卵巢粘液性囊腺癌中DNA复制错误是频发现象

卵巢浆液性囊腺癌(SAC)和粘液性囊腺癌(MAC)是散发性上皮性卵巢癌的两种常见组织学类型。DNA错配修复缺陷在上皮性卵巢癌的发生和发展过程中起一定作用,来自同一个体的肿瘤DNA与正常DNA比较显示:DNA错配修复缺陷能导致简单重复序列(微卫星长度)的改变,这种改变     

上皮性卵巢癌中Survivin的表达及意义

目的　探讨凋亡抑制基因Survivin在上皮性卵巢癌组织中的表达及意义。方法　应用半定量RT-PCR及免疫组化的方法 ,分别检测SurvivinmRNA及蛋白在 5 2例上皮性卵巢癌、 2 5例良性上皮性卵巢肿瘤和 2 0例正常卵巢组织中的表达。结果　SurvivinmRNA及蛋白在 5 2例卵巢癌组织中的阳性表达率分别为 84 6 % (4 4 5 2 )、 6 5 4 % (34 5 2 ) ;在 2 5例良性肿瘤中的阳性表达率分别为 2 4 0 % (6 2 5 )、 0 (0 2 5 ) :在 2 0例正常卵巢组织中的阳性表达率分别为 15 0 % (3 2 0 )、 0 % (0 2 0 )。三者比较均差异有极显著性 (P <0 0 0 1) ;5 2例上皮性卵巢癌中 ,浆液性囊腺癌 30例 ,粘液性囊腺癌 16例 ,其他类型癌 6例 ,各种类型上皮性卵巢癌中SurvivinmRNA及蛋白阳性表达率比较 ,差异均无显著性意义 (P >0 0 5 ) ;上皮性卵巢癌中 ,临床分期Ⅰ～Ⅱ期 16例 ,Ⅲ～Ⅳ期 36例。组织学分级G1 ～G2 19例 ,G333例。SurvivinmRNA及蛋白在卵巢癌组织中的表达随着卵巢癌临床分期及组织学分级的升高而显著增加 (P <0 0 5 )。结论　Survivin基因在卵巢癌的发生发展中起一定作用。     

上皮性卵巢癌PTEN蛋白表达分析

目的：探讨抑癌基因PTEN的蛋白表达与上皮性卵巢癌的发生、发展之间的关系。方法：对74例上皮性卵巢癌应用免疫组化方法检测PTEN蛋白的表达。结果：上皮性卵巢癌中PTEN蛋白有一定的表达缺失，在G1、G2级组织表达率（90．62％）高于G3级组织表达率（66．67％），二者差异有显著性；不同的临床分期中，I、Ⅱ期阳性表达为22／24（91．67％），Ⅲ、Ⅳ期阳性表达为35／50（70％），二者差异有显著性。在浆液性和粘液性两种不同的组织类型间，表达率分别为82．98％和66．67％，二者无明显差别。结论：PTEN蛋白的表达缺失在上皮性卵巢癌的发生、发展过程中有一定的作用，且与病变进展和分化有关。     

卵巢上皮性肿瘤多种癌基因改变及蛋白表达的研究

目的 :检测卵巢上皮性肿瘤中c erbB2、c myc和k ras12 ,13在基因和蛋白质水平的改变 ,探讨促使卵巢癌发生的癌基因谱成员。方法 :免疫组化检测c erbB2、c myc的蛋白质表达 ,原位杂交和Southern杂交检测c erbB2、c myc的基因改变 ,PCR检测k ras12 ,13的点突变。结果 :卵巢囊腺癌中c erbB2、c myc的基因扩增率和蛋白质过表达率均显著高于卵巢囊腺瘤 ,卵巢粘液性肿瘤的k ras12 ,13突变率高于浆液性肿瘤。结论 :在卵巢癌的发生中c erbB2和c myc起一定作用 ,c erbB2起重要作用。两者均可为卵巢癌的癌基因谱成员 ;k ras12 ,13点突变在卵巢浆液性肿瘤中作用不明显。在粘液性肿瘤中 ,k ras点突变除在细胞过度增殖中起作用外 ,还能促进细胞的粘液性分化。     

上皮性卵巢癌中USP39的表达及其临床意义

目的:探讨USP39在上皮性卵巢癌中的表达及临床意义。方法:收集2011～2014年郑州大学第一附属医院病理科的118例上皮性卵巢癌组织(54例卵巢浆液性囊腺癌、28例卵巢黏液性囊腺癌、19例卵巢内膜细胞癌、17例卵巢透明细胞癌)及40例卵巢良性肿瘤组织(20例卵巢浆液性囊性瘤、20例卵巢黏液性囊腺瘤)、24例正常卵巢组织的石蜡包埋组织。免疫组化法检测USP39表达,分析其表达与上皮性卵巢癌临床病理特征的相关性。结果:卵巢癌组织中USP39高表达率为72.03%(85/118),与卵巢良性肿瘤(19/40)及正常卵巢组织(5/24)相比,差异有统计学意义(P<0.05)。浆液性癌的USP39高表达率是85.19%(46/54),高于其他类型的癌,差异有统计学意义(P=0.032)。浆液性囊腺瘤(12/20)与黏液性囊腺瘤(7/20)相比,USP39高表达率无统计学差异(P=0.113)。上皮性卵巢癌中,USP39表达与患者年龄、肿瘤大小及肿瘤分化程度无关(P>0.05),而与病理类型、FIGO分期及淋巴结转移显著相关(P<0.05)。USP39高表达、FIGO分期及淋巴结转移是影响上皮性卵巢癌预后的独立危险因素(P<0.05)。结论:USP39表达升高与上皮性卵巢癌的发生发展有关,可能成为治疗上皮性卵巢癌的新靶点和评估预后的有力指标。     

子宫内膜癌和卵巢上皮性癌PTEN基因突变及其蛋白表达的意义

目的　探讨子宫内膜癌和卵巢上皮性癌组织中抑癌基因PTEN的突变及其蛋白表达与肿瘤发生、发展的关系。方法　应用聚合酶链反应 单链构象多态性分析 (PCR SSCP)和DNA序列分析法 ,检测子宫内膜癌 (5 2例 )、卵巢上皮性癌 (6 0例 )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。结果　子宫内膜癌组织 :(1)PTEN基因突变率为 2 5 % ,高于正常子宫内膜 (0 ,P <0 0 5 ) ;PTEN基因突变率与子宫内膜癌的病理分级、组织类型、肌层浸润深度密切相关(P <0 0 5 )。(2 )PTEN蛋白缺失率为 6 0 % ,高于正常子宫内膜组织 (0 ,P <0 0 5 ) ;子宫内膜癌组织中PTEN蛋白表达率与病理分级和组织类型密切相关 (P <0 0 5 ) ,而与手术病理分期和肌层浸润深度无关 (P >0 0 5 )。卵巢上皮性癌组织 :(1)PTEN基因的突变率为 5 % ,与正常卵巢组织 (0 )和良性卵巢肿瘤 (0 )相比 ,差异无显著性 (P >0 0 5 )。 (2 )PTEN蛋白缺失率为 2 3% ,显著高于良性卵巢肿瘤和正常卵巢组织 (均为 0 ,P <0 0 5 ) ;卵巢上皮性癌组织中的PTEN蛋白缺失率与其组织类型及患者的年龄、绝经与否无明显相关性 (P >0 0 5 ) ,与临床分期和病理分级有关 (P <0 0 5 )。结论　PTEN基因的突变和蛋白表达缺失均参与子宫内膜癌的发生发     

G蛋白耦联受体30(GPR30)在上皮性卵巢癌中的表达与增殖相关基因c-fos、cyclinD1表达的相关性

目的:探索新型雌激素受体G蛋白耦联受体30(G protein coupled receptor 30,GPR30)在人上皮性卵巢癌发生发展中的作用。方法:采用免疫组织化学SP法检测30例上皮性卵巢癌组织中GPR30、增殖相关基因c-fos和cyclinD1的表达,并以9例良性卵巢肿瘤、4例正常卵巢组织作对照。结果:GPR30在上皮性卵巢癌的表达水平(80.0%)显著高于良性卵巢肿瘤(44.4%)和正常卵巢组织(25.0%)(P<0.01;P<0.05)。GPR30和c-fos的表达与上皮性卵巢癌的病理类型、FIGO分期有关,在浆液性囊腺癌、FIGOⅢ-Ⅳ期的表达水平显著升高(P<0.05)。未见cyclinD1的表达与上皮性卵巢癌临床病理参数的关系(P>0.05)。上皮性卵巢癌中GPR30与c-fos、cyclinD1的表达具有正相关性(P<0.01;P<0.05)。结论:GPR30可能通过c-fos、cyclinD1促进卵巢癌增殖,参与上皮性卵巢癌的发生、发展。     

卵巢浆液性囊腺癌中MTS_1/p16基因突变及其蛋白表达的研究

目的：探讨抑癌基困MTS1／p16在人卵巢浆液性囊腺癌发生发展中的作用。方法：应用免疫组化检测10例正常卵巢组织,20例浆液性囊腺瘤,20例交界性策液性囊腺瘤,65例浆液性囊腺癌及有癌转移的阳性盆腔淋巴结中p16基因蛋白表达,用PCR－SSCP分析10例浆液性囊腺癌中有无p16基因第1、2外显子的突变。结果：正常卵巢、浆液性囊腺瘤、交界性浆液性囊腺瘤、浆液性囊腺癌及有癌转移的盆腔淋巴结中,p16基因蛋白表达阳性率分别为60％、55％、55％、12．3％、0％;10例浆液性囊腺癌均未发现p16基因第1、2外显子的突变。结论：p16基因功能失活可能与卵巢癌发生、发展相关,p16基因表达的检测可能成为判断浆液性卵巢肿瘤恶性度及预后的指标;浆液性卵巢癌p16基因突变率较低,可进一步扩大检测范围并作进一步研究。     

人卵巢浆液性囊腺癌中p16~(INK4a)基因失活机制探讨

目的 :探讨人卵巢浆液性囊腺癌中p16INK4a基因表缺失的机制 ,为p16INK4a相关性基因治疗提供理论依据。方法 :采用PCR、PCR SSCP、甲基化特异性PCR和DNA测序等方法重点检测p16INK4a蛋白表达缺失的卵巢浆液性肿瘤组织中p16INK4a基因缺失、突变和5’ CpG岛甲基化 ,分析它们与肿瘤预后的关系。结果 :4 3份p16INK4a蛋白表达阴性标本中检测到p16INK4a基因纯合缺失 4例 ,第 1、2外显子各 2例 ;第 2外显子点突变 2例 ,经DNA测序确定 1例为第 2外显子 4 94位G→T变异 ,位于非编码区 ;1例为第 2外显子 34 3位G→T变异 ,相应的氨基酸变异为第 115位缬氨酸 (GTG)→亮氨酸 (TTG) ;应用MSP法检测出 14例 (32 .6% ) 5’ CpG岛甲基化并经DNA测序证实。p16INK4a蛋白表达阳性的 14份标本中仅检测到 1例 (7.14% ) 5’ CpG岛甲基化 ,而未发现基因缺失和点突变证据。 34例卵巢浆液性囊腺癌患者中p16INK4a基因异常 16例 ,较无异常 18例预后更差 (P =0 .0 0 0 8)。结论 :5’ CpG岛甲基化可能是卵巢浆液性囊腺癌中p16INK4a基因表达缺失的主要原因 ,去甲基化治疗可能成为该类肿瘤一种有用的生物治疗方法     

端粒酶活性与卵巢上皮性肿瘤临床病理因素相关性分析

目的 探讨端粒酶在上皮性卵巢肿瘤发生发展中的作用,评价端粒酶作为卵巢癌诊断及预后指标的价值。方法 采用端粒酶PCR-ELISA法对25例卵巢上皮性肿瘤包括8例良性(5例浆液性、3例粘液性)、3例交界性(浆液性)和14例恶性(8例浆液性,4例粘液性,2例内膜样),6例正常卵巢表面上皮进行端粒酶活性定量检测。结果 2例良性、2例交界性和12例恶性卵巢上皮性肿瘤及1例正常上皮存在端粒酶活性,端粒酶活性的吸光度(A)平均值分别为0.080±0.070、0.408±0.208、1.659±0.930和0.086±0.060,统计学分析表明恶性卵巢肿瘤中端粒酶活性明显高于良性、交界性肿瘤和正常卵巢组织,端粒酶活性和卵巢上皮性肿瘤组织学类型、临床分期无关;而与肿瘤的分化程度呈负相关。结论 研究结果初步证明端粒酶活性增高在卵巢癌的无限增殖中是一重要环节,并提示端粒酶表达有可能成为卵巢癌早期诊断及判断预后的肿瘤标志物。端粒酶PCR-ELISA法具有定性又定量、特异性较高、敏感性强、简易快速、可避免同位素污染等优点。     

Common genetic changes between endometriosis and ovarian cancer

We analyzed 81 ovarian cancers for loss of heterozygosity (LOH) on 10q23 and for mutations in PTEN. LOH was common among the endometrioid (43%) and serous (28%) cancers, but was infrequent among the other histological subtypes. Somatic PTEN mutations were detected in seven (21%) endometrioid cancers and the mutation in all informative cases was accompanied by loss of the wild-type allele. One mucinous cancer without 10q23 LOH was shown to harbor two somatic PTEN mutations. Frequent LOH was observed on chromosome 6q (60.0%) and chromosome 10q (40.0%) in ovarian atypical endometriosis, but no PTEN mutations were observed. These findings support the hypothesis that endometrioid and clear cell ovarian carcinomas may arise through malignant transformation of endometriotic lesions.     

p63 expression in epithelial ovarian tumors

Ovarian cancer is a highly lethal disease and its underlying biology is poorly understood. The p63 is a homologue gene of the tumor suppressor p53. p63 appears to be important for the development and differentiation of reproductive epithelium and interacts with p53 in human tumorigenesis. This study presents the immunoexpression of the p63 in benign and malignant epithelial ovarian tumors. We evaluated the p63 immunoexpression in 91 ovarian benign cystadenomas (29 mucinous and 62 serous) and in 29 ovarian malignant tumors (3 mucinous borderline, 3 serous borderline, 17 serous carcinomas, 2 endometrioid, 2 undifferentiated, 1 mucinous, and 1 clear-cell carcinoma) using a monoclonal antibody clone 4A4 (1:200), which recognizes all p63 variants. The tumors were considered p63 positive if 5% or more cells presented nuclear immunostaining. We observed 85.7% of positivity in benign tumors, 50% in borderline tumors, and 8.7% in invasive ovarian cancer (P < .0001). The benign serous cystadenomas were positive in 91.9% of cases and benign mucinous cystadenomas in 72.4% (P= .02). These data suggests an important role of p63 in the control of ovarian epithelium behavior. The p63 may be involved in the development of benign and malignant epithelial ovarian tumors.     

Role of KRAS and BRAF gene mutations in mucinous ovarian carcinoma

OBJECTIVES: The goals of this study were to perform a comprehensive assessment of the prevalence of KRAS oncogene mutations in invasive epithelial ovarian carcinomas of various histologic subtypes, and for any subgroup(s) in which KRAS mutation was found to be common, to address the hypothesis that those tumors without KRAS mutation had sustained alternative activation of this signaling pathway through mutation of the BRAF oncogene. METHODS: A total of 104 primary, invasive epithelial ovarian carcinomas from a 10-year period at this institution were selected for study based on histologic classification. The histologic cell type was serous in 21 cases, endometrioid in 30 cases, clear cell in 31 cases, and mucinous in 22 cases. Additional clinical and pathological information was abstracted from patient records, and pathology review was performed for all cases. Direct sequence analysis of exon 2 of the KRAS gene, containing codon 12, was performed using DNA isolated from all tumor specimens. Sequence analyses of exons 11 and 15 of the BRAF gene were performed for the 22 cases of mucinous ovarian carcinoma. RESULTS: Activating KRAS mutations were more common in mucinous tumors (50%) than in all other histologic types combined (5%; P < 10(-7)). Mutation of KRAS was more common in stage I tumors than in advanced stage tumors (P = 0.0004). Of the 11 mucinous tumors with KRAS mutations, 6 were of Mullerian (endocervical) type and 5 were of gastrointestinal type. No mucinous tumor was found to harbor a BRAF mutation. CONCLUSIONS: These data indicate that KRAS oncogene mutations exist in several histologic types of invasive epithelial ovarian carcinoma, especially stage I tumors, but are common only in tumors of mucinous histology. Mutations are equally prevalent in mucinous ovarian cancers of Müllerian and gastrointestinal types. In contrast to other solid tumor types frequently affected by KRAS mutation, mucinous ovarian cancers without a KRAS mutation have not sustained alternative activation of this signaling pathway through mutation of the BRAF oncogene.     

Molecular pathology of epithelial ovarian cancer

Ovarian cancer is the most lethal gynaecological malignancy and it most commonly occurs in postmenopausal women. Ninety per cent of ovarian cancers are derived from the ovarian surface epithelium and these neoplasms are classified into serous, mucinous, endometrioid, clear-cell and transitional-cell types. The molecular pathology of ovarian carcinomas is heterogeneous and involves various putative precursor lesions and multiple pathways of development. The most common subtype, high-grade serous carcinoma, is characterized by p53 mutations, and BRCA1 and/or BRCA2 dysfunction. It most likely arises from epithelium within inclusion cysts or from the surface of the ovary. In contrast, low-grade serous carcinomas are characterized by KRAS or BRAF mutations and appear to arise via an adenoma-borderline-carcinoma sequence. Similarly, mucinous carcinomas have KRAS mutations and probably develop via an adenoma-borderline-carcinoma sequence. Low-grade endometrioid carcinomas, however, are characterized by mutations in PTEN and CTNNB1, and microsatellite instability, and may arise from ovarian endometriosis or borderline endometrioid tumours. High-grade endometrioid carcinomas have similar changes to high-grade serous carcinomas. Clear-cell carcinomas are characterized by mutations of TGFbetaR2 and over-expression of HNF-1beta, and probably arise from ovarian endometriosis. The molecular changes in transitional-cell carcinomas of the ovary remain largely unknown. The identified molecular changes and pathways of development in epithelial ovarian cancer will facilitate the rationalized development of new diagnostic modalities and tailored therapies for this malignancy.     

Risk factors for different histological types of ovarian cancer

Various histological types of ovarian cancer may develop from different etiological aspects. Data separated by histological subtypes collected in the framework of a large case-control study on ovarian cancer conducted in Italy were analyzed. The cases were women below the age of 75 years, admitted to a network of hospitals in Milan. Cases were grouped into four categories by histological type: mucinous tumor (n = 52), serous tumor (n = 680), endometrioid tumor (n = 41), and other histologies including clear-cell and undifferentiated epithelial tumors (n = 50). Controls were 2758 patients admitted to the same network of hospitals for a wide spectrum of acute, nongynecological, non-hormone-related, non-neoplastic conditions. In comparison with nulliparae, the risk of serous, endometrioid, and other histologies of ovarian cancer tended to be lower in parous women, but the odds ratios (OR) were above unity for mucinous ovarian cancer. Oral contraceptive use was associated with OR lower than unity for serous (OR = 0.7) and endometrioid (OR = 0.8) ovarian cancers but not for mucinous (OR = 1.4) and other histologies (OR = 1.6). Finally, our results on dietary fat intake did not show substantial differences in all histological types of ovarian cancer.     

Treatment of ovarian cancer in young women

Ovarian cancer accounts for approximately 22,000 cases annually in the United States. Although the vast majority of ovarian cancers occur in postmenopausal women and are of advanced stage, a significant subset occurs in young women. Among those subtypes having a predisposition for young women are malignant ovarian germ cell tumors, sex cord-stromal ovarian tumors, and tumors of low malignant potential. However, invasive epithelial ovarian cancers may also occur in young women, particularly the subtypes of low-grade serous carcinoma and mucinous carcinoma. This article details the diagnosis and optimal treatment of ovarian cancers subtypes in young women.     

Risk Factors for Epithelial Borderline Ovarian Tumors: Results of a Swedish Case–Control Study

OBJECTIVE: Borderline ovarian tumors have a favorable prognosis. Previous epidemiological studies indicate common risk factors for invasive epithelial ovarian cancers and borderline tumors, but it remains unresolved whether these tumors are precursors of invasive cancers or a separate disease entity. The objective of this population-based case-control study conducted in 1993-1995 was to examine reproductive and other factors in relation to the risk of borderline ovarian tumors. METHODS: Subjects were 193 histologically verified incident epithelial borderline tumor cases and 3899 randomly selected controls aged 50-74 years, whose data were collected through mailed questionnaires. Risk estimates were calculated by unconditional logistic regression. RESULTS: Ever parous women were at reduced risk, with odds ratios of 0.44 (95% confidence interval (CI) 0.26-0.75) for serous and 0.63 (95% CI 0.34-1.19) for mucinous tumors. No clear trends emerged for age at first birth, at menarche, and at menopause. Lactation reduced tumor risk. Oral contraceptive ever use conferred no protection, with odds ratios of 1.40 (95% CI 0.87-2.26) for serous and 1.04 (95% CI 0.61-1.79) for mucinous tumors. The odds ratio for serous tumors following unopposed estrogen ever use was 2.07 (95% CI 1.08-3.95), whereas no risk increase appeared with estrogens supplemented by cyclic or continuous progestins. Mucinous tumors were not associated with hormone replacement therapy. The odds ratio for serous tumors in the highest category of body mass index was 6.47 (95% CI 3.09-13.5). CONCLUSIONS: Increasing parity and lactation reduce the risk of borderline ovarian tumors in women aged 50-74, while no protection follows oral contraceptive use. Hormonal situations such as unopposed estrogen use and obesity, where estrogens are not counteracted by progestins, may increase the risk of serous tumors.     

Histologic subtypes and laterality of primary epithelial ovarian tumors

OBJECTIVES: To determine if the likelihood of bilateral primary ovarian tumors differs by histologic subtype. METHODS: Using data collected by the Surveillance Epidemiology and End Results (SEER) program, the analysis included 22,328 women 25-84 years of age who were diagnosed with a borderline or malignant epithelial ovarian tumor during 1992-2000, categorized as to laterality and histologic subtype. RESULTS: Malignant serous tumors were bilateral in 57.5% of cases. Corresponding figures for mucinous, clear cell, endometrioid and other epithelial tumors were 21.3%, 13.3%, 26.8%, and 35.6%, respectively. Borderline serous tumors were bilateral in 29.8% of the cases compared to only 7.0% of mucinous tumors. The tendency for serous tumors to present as bilateral was consistent across all categories of race, age, and stage. CONCLUSIONS: Serous tumors of the ovary are more commonly bilateral than ovarian tumors of other histologic subtypes. The reasons for this tendency remain to be determined.     

Cigarette smoking and epithelial ovarian cancer by histologic type

OBJECTIVE: To examine cigarette smoking as a risk factor for different types of epithelial ovarian cancer. METHODS: We used data from the Cancer and Steroid Hormone Study, a multicenter, population-based, case control investigation. Cases were 447 women aged 20-54 years with diagnoses of epithelial ovarian cancer. Controls were 3868 women selected by random-digit dialing. Conditional logistic regression was used to obtain odds ratios (ORs) and 95% confidence intervals (CIs) as estimators of the relative risk of ovarian cancer. With age and study site as conditioning variables, OR point estimates were additionally adjusted for parity and use of oral contraceptives. RESULTS: The OR of mucinous epithelial ovarian cancer for women who had ever smoked was 2.3 (95% CI 1.4, 3.9) and for current smokers was 2.9 (95% CI 1.7, 4.9). The OR of mucinous tumors for current smokers was significantly elevated regardless of years since first cigarette or age at which women first smoked. The OR of mucinous tumors for current smokers increased slightly as cumulative pack-years of smoking increased, although the trend was not significant. Similar patterns of elevated risk were not observed among serous, endometrioid, or other histologic types. Odds ratio point estimates for former smokers were not significantly elevated for any histologic type. CONCLUSION: Current cigarette smoking was a risk factor for mucinous epithelial ovarian cancer, but not other histologic types.     

卵巢上皮性癌组织中磷酸化蛋白激酶B和PTEN蛋白的表达及其意义

目的探讨磷酸化蛋白激酶B（pAKT）和FYEN蛋白在卵巢上皮性癌（卵巢癌）组织中的表达及其相互关系,并分析两者与卵巢癌患者预后的关系。方法应用免疫组化法,检测12份正常卵巢、20份卵巢良性上皮性肿瘤、12份卵巢交界性上皮性肿瘤、80份卵巢癌组织中pAKT和PTEN蛋白的表达,并分析两者间的关系。采用单因素和多因素生存分析法分析pAKT和FYEN蛋白表达与卵巢癌患者预后的关系。结果pAKT蛋白在正常卵巢、卵巢良性上皮性肿瘤组织中的阳性表达率分别为8％、10％。显著低于卵巢癌组织的55％（P〈0．01）;而FYEN蛋白在卵巢癌组织中的阳性表达率为45％,显著低于正常卵巢和良性上皮性肿瘤组织的100％、80％（P〈0．01）。pAKT和FYEN蛋白在交界性肿瘤组织中的阳性表达率分别为25％、67％,分别与卵巢癌组织比较,差异均无统计学意义（P〉0．05）。pAKT和FYEN蛋白表达与卵巢癌手术病理分期、病理分级、有无淋巴结转移和远处转移有关（P〈O．05）,而与年龄、病理类型、有无腹水无关（P〉0．05）。卵巢癌组织中pAKT和PTEN蛋白间的表达呈明显负相关关系（r=-0．444,P〈0．01）。单因素生存分析显示,手术病理分期、病理分级、有无淋巴结转移和远处转移、pAKT和FrEN蛋白阳性表达与患者预后有关（P〈0．05）。Cox回归多因素分析表明,FYEN蛋白阳性表达和手术病理分期是影响卵巢癌患者预后的独立危险因素（P〈0．05）。结论pAKT蛋白过度表达伴随PTEN蛋白表达缺失可能参与卵巢癌的发生、发展,PTEN蛋白表达缺失是卵巢癌患者预后不良的独立危险因素。