表达率明显高于分泌期,P＜0．05。ER、PR在不孕组增生期子宫内膜上皮细胞及间质细胞中阳性表达率明显高于正常组,P均〈0．05;分泌期不孕组子宫内膜间质细胞ER、PR阳性表达率明显低于对照组。P均〈0．05。提示HOXA-11基因在子宫内膜的表达呈周期性变化,且与子宫内膜“着床窗”期-致,其在子宫内膜表达异常可能是女性不孕原因之-;HOXA-11基因对子宫内膜的作用通过ER、PR调节。     

子宫内膜癌组织中PR及其亚型PRA、PRB的表达变化及意义

目的观察子宫内膜癌组织中孕激素受体（PR）及其亚型PRA、PRB表达变化,并探讨其临床意义。方法采用免疫组化SP法检测正常子宫内膜（正常组）、不典型增生内膜（不典型增生组）及子宫内膜样腺癌内膜（内膜癌组）组织中的PR及其亚型PRA、PRB表达情况。结果不典型增生组和内膜癌组PR阳性表达率明显低于正常组（P均〈0.05）,内膜癌组PR表达强度低于正常组和典型增生组（P均〈0.05）。正常组、不典型增生组、内膜癌组PRA阳性表达率分别为100%、86.7%（13/15）、74.5%（41/55）,PRB阳性表达率分别为100%、80%（12/15）和69.1%（38/55）,内膜癌组PRA、PRB阳性表达率与正常组和不典型增生组相比均明显降低（P均〈0.05）。正常组25例（82.5%）PRA、PRB表达强度相等,不典型增生组和内膜癌组分别为7例（46.7%）、12例（21.8%）,内膜癌组明显低于正常组和不典型增生组,P均〈0.01。内膜癌组只表达PRA或PRA占优势者24例（43.6%）,明显多于正常组的5例（12.5%）和不典型增生组的4例（26.7%）,P均〈0.05。PRA表达与子宫内膜癌分化程度有关,PRB表达与子宫内膜癌分化程度、淋巴结转移和FIGO分期有关（P均〈0.05）。结论子宫内膜癌患者子宫内膜组织中PR、PRA、PRB表达均明显降低。子宫内膜组织PR亚型表达缺失、比例失衡,尤其是PRB表达缺失可能与子宫内膜癌的发生有关。     

HER-2、PTEN蛋白及ERα在子宫内膜癌中的表达及其临床意义

目的检测子宫内膜癌组织中HER-2、PTEN蛋白及雌激素受体亚型(ERα)表达并探讨其临床意义。方法采用免疫组织化学法检测60例子宫内膜癌、32例正常子宫内膜组织中HER-2、PTEN蛋白及ERα的表达。结果在正常的子宫内膜HER-2蛋白为低表达,子宫内膜癌中HER-2的表达率明显增高(P0.05),而且HER-2的表达与肿瘤组织学分级、病理学分期以及肿瘤浸润子宫肌层深度显著相关(P0.05),其表达与组织学类型、有无淋巴结转移无关(P0.05)。子宫内膜癌组织中PTEN缺失率高于正常子宫内膜组织(P0.05)。PTEN表达在G1级肿瘤高于G2、G3级(P0.05),PTEN蛋白缺失率与肿瘤组织类型有关(P0.05),与肌层浸润、淋巴结转移及病理分期无明显关系(P0.05)。HER-2与PTEN的表达呈呈明显负相关。ERα在子宫内膜癌表达低于正常子宫内膜,且随着病理分期表达显著降低(P0.05)。结论 PTEN表达缺失与临床病理参数无关,蛋白表达缺失常发生细胞分化较差的子宫内膜癌。PTEN蛋白表达缺失与HER-2表达水平有关。     

子宫内膜间质肿瘤免疫表型分析

对子宫内膜间质结节(ESN)、子宫内膜间质肉瘤(ESS)、未分化子宫内膜肉瘤(UES)患者分别进行CD10、重型钙调蛋白结合蛋白(h-caldesmon)、CD44v3、Ki-67、雌激素受体(ER)、孕激素受体(PR)免疫组化检测,并与其病理组织形态、临床表现、鉴别诊断及随访结果进行对照.结果 子宫内膜间质肿瘤(EST)中CD10阳性率89.7%;UES与ESN、ESS比较,CD10、Ki-67及PR均有统计学意义(P＜0.05),h-caldcsmon、CD44v3、ER均无统计学意义(P＞0.05),CD10、PR在ESN、ESS、UES中表达逐渐减弱,而Ki-67则逐渐增强;9例伴平滑肌分化.认为ESN、ESS、UES均可伴平滑肌分化;CD10是诊断子宫间质肿瘤比较特异的抗体,结合组织形态及h-caldesmon、CD44v3可增加其特异性;EST生物学行为和预后可能与CD10、PR、Ki-67阳性表达的数量和强度有关;ER、PR常规检测主要用于指导孕激素辅助治疗.     

PTEN immunohistochemical expression is suppressed in G1 endometrioid adenocarcinoma of the uterine corpus

Purpose PTEN is a tumor suppressor gene that inhibits cell proliferation by regulating intracellular signaling pathways, and this activity can be abolished by mutations of the PTEN gene. This study was designed to examine the correlation of PTEN expression with the expression of cell cycle regulators and with clinicopathological parameters in endometrioid adenocarcinoma of the uterine corpus.Methods Tissue samples of 117 endometrioid adenocarcinomas in addition to those of 19 normal endometria and 20 endometrial hyperplasias were used for the study. Immunohistochemical staining for PTEN protein was performed with the labeled streptavidin-biotin method on formalin-fixed and paraffin-embedded tissue samples. PTEN expression was represented as the staining score.Results Immunohistochemistry showed that the nuclei of cells were positive for PTEN. The PTEN staining score of normal endometrium was significantly higher in the proliferative phase than in the secretory phase. The scores of various endometrial hyperplasias were not significantly different from each other, regardless of the type of hyperplasia. The PTEN staining scores of endometrioid adenocarcinomas were 7.6±5.2 in G1, 9.6±5.2 in G2, and 11.9±3.7 in G3, and increased significantly as the histological grade increased. PTEN staining score was not significantly correlated with clinicopathological parameters such as FIGO stage, myometrial invasion, lymph-vascular space invasion (LVSI), lymph node metastasis or group, but was significantly correlated with labeling indices (LIs) of cell cycle regulators such as Ki-67, cdk2, cyclin A, cyclin D1, cyclin E, p27, and p53. The PTEN staining score of p53-wild cases was significantly lower than that of p53-mutant ones, but there was no significant difference of the score in cases with different PTEN gene status. PTEN expression was significantly lower in cases with both high levels of estrogen receptor and progesterone receptor.Conclusion PTEN protein expression was decreased in well-differentiated and less growth-aggressive endometrial carcinoma with wild-type p53 gene and high levels of ER and PR. This suggests that disturbed PTEN expression occurs in an early phase of the tumorigenesis of well-differentiated endometrial carcinoma.     

Vav3蛋白在子宫内膜癌组织中的表达及其与雌激素受体相关性的研究

目的探讨Vav3基因在子宫内膜癌组织中的表达及其与雌激素受体（ER）和临床病理特征的关系。方法应用免疫组织化学SP法检测正常子宫内膜组织、非典型增生子宫内膜组织、子宫内膜癌组织中Vav3蛋白表达,并对其及ER与临床病理特征的关系进行分析。结果①Vav3在正常子宫内膜、非典型增生子宫内膜、子宫内膜癌组织中阳性表达率逐渐增高,三组间差异有统计学意义（P〈0．01）,而在非典型增生组织中与子宫内膜癌组织中差异无统计学意义。②非典型增生子宫内膜中Vav3与ER表达无明显相关,而在子宫内膜癌中二者表达存在相关性（rs=0．225,P〈0．05）。③Vav3表达在I、Ⅱ型子宫内膜癌之间无明显差异,Vav3在I型子宫内膜癌中的表达与患者FIGO分期、组织学分级、肌层浸润呈正相关（rs=0．276、0．238、0．237,P〈0．05）,而与是否绝经、淋巴结有无转移无明显相关。结论Vav3基因在子宫内膜癌的发生发展中可能起重要作用,与ER可能存在交联对话。     

Expression of cyclin A in endometrial adenocarcinoma and its correlation with proliferative activity and clinicopathological variables

Purpose: Cyclin A is known as an S- and G2-M phase regulatory protein and its abnormal expression has been reportedly implicated in cellular proliferation. This study was designed to investigate the correlation of cyclin A expression with tumorigenesis of the endometrium and clinicopathological variables. Methods: Immunohistochemical staining using labeled streptavidin-biotin complex was performed on formalin-fixed, paraffin-embedded tissue of normal endometrium (15 cases), endometrial hyperplasia (23 cases), and endometrial adenocarcinoma (endometrioid type) (112 cases). Results: Immunohistochemistry showed that the nuclei of the cells were positive for cyclin A. In normal endometrium, only proliferative phase was focally positive for cyclin A. Cyclin A was also positive for endometrial hyperplasia. Its expression in hyperplasia was significantly more frequent than that of proliferative phase and less than that of endometrioid adenocarcinoma. The labeling index (LI) of cyclin A in endometrioid adenocarcinoma was 16.3Lj.9 in well-differentiated, 18.3NJ.8 in moderately differentiated, and 30.2ᆟ.8 in poorly differentiated adenocarcinoma, respectively. Cyclin A expression increased significantly more in high histological grades. The area of squamous metaplasia in endometrioid adenocarcinoma was negative for cyclin A. The LI of cyclin A was positively correlated with that of Ki-67 and cyclin-dependent kinase 2. Cyclin A expression was significantly associated with carcinoma without coexisting endometrial hyperplasia and lymphovascular space involvement (LVSI), but not with FIGO stage, myometrial invasion, lymph node metastasis, estrogen receptor, progesterone receptor, and menopause as well as recurrence. Conclusions: Cyclin A expression was involved in the progression to malignancy of the endometrium and was correlated with proliferative activity and prognostic features including histological grade, without coexisting endometrial hyperplasia and LVSI.     

Biochemical analysis of estrogen receptor and progesterone receptor in normal uterus and endometrial carcinoma

In this study, human uterine endometrial estrogen receptor (ER) and progesterone receptor (PR) in normal menstrual cycle were estimated, and biochemical characterization of ER and PR in normal endometrium and endometrial carcinoma were also investigated. Following results were obtained in this study. In normal menstrual cycle, ER and PR levels in endometrial cytosol gradually rose to peaks in the late proliferative phase, but PR in nuclear fraction rose to a peak in the early secretory phase. Scatchard analysis of ER in normal endometrium and myometrium contains two estradiol (E2) binding sites with dissociation constants (Kd) of 10(-9) M and 10(-10) M, but endometrial carcinoma contains a single population of E2 binding site with Kd's 10(-10) M. Total binding sites for ER and PR of normal endometrium have 2 approximately 3 times much more than those of endometrial carcinoma. In normal endometrium, specific binding of 40nM 3HE2 on isoelectric focusing (IEF) indicated three binding activities with elution pH's (EPH) of 4, 6 and 8. But specific binding of 2nM 3HE2 indicated only one binding activity with EPH of 6 in endometrial carcinoma. Specific binding of EPH 6 indicated high affinity ER (type 1 ER) and specific binding of EPH 8 indicated low affinity ER (type 2 ER) in the result of IEF and Scatchard analysis. Loss of type 2 receptor is important result in endometrial carcinoma. The above results suggest that increase in blood E2 level increases endometrial ER and PR, and increase in blood progesterone level after ovulation decreases endometrial ER and PR for anti-ER and PR effect of progesterone. If type 2 ER could transport hormone receptor complex to the nucleus, loss of type 2 ER would be the important cause of ER and PR decrease and get resistance of hormone therapy to endometrial carcinoma.     

肿瘤抑制基因PTEN蛋白在乳腺癌中的表达及意义

采用免疫组化法检测 138例乳腺癌患者的 PTEN蛋白、ER和 PR的阳性表达。结果示 PTEN阳性率(4 7.83% )与 ER阳性率 (39.86 % )和 PR阳性率 (4 2 .0 3% )接近。PTEN阳性病例中淋巴结转移率 (2 7.6 9% )远低于 PTEN阴性者 (6 1.6 4% ) ,两者差异显著 (P〈0 .0 5 )。认为 PTEN、ER和 PR表达具有较强的一致性 ,推测 PTEN基因的突变和缺失可能与乳腺癌的发生、发展有关 ;PTEN与 ER的表达与淋巴结转移有明显相关性 ,可作为判断乳腺癌预后的指标。     

行激素补充疗法的绝经后妇女子宫内膜安全性监测

目的　探讨应用激素补充疗法(HRT)的绝经后妇女子宫内膜安全性的监测方法。　方法　对60例绝经后行HRT妇女进行血清雌二醇(E2)测定;阴道B超(TVS)监测子宫体积和子宫内膜厚度;对部分患者行子宫内膜的病理学检查和雌激素受体(ER)、孕激素受体(PR)半定量检测。　结果　应用HRT后,子宫内膜明显增厚,均值从2.8mm升至3.9mm(P＜0.05);E2显著上升,由(20.6±6.9)ng/L升至(33.8±11.7)ng/L（P＜0.01）;子宫内膜厚度与E2呈正相关关系(r=0.94,P＜0.01);20例送检内膜中,2例简单型增生过长,1例复杂型增生过长,余为萎缩型;ER(+)19例,ER(++)1例;PR均为(+)。　结论　根据临床表现,并结合血清E2和TVS检测子宫内膜厚度,可对子宫内膜安全性进行初步评估;当E2＞45ng/L,子宫内膜厚度≥5mm时,则需进一步行子宫内膜病理学检查和ER测定。     

Immunohistochemical expression of cyclin E in endometrial adenocarcinoma (endometrioid type) and its clinicopathological significance

PURPOSE: Cyclin E is known as a G1-S phase regulatory protein and its abnormal expression has been implicated in cellular proliferation. This study aimed to investigate the correlation of cyclin E expression with tumorigenesis of the endometrium, proliferative activity, and clinicopathological features of endometrial adenocarcinoma. METHODS: Immunohistochemical staining for cyclin E in addition to cyclin-dependent kinase 2 (cdk2), Ki67, p27, and p53 was performed by the labeled streptavidin-biotin method on formalin-fixed, paraffin-embedded tissues of normal endometria (20 cases), endometrial hyperplasias (20 cases), and endometrial adenocarcinomas (endometrioid type) (127 cases). Positive staining was expressed as a labeling index (LI) based on percentages of positive nuclei in tumor cells. RESULTS: Immunohistochemistry showed that the nuclei of the cells were positive for cyclin E. Both proliferative and secretory endometria, and endometrial hyperplasia regardless of type were negligible for cyclin E expression. The expression in normal endometrium and hyperplasia was significantly less than that in endometrial adenocarcinomas (P<0.0001). LIs of cyclin E in well-differentiated, moderately differentiated, and poorly differentiated endometrial adenocarcinomas were 31.5+/-33.3%, 37.8+/-31.9%, and 51.1+/-30.8%, respectively. Cyclin E expression increased significantly more in histological grades. The LI of cyclin E in carcinoma was positively correlated with that of cdk2, Ki67, and p53 but not with p27. The cyclin E expression was correlated with myometrial invasion and lymph-vascular space involvement, but not with FIGO stage, lymph node metastasis, coexisting endometrial hyperplasia, estrogen receptor, progesterone receptor, and menopause. CONCLUSION: Cyclin E as a complex with cdk2 is associated with carcinogenesis and disease progression in endometrial adenocarcinoma, and might be a prognostic indicator of endometrial adenocarcinoma.     

Cyclic changes in the expression of steroid receptor coactivators and corepressors in the normal human endometrium

To examine the sex steroid-dependent growth mechanisms of the human endometrium, the expression of steroid receptor coactivators [steroid receptor coactivator-1 (SRC-1) and p300/CREB-binding protein (p300/CBP)] and corepressors (nuclear receptor corepressor and silencing mediator for retinoid and thyroid hormone receptors) was examined by immunohistochemistry, using 50 samples of normal endometria, and was compared with that of estrogen receptors (ER), progesterone receptors (PR), and proliferation marker Ki-67. In addition, actual binding of the coactivators to ER or PR was analyzed by immunoprecipitation. The expression of SRC-1 was diffusely observed in glandular and stromal cells in the proliferative phase and drastically decreased in the secretory phase. Such change in the expression pattern of SRC-1 resembled that of ER, PR, and Ki-67. On the other hand, p300/CBP expression was relatively constant throughout the menstrual cycle, with slight predominance in the proliferative phase. The expression of corepressors nuclear receptor corepressor and silencing mediator for retinoid and thyroid hormone receptors was focal in the endometrium. Immunoprecipitation, using tissue samples of both proliferative and secretory phases, revealed the complex formation between the coactivators and receptors. Binding of SRC-1 to ER was observed in the proliferative (but not in the secretory) endometrium. In contrast, binding p300/CBP to ER was noted in the endometria of both phases. Complex formation between p300/CBP and PR was noted in the secretory endometrium, whereas that between SRC-1 and PR was not apparent. Accordingly, we showed the expression pattern of steroid receptor coactivators and corepressors in the normal endometrium. Cyclic change in the expression of SRC-1 during the menstrual cycle might be important in the estrogen-action for the glandular and stromal cells.