子宫内膜癌组织中PTEN mRNA表达的研究

目的:探讨子宫内膜癌组织中PTENmRNA的表达及临床病理意义。 方法:应用逆转录 -聚合酶链反应(RT-PCR)分别扩增65例子宫内膜癌和15例正常子宫内膜组织中PTEN基因外显子1 -8、5 -9和5-8片段 ,并结合临床病理资料进行分析。结果:在65例子宫内膜癌组织中 ,PTENmRNA的表达缺失率在外显子1 -8、5-9和5-8分别为49.23 %(32/65)、38.46 %(25/65)和32.31 %(21/65) ,而正常子宫内膜组织中全部呈阳性表达。二者在三组中表达缺失率的差别显著(P<0.05)。而且子宫内膜癌组织中的表达缺失率在特殊类型癌和G3 级组织中分别高于内膜样腺癌和G1～2 级组织(P<0.05)。 结论:子宫内膜癌组织中存在较高比例的PTENmRNA表达缺失 ,表明PTEN基因转录水平异常在子宫内膜癌的发生发展中起重要作用     

PTEN和P53蛋白在子宫内膜癌中的表达及临床意义

目的：探讨PTEN和P53蛋白在子宫内膜癌中的表达及临床意义。方法：采用免疫组织化学S-P法检测42例子宫内膜癌、28例子宫内膜增殖症和20例正常增生期子宫内膜组织中PTEN和P53蛋白的表达。结果：与增生期子宫内膜100％表达率相比，PTEN蛋白子宫内膜非典型增生及子宫内膜癌中的阳性表达率逐渐降低，分别为66．7％和53．1％。随着子宫内膜癌临床分期的升高、病理分级的降低及肌层浸润的加深，PTEN蛋白的表达呈逐渐降低的趋势。子宫内膜癌组织中PTEN蛋白的失表达主要局限于子宫内膜样腺癌，占46．9％，10例子宫内膜浆液性腺癌中则未见PTEN的失表达，PTEN失表达在这两组肿瘤间的差异有统计学意义（P=0．001）。P53蛋白过表达在子宫内膜样腺癌中占25％，在子宫内膜浆液性腺癌中为80％，两组间差异有统计学意义（P=0．001）。结论：PTEN的缺失和P53过表达与子宫内膜癌的发生、发展有关，同时预示着子宫内膜癌的不良预后。     

Beclin1、PTEN在子宫内膜癌组织中的表达及其意义

背景与目的:子宫内膜癌的确切发病机制尚不明确。本研究旨在探讨抑癌基因Beclin1(BECN1)、PTEN在子宫内膜癌组织中的表达情况及其与临床病理参数之间的关系。方法:采用免疫组织化学PowerVision二步法测定79例子宫内膜癌、34例子宫内膜增殖症以及22例正常子宫内膜组织中BECN1、PTEN的表达并加以分析。结果:BECN1在正常子宫内膜组织、子宫内膜增殖症、子宫内膜癌组织中的阳性率分别为93.33%、58.82%、34.18%;PTEN的阳性率分别为93.33%、64.71%、32.91%。BECN1、PTEN在正常子宫内膜组织、子宫内膜增殖症、子宫内膜癌组织中的表达率逐渐下降差异有显著性(χ2=42.318,P<0.001;χ2=31.746,P<0.001)。BECN1表达程度与子宫内膜癌细胞分化、组织学类型相关,与手术病理分期和肌层浸润深度无关。PTEN蛋白表达与细胞分化程度、组织学类型以及肌层浸润深度有关,而与手术病理分期无关。BECN1与PTEN表达之间呈正相关。结论:BECN1、PTEN低表达与子宫内膜样腺癌的发生、发展相关。     

PTEN/PI3K信号转导途径与子宫内膜癌生物学行为的相关性

目的 :研究PTEN/PI3K信号转导途径与子宫内膜癌发生发展的关系。方法 :应用免疫组化和免疫印迹方法对 68例子宫内膜癌和癌前病变组织及 11例正常子宫内膜进行PTEN、p PKB及p Bad蛋白检测。结果 :1)PTEN蛋白的阳性表达率在正常增殖期子宫内膜组织中最高 ( 90 9% ) ,非典型增生组织中开始下降 ,在子宫内膜癌组织中明显降低 ( 4 9 1% ) ,三者之间比较 ,差异有统计学意义 ,P <0 0 1;2 )p PKB及p Bad与PTEN的阳性表达呈相反趋势 ,在非典型增生组织及内膜癌组织中p PBK及p Bad表达阳性率明显增加 ,差异均有统计学意义 ,P <0 0 1,P <0 0 5。在子宫内膜癌PTEN表达阴性组织中p PKB、p Bad蛋白染色积分均明显高于PTEN阳性组 ,P <0 0 5 ,P <0 0 1;3 )相关分析显示PTEN与p PKB及p Bad表达均呈负相关 ,r =-0 67,P <0 0 5 ;r =-0 65 ,P <0 0 5 ;4)PTEN、p Bad蛋白的阳性表达率在不同的临床分期、组织学分级及不同肌层浸润程度之间比较 ,差异均无统计学意义 ,P >0 0 5 ,而PTEN、p PKB只在临床分期间差异有统计学意义 ,P <0 0 5。结论 :PTEN/PI3K信号转导途径与子宫内膜癌的发生密切相关。伴随PTEN表达缺失 ,p PKB、p Bad阳性表达更加明显 ,提示PTEN蛋白表达可作为子宫内膜癌早期诊断指标和基因治疗靶点。     

PTEN基因在子宫内膜癌中的突变表达及其临床意义

目的:探讨子宫内膜癌组织中PTEN抑癌基因突变、蛋白表达异常及其与子宫内膜癌发生发展的关系。方法:采用聚合酶链反应—单链构象多态性分析方法和DNA测序技术,检测52例子宫内膜癌组织中PTEN基因突变高发区外显子5、8的突变情况,同时应用链霉菌抗生物素蛋白—过氧化酶免疫组织化学方法检测PTEN蛋白的表达。结果:1)52例组织中PTEN外显子5突变率为17.31%,外显子8突变率为7.69%,总突变率为25.00%。统计分析表明,PTEN基因突变与子宫内膜癌的组织学分级、组织病理类型和肌层浸润深度密切相关(P<0.05)。2)52例组织中PTEN蛋白表达缺失率为59.62%,蛋白表达缺失率与组织学分级和组织学分类密切相关(P<0.05)。3)52例中21例PTEN蛋白表达阳性,31例表达阴性,表达缺失组织中13例发生PTEN基因突变。结论:1)PTEN蛋白表达异常与PTEN基因突变有关,基因突变是基因失活的重要机制之一。2)PTEN蛋白表达缺失、PTEN基因突变与子宫内膜癌的发生和发展密切相关。     

PTEN,Bcl-2基因蛋白在子宫内膜腺癌中的表达及临床病理意义

目的:研究PTEN、Bcl-2在子宫内膜腺癌发生、发展中的作用。方法:应用免疫组化S-P法检测PTEN,Bcl-2在10例正常子宫内膜,10例子宫内膜不典型增生,58例子宫内膜腺癌中的表达,并分析它们与子宫内膜腺癌临床病理指标的关系。结果:PTEN蛋白在正常子宫内膜,子宫内膜不典型增生和子宫内膜腺癌中的阳性表达逐渐降低,差异有显著性(P<0.05)。在子宫内膜腺癌中PTEN的表达与临床分期、组织分化、肌层浸润及淋巴结转移无关。Bcl-2蛋白在正常子宫内膜,子宫内膜不典型增生和子宫内膜腺癌中的阳性表达逐渐降低,差异有显著性(P<0.005)。在子宫内膜腺癌中Bcl-2的表达与临床分期、组织分化、肌层浸润及淋巴结转移均显著相关(P<0.05)。结论:PYEN和Bcl-2在子宫内膜腺癌的发生,发展中起着不同程度的作用。它们的检测可对子宫内膜腺癌的早期诊断、恶性程度、预后的判断和进一步治疗提供依据。     

PTEN和CyclinA蛋白在子宫内膜癌组织中的表达及临床意义

目的：探讨PTEN和CyclinA在子宫内膜癌中的表达及其在癌发生发展中的作用。方法：采用免疫组化SP法检测PTEN和CyclinA蛋白在30例正常子宫内膜、30例子宫内膜增生、20例子宫内膜不典型性增生、55例子宫内膜癌组织中的表达。结果：不典型增生组和子宫内膜癌组中PTEN阳性表达率分别为55．00％（11／20）、45．45％（25／55），与全部为阳性表达的正常内膜及阳性表达率为90．00％（27／30）的子宫内膜增生组比较，不典型增生组和癌组中PTEN阳性表达均显著低于正常子宫内膜和子宫内膜增生组（P〈0．05）。CyclinA在不典型增生组和癌组中阳性表达率分别为45．00％（9／20）、67．27％（37／55），显著高于全部阴性表达的正常子宫内膜组和子宫内膜增生组（10．00％，3／30）（P〈0．05）。两者在不典型增生和子宫内膜癌组中的表达均呈显著性负相关（r=-0．5330，r=-0．5556；P〈0．001）。癌组中PTEN阳性表达的缺失与组织学分级有关（P〈0．05），但与肿瘤的浸润转移、临床分期和复发无关（P〉0．05）；CyclinA的阳性表达率与组织学分级、肿瘤的浸润转移和临床分期、复发有关。结论：PTEN表达缺失和CyclinA的过度表达涉及子宫内膜癌的发生、发展过程，二者联合检测可作为子宫内膜癌早期诊断、判断肿瘤生物学行为的免疫学指标。     

Loss of PTEN expression is associated with metastatic disease in patients with endometrial carcinoma

BACKGROUND: The PTEN tumor suppressor gene frequently is involved in endometrial carcinoma. Loss of heterozygosity and mutations reportedly are common, although the biologic importance of these changes remain largely unknown. The objective of this study was to assess the pattern of PTEN expression by immunohistochemistry in a large series of patients with endometrial carcinoma. METHODS: A population-based series of 316 patients with endometrial carcinoma who had long and complete follow-up was investigated for PTEN expression and its correlation with clinicopathologic variables, tumor markers, and survival. RESULTS: PTEN protein expression was mainly cytoplasmic in tumor cells, with no expression seen in 56 of 279 patients (20%) who had evaluable results. A heterogeneous staining pattern was found in 70 tumors (25%). A significant association between the loss of PTEN expression and metastatic disease was identified (P = 0.05). However, PTEN staining did not influence survival significantly. CONCLUSIONS: The loss of PTEN expression is relatively frequent in endometrial carcinoma and is associated significantly with metastatic disease. This indicates that the PTEN system plays an important role in some endometrial carcinomas, but further studies of PTEN protein expression related to various genetic alterations are necessary.     

PTEN expression in tamoxifen-associated endometrial cancers

Tamoxifen is associated with increased rates of endometrial hyperplasia and adenocarcinoma. Our previous work suggested tamoxifen-associated endometrial cancers might be associated with p53 mutations. PTEN, a tumor suppressor gene, is altered in low-grade endometrial carcinoma. This study evaluates PTEN immunohistochemical (IHC) expression in tamoxifen-associated endometrial cancers. MATERIALS AND METHODS: Twenty-eight endometrial carcinoma specimens were examined from patients with a history of breast cancer. Patients who had taken Tamoxifen (15) were compared to non-users (13). IHC staining was performed for PTEN; overexpression was defined as greater than 70% positivity. RESULTS: The mean duration of tamoxifen use was 3.3 years (3-171 months). Four out of 15 (27%) tamoxifen users expressed PTEN compared with 2 out of 13 (15%) of non-users. CONCLUSION: In this study, it appears that tamoxifen-associated endometrial cancers are not significantly different from sporadic endometrial cancer with regards to PTEN IHC expression, although there is a trend towards retained PTEN expression.     

子宫内膜癌组织中抑癌基因PTEN突变和表达的探讨

目的：研究抑癌基因PTEN在子宫内膜癌组织中的突变频率、分布和表达，探讨其在子宫内膜癌发病中的意义。方法：提取40例新鲜子宫内膜癌及癌周组织的基因组DNA，应用聚合酶键式反应—单链构象多态性分析(PCR—SSCP)方法，研究PTEN基因9个外显子的突变情况，并对突变样本进行测序分析。采用免疫组织化学法进行PTEN蛋白表达研究，并与组织学类型、临床分期、病理分级、淋巴结转移和雌孕激素受体状态的相关性进行分析。结果：40例子宫内膜癌中共检测到突变为18例，占45、0％。18例结果显示，8例为错义突变，10例分别为无意义突变、插入和缺失，形成截短蛋白。异常突变点中44、0％为外显子5，28.0％为外显子8，17．0％为外显子3，外显子1和6各有1例。免疫组化结果显示PTEN主要分布于细胞浆中：23／40例(57．5％)子宫内膜癌中PTEN表达完全缺失，10／40例(25．0％)表达部分缺失。PTEN在子宫内膜癌的表达与组织学类型和临床分期有关，与病理分级、肌层侵润及淋巴结转移无明显相关性。PTEN表达缺失率在雌孕激素受体阳性的癌组织中明显高于雌孕激素受体阴性的癌组织。结论：PTEN可能和子宫内膜癌的发生有关。     

PTEN基因对子宫内膜癌细胞生长的抑制作用

目的 探讨PTEN基因在子宫内膜癌基因治疗方面的可行性。方法 通过腺病毒载体(Ad-PTEN)将人野生型PrENcDNA导入Ishikawa细胞,观察外源性PTEN蛋白的表达情况,以及PTEN蛋白对Ishikawa细胞生长的影响,同时还观察了PTEN蛋白是否影响胰岛素样生长因子Ⅱ(IGF-Ⅱ)对Ishikawa细胞的作用。结果 Ad-PTEN感染IsHikaWa细胞后1d,即可见PTEN蛋白表达;第3天时,表达明显增强,并能持续表达10d。感染后的IshikaWa细胞生长受到明显抑制,并且PTEN还能明显抑制IGF-Ⅱ诱导的Ishikawa细胞生长。结论 腺病毒介导的PTEN基因导入能诱导Ishikawa细胞生长受到明显抑制,提示野生型PTEN基因可能是治疗子宫内膜癌的一种新途径。     

子宫内膜癌组织中PTEN蛋白的表达及其临床意义

目的：探讨PTEN蛋白表达与子宫内膜癌病理特征的关系。方法：应用免疫组化方法检测15例正常子宫内膜、18例子宫内膜癌前病变，60例子宫内膜癌组织中的PTEN蛋白表达。结果：正常子宫内膜、子宫内膜癌前病变和子宫内膜癌组织中PTEN蛋白阳性表达率分别为93．3％、66．7％和40．0％，三者之间有显著性差异（P＜0．05）。子宫内膜癌组织中PTEN蛋白表达缺失率与组织学分级、组织类型和临床分期密切相关（P＜0．05），组织分化程度高、临床分期早、内膜样腺癌组织中PTEN蛋白表达缺失率明显低于组织分化程度低、临床分期晚及其他组织类型癌。结论：PTEN蛋白在子宫内膜癌的发生、发展中起重要作用，PTEN蛋白表达与子宫内膜癌的组织学分级、组织类型和临床分期密切相关。     

Correlation between loss of PTEN expression and Akt phosphorylation in endometrial carcinoma.

The tumor suppressor PTEN acts as a lipid phosphatase, regulates the phosphatidylinositol 3-kinase (PI3K)/Akt-signaling pathway, and modulates cell cycle progression and cell survival. Somatic mutations of PTEN have been reported in a variety of cancers, especially in endometrial carcinoma. To clarify whether and how PTEN and the PI3K/Akt pathway relates to endometrial carcinoma, we examined the expression of those pathway-related proteins in patients with endometrial carcinoma. Of 103 endometrial carcinomas, 37 (36%) showed negative immunohistochemical staining of PTEN. Western blotting revealed that the expression of PTEN in PTEN-negative cases was significantly lower compared with that in positive cases. In contrast, phospho-Akt level in negative cases was significantly higher. We found a significant inverse correlation between PTEN and phospho-Akt (r = -0.796). The expression of phospho-Bad was greater in negative cases, suggesting that Bad might be a target for AKT: The present study demonstrates the phosphorylation of Akt accompanied by the loss of PTEN in clinical specimens of endometrial carcinomas.     

Diagnostic utility of phosphatase and tensin homolog, beta-catenin, and p53 for endometrial carcinoma by thin-layer endometrial preparations

BACKGROUND: For the current report, the authors examined the characteristic features of morphology and molecular biology of phosphatase and tensin homolog (PTEN), beta-catenin, and p53 immunocytochemistry in endometrial carcinoma by using thin-layer cytologic preparations. METHODS: During a 6-month period, 120 endometrial samples were collected directly by using the Uterobrush, and thin-layer specimens were prepared. Immunocytochemical expression levels of PTEN, beta-catenin, and p53 were investigated by using 40 specimens of endometrial carcinoma (EC), and 30 specimens each of proliferative endometrium, secretory endometrium, and atrophic endometrium. RESULTS: For PTEN immunoreactivity, the a cutoff value of 50% PTEN expression appeared to be useful for the correct diagnosis of EC in endometrial cytology. For beta-catenin immunoreactivity, an increase in cytoplasmic and nuclear beta-catenin expression and a loss of beta-catenin expression appeared to be useful for the correct diagnosis of EC in endometrial cytology and may aid in the stratification of EC into low grade and high grade EC. For p53 immunoreactivity, the application of a cutoff score >or=4 for nuclear p53 expression appeared to be useful for the diagnosis of high-grade EC in endometrial cytology. CONCLUSIONS: Immunocytochemical findings from a combination of PTEN, beta-catenin, and p53, in addition to cytomorphologic features, appeared to be useful for the more accurate diagnosis of EC in endometrial cytology.     

PTEN、p27~(kip1)、VEGF在子宫内膜癌中的表达及意义

 目的　探讨抑癌基因PTEN、p2 7kip1、VEGF在子宫内膜癌中的表达、意义及三者之间的相关性。方法　采用免疫组化SP法检测 32例子宫内膜腺癌 ,13例子宫内膜不典型增生和 10例正常子宫内膜石蜡切片中PTEN、p2 7kip1及VEGF的表达。结果　子宫内膜腺癌组织与子宫内膜不典型增生、正常子宫内膜组织比较 ,PTEN、p2 7kip1阳性表达率明显降低 ,差异有非常显著性 (χ2 =11.0 9,χ2 =9.4 6 6 ,P <0 .0 1) ,VEGF表达率明显增加 ,差异有非常显著性 (χ2 =2 1.2 5 3,P <0 .0 1)。PTEN表达与肿瘤分化、肌层浸润程度、淋巴结转移有关 (P <0 .0 5 ) ,与临床分期无关 (P >0 .0 5 )。在子宫内膜腺癌组织中 ,PTEN与p2 7kip1表达呈正相关 (r=0 .74 4 ,P <0 .0 1) ,与VEGF表达呈负相关 (r =- 0 .738,P <0 .0 1)。结论　PTEN、p2 7kip1的失表达与VEGF的过表达在子宫内膜腺癌的发生发展中起着一定的作用 ,PTEN与 p2 7kip1、VEGF的异常表达密切相关 ...     

PTEN induces G(1) cell cycle arrest and decreases cyclin D3 levels in endometrial carcinoma cells

Inactivating mutations in the PTEN tumor suppressor gene occur in approximately 30-50% of endometrial carcinomas. PTEN is a phosphatase that negatively regulates the phosphoinositide 3-kinase signaling pathway, including the downstream effector AKT. To evaluate the role of PTEN in endometrial growth regulation, we expressed wild-type or mutant PTEN in endometrial carcinoma cell lines. As expected, expression of exogenous PTEN decreased levels of activated AKT in all cell lines examined. However, PTEN induced a G(1) cell cycle arrest specifically in endometrial carcinoma cells that lack endogenous wild-type PTEN. Growth of cells containing wild-type PTEN was unaffected by exogenous PTEN expression. Growth arrest required a functional phosphatase domain but not the PDZ interaction motif of PTEN. Overall levels of CIP/KIP and INK4 family members, the known inhibitory regulators of the G(1) phase of the cell cycle, were unchanged. However, PTEN induced a specific reduction of cyclin D3 levels and an associated increase in the amount of the inhibitor p27(KIP1) complexed with CDK2. Enforced expression of cyclin D3 abrogated the PTEN-induced cell cycle arrest. Although PTEN signaling directly regulates p27(KIP1) levels in some settings, in endometrial carcinoma cells, PTEN expression indirectly regulated p27(KIP1) activity by modulating levels of cyclin D3. These data support multiple mechanisms of PTEN-induced cell cycle arrest.     

子宫内膜癌组织中PTEN基因突变及蛋白表达的检测

背景与目的:肿瘤抑制基因———第10染色体同源丢失性磷酸酶-张力蛋白基因(phosphataseandtensinhomologdeletedonchromosometen,PTEN)被称为子宫内膜的看家基因。但有关PTEN基因在子宫内膜癌发生发展中的确切作用尚不清楚。本研究旨在检测子宫内膜癌组织中PTEN基因的突变及蛋白表达情况。方法:应用聚合酶链反应-单链构象多态性分析(polymerasechainreaction-singlestranconformationpolymorphism,PCR-SSCP)和DNA序列分析法,检测52例子宫内膜癌组织和10例正常子宫内膜组织中PTEN基因第5和第8外显子的突变;免疫组织化学法检测PTEN蛋白的表达,并结合临床病理特征进行分析。结果:子宫内膜癌组织的PTEN基因突变率和蛋白缺失率分别为25%和60%,高于正常子宫内膜组织(0%),差异有显著性(P<0.05)。病理学分级为G1、G2及肌层浸润深度<1/2的组织的PTEN基因突变率高于病理学分级为G3及肌层浸润深度≥1/2者,而病理学分级为G1、G2组织的PTEN蛋白表达缺失率低于病理学分级为G3者,差异有显著性(P<0.05)。PTEN基因突变率和蛋白表达缺失率在子宫内膜样腺癌和其它组织类型之间比较,差异有显著性(P<0.05),而在不同手术分期之间差异无显著性(P>0.05)。结论:PTEN基因突变和蛋白阳性表达常发生在病理学分级较低的子宫内膜癌病例     

Correlation between NDRG1 and PTEN expression in endometrial carcinoma

N-myc Downstream-Regulated Gene 1 (NDRG1) is known as a differentiation-related gene that plays important roles in cell differentiation, organ formation, and embryonic development. NDRG1 has recently been shown to be associated with carcinogenesis and tumor progression in a wide variety of tumors. Phosphatase and tensin homolog deleted from chromosome (PTEN), a phosphatase and tensin homolog located on chromosome 10, is shown to be a tumor suppressor and is often mutated or deleted in various tumor cells, particularly in endometrial carcinoma. Using an immunohistochemical approach, we investigated the expression of NDRG1 and PTEN in normal endometrium, atypical hyperplasia, and endometrial carcinoma. All tumor tissues harvested in this study were derived from endometrioid carcinoma Type I, that were estrogen-related. Our results demonstrate that the expression of NDRG1 was up-regulated in 5/40 (12.5%), 18/34 (52.94%), and 86/103 (83.5%) normal endometrium, atypical hyperplasia, and endometrial carcinoma cases, respectively ( P <  0.01), while in 6/40 (15%), 20/34 (58.82%), and 89/103 (86.41%) normal endometrium, atypical hyperplasia, and endometrial carcinoma cases, respectively. PTEN expression was significantly decreased ( P <  0.01). Statistical analyzes demonstrated a positive correlation between NDRG1 up-regulation and PTEN down-regulation ( P <  0.01). The expression of NDRG1 had no correlation with the differentiation degree of the tumor cells, lymph-node metastasis, and/or abdominal cavity implantation ( P  > 0.05). Our results indicated that development of endometrial carcinoma is associated with an overexpression of NDRG1 and the loss of PTEN expression. Identification of changes in the NDRG1 and PTEN expression may be a significant diagnostic tool for the early detection of endometrial carcinoma. ( Cancer Sci 2008; 99: 706–710)     

PTEN和CyclinE蛋白在子宫内膜癌组织中的表达

目的探讨子宫内膜良性、癌前病变和恶性病变中PTEN、CyclinE蛋白的表达及其意义.方法采用免疫组化S-P法检测正常子宫内膜、子宫内膜增生、非典型性增生和子宫内膜癌组织中PTEN和CyclinE蛋白.结果非典型性增生组和子宫内膜样癌组中PTEN和CyclinE蛋白阳性表达率分别为60.0%,50.0%和42.0%,62.2%.非典型性增生组中PTEN的阳性表达显著低于正常组和增生组(P<0.02),而CyclinE的阳性表达则显著高于正常组和增生组(P<0.03).PTEN和CyclinE蛋白在子宫内膜样癌组中的表达呈负相关(r=-0.4475,P<0.01).宫内膜样癌中PTEN蛋白阳性表达的缺失与组织学分级(P<0.02)及肌层浸润深度或伴有转移有关(P<0.04),与临床分期无关(P>0.05).CyclinE的阳性表达率则与组织学分级有关(P<0.05),与肌层浸润(P>0.05)和临床分期无关(P>0.05).结论 PTEN表达缺失和CyclinE的过度表达与子宫内膜样癌的发生发展密切相关,二者的联合检测可作为子宫内膜样癌早期诊断的生物学指标.