类胚胎致死性异常视觉基因1表达与卵巢浆液性癌化疗耐药及预后关系研究

目的探讨类胚胎致死性异常视觉基因1(ELAV1)在卵巢浆液性肿瘤组织中的表达与卵巢浆液性癌化疗耐药及预后的关系。方法采用免疫组化法对2010年1月至2013年2月中国医科大学附属盛京医院收治的40例卵巢浆液性癌(化疗耐药20例和化疗敏感20例)、15例卵巢交界性浆液性瘤、20例卵巢良性浆液性瘤及15例正常卵巢组织中的ELAV1蛋白表达进行检测,并对ELAV1表达与患者临床病理资料及生存率的关系进行分析。结果 (1)ELAV1蛋白胞浆在卵巢浆液性癌中的阳性表达率明显高于卵巢交界性浆液性瘤、卵巢良性浆液性瘤和正常卵巢组织(P0.05),且在卵巢癌化疗耐药组织中明显高于化疗敏感组织(P0.05)。(2)ELAV1蛋白胞核阳性表达率在卵巢浆液性癌、卵巢交界性浆液性瘤、卵巢良性浆液性瘤及正常卵巢组织中差异无统计学意义(P0.05)。(3)胞浆ELAV1的表达与卵巢浆液性癌FIGO病理分期及淋巴结转移情况相关(P0.05),与患者年龄、是否绝经及分化程度无关(P0.05)。(4)Kaplan-Meier生存分析提示:ELAV1蛋白胞浆阳性和化疗耐药患者生存时间短。结论 ELAV1可能与卵巢浆液性癌的发生发展相关,可作为预测卵巢浆液性癌化疗耐药及预后的指标。     

精脒合酶蛋白在卵巢浆液性肿瘤组织中表达及其与预后关系研究

目的探讨精脒合酶(Srm)蛋白在卵巢浆液性肿瘤组织中的表达情况及其与卵巢浆液性癌临床病理特征及预后的关系。方法收集中国医科大学附属盛京医院2008年1月至2014年12月经手术治疗并于术后病理证实的卵巢浆液性癌组织石蜡切片80例、卵巢交界性浆液性肿瘤组织蜡块切片26例、卵巢良性浆液性肿瘤组织蜡块切片13例及正常卵巢组织石蜡切片12例。应用免疫组化法检测Srm蛋白在不同组织中的表达情况,分析其表达与卵巢浆液性癌临床病理特征的关系;同时对卵巢浆液性癌患者进行生存随访并进行单因素及多因素的生存分析,研究Srm蛋白表达与卵巢癌患者预后的相关性。结果 Srm蛋白的表达水平与患者是否绝经、卵巢浆液性癌FIGO手术病理分期及组织病理分级程度相关(χ~2=4.752、13.182、5.921,均P0.05),与是否存在淋巴转移情况无关(χ~2=1.537,P0.05)。多因素COX模型生存分析显示:FIGO手术病理分期、Srm蛋白表达程度及有无淋巴结转移是影响卵巢浆液性癌预后的独立危险因素(χ~2=5.941、4.699、4.596,均P0.05)。结论 Srm蛋白的高表达与卵巢浆液性癌发病之间存在联系。Srm蛋白可能参与卵巢浆液性癌发生发展,其高表达可能是影响卵巢浆液性癌预后的独立危险因素之一。     

卵巢上皮性肿瘤中细胞周期素D1蛋白与p16蛋白的表达及其临床意义

目的　探讨细胞周期素D1蛋白 (cyclinD1)与 p16蛋白在卵巢上皮性肿瘤中的表达及临床意义。 方法　 1998年 1月至 2 0 0 0年 1月采用免疫组化SP法 ,检测恶性、交界性、良性卵巢上皮性肿瘤、正常卵巢组织中的cyclinD1蛋白和p16蛋白的表达。结果　cyclinD1蛋白、p16蛋白表达的阳性率分别为恶性 5 0 %和 4 0 %、交界性30 %和 5 0 %、良性卵巢上皮性肿瘤 0和 80 %、正常卵巢组织中 0和 90 %。恶性卵巢上皮性肿瘤与良性卵巢上皮性肿瘤及正常卵巢组织之间比较 ,cyclinD1蛋白的表达差异有显著性意义 (P <0 0 1) ,p16蛋白的表达差异有显著性意义 (P <0 0 5 )。在恶性程度较高 ,组织分化差 ,晚期的恶性卵巢上皮性肿瘤中cyclinD1蛋白表达率高 ,p16蛋白的表达率低。相关性分析显示 ,cyclinD1蛋白与 p16蛋白的表达呈负相关。 结论　cyclinD1蛋白的过度表达与 p16蛋白表达的缺失在恶性卵巢上皮性肿瘤的发生、发展中起一定作用 ,二者可能存在相互抑制机制。     

活化白细胞粘附分子在卵巢浆液性肿瘤中的表达及意义

目的探讨活化白细胞粘附分子(ALCAM)在卵巢浆液性肿瘤中的表达及其意义。方法使用免疫组化法检测ALCAM在卵巢良性、交界性及恶性浆液性性肿瘤病灶中的表达。使用Elisa检测卵巢肿瘤患者术前血清中ALCAM浓度。结果卵巢良性、交界及恶性浆液性肿瘤患者血清均可检测到ALCAM,三组间浓度无统计学差异。ALCAM在卵巢良性、交界性、恶性肿瘤中的阳性表达率分别为:31.8%、28.5%及62.2%。良性与恶性肿瘤组间ALCAM蛋白表达率差异有统计学意义(P=0.001)。卵巢恶性肿瘤组织中ALCAM蛋白的表达与手术分期、是否有淋巴结转移及预后有相关性。ALCAM阳性组卵巢恶性肿瘤患者5年生存率为23.5%,而ALCAM阴性组为50.0%,二者之间差异有统计学意义(P=0.02)。结论卵巢恶性肿瘤组织中ALCAM表达增强为卵巢恶性肿瘤不良预后的指标。     

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。     

卵巢浆液性癌组织中Hugl-1和aPKC的表达及意义

目的探讨原发性卵巢浆液性癌组织中Hugl-1和aPKC的表达及意义。方法选择浙江大学医学院附属妇产科医院2000年6月至2007年6月经手术切除的原发性卵巢浆液性癌组织79例,用免疫组化SP法检测Hugl-1和aPKC蛋白在其组织中的表达。同时检测Hugl-1和aPKC蛋白在25例正常卵巢组织,31例卵巢浆液性囊腺瘤,41例卵巢交界性浆液性肿瘤中的表达,并分析了Hugl-1和aPKC蛋白表达与卵巢癌临床病理参数间的关系。结果Hugl-1蛋白在卵巢浆液性癌组织、正常卵巢、浆液性囊腺瘤及交界性浆液性肿瘤中的强阳性表达率分别为12.7%、48%、58%、41.5%。癌组织中的表达显著低于其余3组,差异有统计学意义(P0.001);aPKC蛋白在卵巢浆液性癌组织、正常卵巢、浆液性囊腺瘤及交界性浆液性肿瘤中的强阳性表达率分别为19%、0、0、0。癌组织中的表达显著高于其余3组,差异有统计学意义(P0.001);Hugl-1和aPKC的表达与组织学分级、手术病理分期、淋巴结转移有一定的相关性(P0.05)。Hugl-1和aPKC在卵巢癌组织中的表达不存在相关性(P0.05)。结论Hugl-1和aPKC可能均参与了卵巢癌的发生与发展。     

环氧合酶-2蛋白及前列腺素类物质与卵巢浆液性癌生物学行为的关系

目的　研究环氧合酶 2 (COX 2 )以及前列腺素类物质与卵巢浆液性肿瘤发生、发展的关系。方法　采用免疫印迹法及放射免疫法对 5 4例卵巢浆液性肿瘤组织 (其中良性卵巢浆液性肿瘤 11例 ,交界性良性卵巢浆液性肿瘤 10例 ,卵巢浆液性癌 3 3例 )和 10例正常卵巢组织进行COX 2蛋白、前列腺素 (PG)E2 、6 酮 前列腺素F1α(6 keto PGF1α)及血栓素 (TX)B2 水平检测。结果　 (1)COX 2蛋白表达 :卵巢浆液性癌组织的阳性表达率为 82 % (2 7/ 3 3 )、相对含量为 2 0 0 8± 3 5 3 ,交界性卵巢浆液性肿瘤分别为 90 % (9/ 10 )、2 0 61± 3 0 3 ,均明显高于良性卵巢浆液性肿瘤及正常卵巢 (阳性表达率均为0 ,相对含量分别为 15 0 4± 0 12及 15 3 3± 0 60 ) ,差异均有显著性 (P <0 0 5 ) ;卵巢浆液性癌患者不同临床分期 (Ⅰ～Ⅱ期与Ⅲ～Ⅳ期 )、病理分级及有无腹水、有无淋巴结转移间比较 ,差异均无显著性 (P>0 0 5 )。 (2 )前列腺素类物质PGE2 、6 keto PGF1α及TXB2 水平 :卵巢浆液性癌明显高于交界性、良性肿瘤和正常卵巢 (P <0 0 5 ) ,而后 3者间比较 ,差异无显著性 (P >0 0 5 ) ;卵巢浆液性癌患者不同临床分期 (Ⅰ～Ⅱ期与Ⅲ～Ⅳ期 )、病理分级及有无腹水、有无淋巴结转移间比较 ,差异均无显著性 (     

c-kit基因及其靶体SCF在卵巢上皮性肿瘤中的表达

目的:研究c-kit基因及其靶体干细胞因子(stem cell factor,SCF)在卵巢上皮性肿瘤的表达及临床意义,探讨其在卵巢上皮性癌发生发展中的可能作用。方法:免疫组化SP法测定10例正常卵巢组织,20例卵巢良性上皮性肿瘤,16例卵巢交界性上皮性肿瘤,58例卵巢上皮性癌标本中c-kit、SCF蛋白的表达。结果:(1)卵巢上皮性癌中c-kit蛋白阳性表达率为63.79%,明显高于正常卵巢组织(0%)及卵巢良性上皮性肿瘤(10.00%),差异有显著性(P<0.01);卵巢交界性上皮性肿瘤中c-kit阳性表达率为43.75%(7/16),也高于正常卵巢组织及卵巢良性上皮性肿瘤,差异有显著性(P<0.05);(2)卵巢上皮性癌中,低分化组的c-kit蛋白阳性表达率高于高、中分化组(P<0.05),c-kit蛋白的阳性表达率随FIGO分期的进展及淋巴结转移而升高(P<0.05);(3)c-kit阳性患者的预后比c-kit阴性患者差(P<0.05);(4)SCF在正常卵巢上皮、卵巢良性上皮性肿瘤、卵巢交界性上皮性肿瘤、卵巢上皮性癌中的阳性表达率分别为30.00%、35.00%、62.50%和74.14%,卵巢上皮性癌的阳性表达率显著高于正常卵巢组织及卵巢良性上皮性肿瘤(均P<0.01)。卵巢癌低分化组SCF的阳性表达率显著高于高、中分化组(P<0.05)。且随FIGO分期的进展及淋巴结转移而升高(P<0.05);(5)c-kit与SCF表达具有明显相关性(r=0.302,P<0.05)。结论:(1)c-kit、SCF表达异常可能在卵巢上皮性癌的发生发展中起重要作用;(2)c-kit、SCF在卵巢上皮性癌中的表达具有相关性,SCF作为c-kit的配体,可促使c-kit活化,两者具有协同作用(3)c-kit蛋白表达与卵巢上皮性癌患者的预后有关,可作为判断卵巢上皮性癌患者预后的指标之一。     

细胞周期p16-cyclin D1-pRb调节通路与人卵巢浆液性囊腺癌的相关性研究

目的 :探讨细胞周期 p16 - p Rb- cyclin D1调节通路及各因子在浆液性卵巢肿瘤发生和发展中的作用。方法 :应用免疫组化 L s AB法检测一组浆液性卵巢肿瘤中 p16、p Rb和 cyclin D1蛋白表达情况。结果 :卵巢浆液性囊腺癌原发灶和淋巴结转移灶中 p16表达阳性率明显低于正常卵巢、良性肿瘤和交界性肿瘤 ;p16 - p Rb- cyclin D1调节通路异常率却呈相反趋势变化 ,且通路异常与浆液性囊腺癌 FIGO分期、组织学分级及预后无明显相关性。 p16表达阳性患者术后生存率高于阴性患者 (P=0 .0 0 0 6 )。p Rb和 cyclin D1表达情况与卵巢浆液性囊腺癌组织学分级、FIGO分期无明显关系。卵巢浆液性肿瘤组织中 p16和 p Rb蛋白表达呈负相关。结论 :p16蛋白在卵巢浆液性肿瘤的发生、发展中可能起着较为重要的作用。 p16 - p Rb- cyclin D1调节通路异常在浆液性卵巢肿瘤虽很常见 ,但其具体作用尚不清楚     

eIF4A在卵巢上皮性癌中表达及其与预后的关系

目的:检测真核细胞起始因子4A(e IF4A)在不同卵巢组织中的表达,探讨其临床意义及其与预后的关系。方法:利用荧光实时定量PCR及Western blot法检测42例卵巢上皮性癌(EOC)组织、15例卵巢交界性上皮性肿瘤组织、15例卵巢良性上皮性肿瘤组织和20例正常卵巢组织中e IF4A mRNA及蛋白的表达情况,同时采用免疫组化SP法检测123例EOC石蜡切片中e IF4A蛋白表达情况,并评估影响患者总生存率的高危因素。结果:EOC中e IF4AmRNA及蛋白表达显著高于交界性、良性及正常卵巢上皮组织(P0.05);交界性上皮肿瘤组织明显高于良性及正常卵巢上皮组织(均P0.05);卵巢良性上皮性组织略高于正常卵巢组织,但差异无统计学意义(P0.05)。EOC中e IF4A表达与FIGO手术病理分期、组织学分级、淋巴结转移及腹水情况有关(P均0.05),而与年龄及组织学类型无关(P0.05)。Kaplan-Meier生存曲线显示,e IF4A蛋白高表达者的总生存率明显低于低表达者(Log-Rank检验,P0.05)。COX比例风险模型分析发现,临床病理分期、组织学分级及术后有无残余瘤灶是EOC患者的独立预后因素(P0.05)。结论:e IF4A在EOC的发生进展中可能起重要作用,有可能成为判断预后的指标之一。     

卵巢上皮性肿瘤的临床病理特征及其细胞周期素D1和p53蛋白表达的研究

目的研究卵巢上皮性癌（卵巢癌）和交界性上皮性肿瘤的临床病理特征及其细胞周期素D1（cyclin D1）和p53蛋白表达的情况,探讨卵巢癌和交界性上皮性肿瘤在发病机制上的联系。方法分析45例卵巢癌（卵巢癌组）和54例卵巢交界性上皮性肿瘤（交界性肿瘤组）的临床病理资料,采用免疫组化法检测两组组织中cyclin D1、p53蛋白的表达情况,并分析其与临床病理特征的相关性。结果（1）临床病理特征：①年龄：交界性肿瘤组平均年龄为42．5岁（14～82岁）,中位数年龄41岁;卵巢癌组平均年龄为53．5岁（26～80岁）,中位数年龄51岁。②分期：按国际妇产科联盟（FIGO）分期标准,交界性肿瘤组Ⅰ期48例、Ⅱ期3例、Ⅲ期3例;卵巢癌组Ⅰ期6例、Ⅱ期8例、Ⅲ期26例、Ⅳ期5例。③病理类型：交界性肿瘤组以黏液型为主[占56％（30／54）],其次为浆液型[其中普通型11例,微乳头型5例;占30％（16／54）];卵巢癌组以浆液型（其中低度恶性19例,高度恶性3例）为主[占49％（22／45）]。④病理分化程度：卵巢癌组高分化5例,中分化17例,低分化或未分化23例。⑤预后：交界性肿瘤组5年生存率为98％,卵巢癌组为51％,两组比较,差异有统计学意义（P=0．000）。（2）cyclin D1和p53蛋白的表达及其与卵巢癌和交界性肿瘤临床病理特征的相关性：卵巢癌组cyclin D1和p53蛋白的阳性表达率分别为31％（14／45）和56％（25／45）,p53蛋白表达强度与病理分化程度呈正相关（r=0．320,P=0．032）;交界性肿瘤组cyclin D1和p53蛋白的阳性表达率分别为69％（37／54）和6％（3／54）。其中,普通型浆液性交界性肿瘤与高度恶性浆液性癌比较（两者cyclin D1蛋白阳性表达率分别为91％和26％,p53蛋白分别为0和58％）,差异有统计学意义（P〈O．01）;而微乳头型浆液性交界性肿瘤与低度恶性浆液癌比较（两者cyclin D1蛋白阳性表达率分别为3／5和2／3,p53蛋白分别为1／5和1／3）,差异则无统计学意义（P〉0．05）。结论cyclin D1蛋白的过度表达常见于卵巢浆液性交界性肿瘤及低度恶性浆液性癌组织中,而p53蛋白的过度表达更多见于高度恶性浆液性癌组织中。卵巢浆液性交界性肿瘤与高度恶性浆液性癌具有不同的发病机制,而微乳头型浆液性交界性肿瘤与低度恶性浆液性癌的关系可能更为密切。     

Pathology of borderline (low malignant potential) ovarian tumours

Recent studies suggest that the borderline group of ovarian tumours can be subclassified into benign and malignant neoplasms. The survival for patients with serous borderline tumours confined to the ovaries is virtually 100%. Patients with serous borderline tumours with invasive peritoneal implants, and with micropapillary serous carcinomas (a distinctive neoplasm previously included in the borderline category), have a 30-40% mortality rate and therefore these tumours are classified as carcinomas. After these neoplasms are excluded, the remaining advanced stage serous borderline tumours (those with non-invasive implants) have a survival rate of nearly 100% and should be considered benign. Similarly, nearly all mucinous borderline tumours reported to display aggressive behaviour have been associated with pseudomyxoma peritonei, a condition now known to be of appendiceal origin. The remaining mucinous borderline tumours are always confined to the ovaries and have a benign behaviour. Since borderline tumours can now be classified into benign and malignant types, the category has no further utility.     

Antimetastasis gene expression and numerical chromosomal abnormalities of chromosomes 1 & 17 in serous tumours of the ovary

OBJECTIVE(S): The aim of this study was to examine the expression of the antimetastasis gene nm23 and numerical changes on chromosome 1 and 17 in ovarian tumours. METHODS: In this study 20 serous cystadenocarcinomas, ten borderline and five benign tumours were analysed for expression of the nm23 antimetastasis gene by immunohistochemistry and for numerical chromosomal abnormalities of chromosomes 1 and 17 by interphase cytogenetics. RESULTS: Strong intracytoplasmic immunoreactivity with the antimetastasis gene was observed in late stage carcinomas but not in benign or borderline tumours or in lymph node metastases. Numerical abnormalities were only observed in carcinomas. CONCLUSION(S): These sets of data are consistent with the majority of benign and borderline tumours lacking invasive potential. Odds Ratio (OR) assessment indicates that the presence of numerical aberrations correlates with immunopositivity.     

Overexpression of cyclin D1 and c-Myc gene products in human primary epithelial ovarian cancer

Cyclin D1 and c-Myc are key participants in the cell-cycle pathway, in which aberrancies have been associated with malignant transformation. To date, data on the relationship of expression of these proteins and histologic subtype of epithelial ovarian cancer are still scarce and discordant. Immunohistochemical analysis was performed on 12 normal ovaries and 47 cases of serous, mucinous, endometrioid, and clear cell ovarian carcinomas. No abnormal expression of cyclin D1 or c-Myc was demonstrated in any of the 12 normal ovarian specimens. However, compared to normal ovarian tissues, overexpression of cyclin D1 and c-Myc was observed in 42.6% (20/47) and 65.9% (31/47) of tumors examined, respectively. There was no significant difference of overexpression of cyclin D1 or c-Myc gene products between these four histologic subtypes of ovarian adenocarcinomas. This study shows that cyclin D1 and c-Myc are frequently overexpressed in epithelial ovarian carcinomas, but they are not correlated with a particular histologic subtype. Although our preliminary results need to be validated in a larger number of tumors, the abnormal expression of cyclin D1 and c-Myc in epithelial ovarian cancer reaffirms the notion that they are crucial components in the pathway of tumorigenesis and deserve further study.     

Biological relevance of E-cadherin-catenin complex proteins in primary epithelial ovarian tumours

This study analysed the biological relevance of E-cadherin, alpha-catenin, beta-catenin and gamma-catenin immunoexpression pattern (reduced vs. preserved phenotype) in epithelial ovarian tumours. Immunohistochemistry was used to evaluate the expression of these proteins in 154 epithelial ovarian tumours, consisting of 17 benign, 33 borderline and 104 malignant tumours. In borderline tumours, the immunoexpression pattern of E-cadherin (p = 0.014) and alpha-catenin (p = 0.030) associated with histological type. In malignant tumours, the immunoexpression pattern of E-cadherin was related with histological type (p = 0.001). The immunoexpression pattern of beta-catenin associated with histological type and tumour differentiation (p = 0.005, p = 0.025, respectively). The preserved phenotype of E-cadherin was most frequently observed in mucinous tumours, whereas reduced E-cadherin was most frequently observed in serous tumours. The preserved phenotype of beta-catenin associated with endometrioid carcinomas, while reduced beta-catenin associated with poorly differentiated serous and clear cell carcinomas. Although the reduced phenotype was the most frequent immunoexpression observed for all proteins of the E-cadherin-catenin complex in epithelial ovarian tumours, only beta-catenin showed a significant difference between benign, borderline and malignant tumours (p = 0.045), since borderline and malignant tumours most frequently showed the reduced phenotype. The immunohistochemical profile of beta-catenin was shown to be of biological relevance: reduced beta-catenin was correlated with loss of tumour differentiation and serous carcinomas that are known to depict aggressive biological behaviour in epithelial ovarian tumours.     

K-ras alterations in Danish ovarian tumour patients. From the Danish "Malova" Ovarian Cancer study

OBJECTIVE: Activation of ras oncogenes has been demonstrated in ovarian tumours. All the reported studies are based on a relatively small number of patients and the results therefore remain a subject of debate. METHODS: In this study, we analyzed the presence of mutations at codons 12 and 13 of the K-ras gene in 165 Danish women with ovarian tumours, including 138 invasive ovarian cancers and 27 borderline ovarian tumours, using a restriction fragment length polymorphism-polymerase chain reaction technique and evaluated whether such alterations were associated with the clinicopathological parameters of the patients and survival. RESULTS: K-ras codon 12 gene mutations were found in 8.7% of ovarian cancer patients and in 14.8% of the borderline ovarian tumour patients. A K-ras codon 13 gene mutation was found in 1.5% of ovarian cancer patients. K-ras mutations were found with a significantly higher frequency in mucinous tumours compared to serous tumours (P = 0.011). CONCLUSIONS: Mutation frequency was correlated with the histological type of tumour, but not with stage, radicality of operation, and age. Furthermore, no significant difference in survival was demonstrated between patients with or without K-ras mutation, neither in the univariate nor in the multivariate survival analyses.     

Implication of malignancy and prognosis of p27(kip1), Cyclin E, and Cdk2 expression in epithelial ovarian tumors

OBJECTIVE: The aim of this study was to further evaluate whether the expression of p27(kip1), cyclin E, and cdk2 is related to the malignancy of ovarian tumors and whether their expressions, alone or in combination, are associated with prognosis in epithelial ovarian carcinoma. METHODS: Immunohistochemical analysis using anti-p27(kip1), anti-cyclinE, and anti-cdk2 antibodies was carried out for 103 cases consisting of benign, borderline, and malignant ovarian tumors, and Western blot analysis and cdk2 activity assay were performed in 26 fresh ovarian tumor samples. RESULTS: p27(kip1) expression was reduced in ovarian carcinomas in contrast to benign and borderline tumors. The expression of cyclin E and cdk2 gradually increased from benign to borderline to malignant tumors. Kaplan-Meier survival analysis showed that patients with p27(kip1) expression had a high overall survival rate. Patients with cyclin E overexpression had a low overall survival rate. When the combination of these proteins was analyzed, patients with the p27(kip1) (-)/cyclin E (++)/cdk2 (++) phenotype were significantly associated with the poorest overall survival. In multivariate Cox regression analysis, the combined phenotype of p27(kip1) (-)/cyclin E (++)/cdk2 (++) was independently related to poor prognosis. CONCLUSIONS: Our results suggest that loss of p27(kip1) expression and overexpression of cyclin E or cdk2 were significantly associated with malignancy in ovarian tumors. p27(kip1) and cyclin E proteins may be valuable prognostic factors for epithelial ovarian carcinoma patients. Furthermore, the combined evaluation of p27(kip1)/cyclin E/cdk2 may provide the most important prognostic implication.     

Developments in the pathology of ovarian tumours

The understanding of the pathogenesis and pathology of ovarian tumours is constantly evolving. Dominant themes in recent studies of ovarian tumours include prognostic features in borderline tumours, molecular events in the pathogenesis of ovarian tumours, the assessment of tumour features that may have prognostic or treatment implications, and the development of techniques that may enhance diagnostic accuracy. The literature has been reviewed with an aim to identifying those studies that can potentially impact practice and improve patient care. The most noteworthy developments include: the understanding that so-called 'tumours of low malignant potential' are virtually always benign, and that one can identify those rare cases with malignant potential; the importance of the recognition of micropapillary serous carcinomas; an improved understanding of early invasive carcinomas and their impact on screening practices; an understanding of the association of endometriosis with ovarian cancer; further awareness of factors in ovarian tumours that influence prognosis, such as refinements in grading and molecular markers such as P27; and refinements in diagnosis so as to distinguish primary from metastatic cancer and benign lesions from malignant tumours more effectively.     

Borderline ovarian tumors: clinical analysis of 114 cases]

OBJECTIVES: The aim of this study was to analyse the group of patients with borderline ovarian tumours. DESIGN: The analysis included 114 patients, operated for ovarian tumours of borderline malignancy in the Gynaecological Department of Medical University of Gdańsk between 1978-1997. The study takes into account comparison of: age of patients, obstetrical past, clinical signs and symptoms, clinical stage (according to FIGO), type of surgery, tumour pathology, post surgical treatment. Furthermore, long-term follow up was assessed. RESULTS: Middle age in the group was 48 years, main symptoms: pain of lower part of abdomen (47%) and ascites (26%). 92% of tumours were recognised in stage I (FIGO). 44.7% of the tumours were histological serous, 36% were mucinous. All patients were treated by surgery and 12% received additional treatment. Mean follow up was 104 months (1-247). 9.6% of the patients died because of main disease, next ten persons for reasons not connected with the main disease. 5 year survival rate was 91.2%, 10-year 84.2%. CONCLUSIONS: 1. Borderline ovarian tumours are most frequently recognised in stage I. 2. Serous and mucinous borderline ovarian are dominant. 3. Type of surgery is dependent on age of patients, obstetrical past, clinical stage and tumour pathology. 4. Prognosis in borderline ovarian tumours is excellent.