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。     

上皮性卵巢肿瘤患者血清和肿瘤组织中VEGF水平的检测

目的　通过对上皮性卵巢肿瘤患者肿瘤组织中血管内皮生长因子 (VEGF)表达的观察以及对术前血清VEGF水平的检测 ,探讨VEGF与上皮性卵巢肿瘤临床病理因素之间的关系。方法　应用免疫组织化学和ELISA方法 ,对 79例上皮性卵巢肿瘤患者 (包括 2 1例卵巢良性囊腺瘤 ,1 2例交界性卵巢肿瘤和 4 6例上皮性卵巢癌 )术前血清VEGF水平和术后组织标本中VEGF的表达进行了检测。结果　①上皮性卵巢癌组织VEGF阳性表达率 (78 2 6 % )显著高于交界性肿瘤 (4 1 6 7% )和良性囊腺瘤 (33 33% ) (P <0 0 1 ) ;上皮性卵巢癌中 ,晚期癌 (Ⅲ、Ⅳ期 )的VEGF阳性表达率 (92 0 0 % )显著高于早期癌 (Ⅰ、Ⅱ期 ) (6 1 90 % ) (P <0 0 1 ) ,且强阳性表达率 (5 2 0 0 % )也显著高于早期癌 (1 4 2 9% ) (P <0 0 5 ) ;有腹水组VEGF阳性表达率 (87 5 0 % )显著高于无腹水组 (5 7 1 4 % ) (P <0 0 5 ) ;②上皮性卵巢癌患者血清VEGF水平也明显高于良性囊腺瘤患者和交界性肿瘤患者 (P <0 0 1 ) ,卵巢癌中 ,低分化患者血清VEGF水平高于高、中分化患者 (P <0 0 1 ) ,血清VEGF水平在临床Ⅲ、Ⅳ期患者明显高于Ⅰ、Ⅱ期患者 (P <0 0 5 ) ,有明显腹水者比无腹水者高 (P <0 0 1 )。结论　VEGF在上皮性卵巢癌肿瘤组织中表达的增加以及血     

细胞周期素D1与p53蛋白在卵巢上皮性肿瘤的表达及意义

目的　探讨细胞周期素D1(CyclinD1)与 p5 3蛋白在卵巢上皮性肿瘤的表达及意义。 方法　 1990～1995年应用免疫组化法对 4 0例恶性卵巢上皮性肿瘤及 2 0例良性卵巢上皮性肿瘤组织进行CyclinD1与 p5 3蛋白检测。结果　良性卵巢上皮性肿瘤CyclinD1阳性表达为 10 0 % ,而恶性卵巢上皮性肿瘤CyclinD1阳性表达为37 5 %。良性卵巢上皮性肿瘤p5 3阳性表达为 15 0 % ,恶性卵巢上皮肿瘤 p5 3阳性表达为 4 7 5 %。CyclinD1在卵巢上皮癌G1与G2 、G3 中的阳性表达统计学差异有显著性 (P <0 0 5 ) ,p5 3蛋白在早期卵巢上皮癌与晚期卵巢上皮癌组织中的阳性表达 ,统计学差异有显著性 (P <0 0 5 ) ,p5 3蛋白的阳性表达在卵巢癌G1与G2 、G3 比较差异有显著性 (P <0 0 5 )。CyclinD1过表达的细胞同时也有 p5 3的过表达。 结论　CyclinD1与 p5 3蛋白在卵巢上皮性肿瘤的共同表达可能是促进卵巢上皮性肿瘤发展的因素。     

脆性组胺酸三聚体蛋白在上皮性卵巢肿瘤中的表达

目的 :探讨脆性组胺酸三聚体 (FHIT)蛋白在上皮性卵巢肿瘤组织中的表达及其意义 ,分析FHIT与P5 3蛋白、nm2 3 H1产物表达之间的相关性。方法 :应用免疫组化二步法检测 83例上皮性卵巢肿瘤蜡块组织标本中FHIT蛋白、P5 3蛋白及nm2 3 H1产物的表达。结果 :FHIT蛋白缺失仅见于恶性上皮性卵巢肿瘤 ,缺失率为 17.0 %。在良性与交界性上皮性卵巢肿瘤中未见FHIT蛋白缺失。在上皮性卵巢癌不同组织学分级中FHIT蛋白的缺失率分别为G10 / 6、G2 8.0 %、G331.8% ,低分化肿瘤FHIT蛋白缺失率显著高于高中分化肿瘤 (P <0 .0 5 ) ;在不同组织学类型中 ,FHIT蛋白缺失仅见于浆液性癌和透明细胞癌 ,缺失率分别为 2 5 .0 %和 1/ 3,在粘液性癌和子宫内膜样癌中未见FHIT蛋白缺失 ,但差异无显著性 (P >0 .0 5 ) ;FHIT蛋白缺失与淋巴结转移、残留癌灶大小及nm2 3 H1产物表达有明显相关性 ,与FIGO分期、有无腹水及P5 3蛋白表达无明显相关性。结论 :FHIT蛋白缺失是恶性上皮性卵巢肿瘤的特征 ,FHIT蛋白表达缺失在卵巢肿瘤的发生发展过程中有一定的作用 ,可能与上皮性卵巢癌的恶性进展及转移有关     

研究C-erbB-2、P53在卵巢上皮性肿瘤中表达及临床意义

目的　探讨癌基因C -erbB - 2 ,抑癌基因P5 3在卵巢上皮性肿瘤发生发展中的作用及临床意义。方法　采用免疫组化技术对 6 7例卵巢上皮性肿瘤组织、其中 1 0例良性肿瘤 ,1 4例交界性卵巢瘤、 4 3例卵巢癌的石蜡包埋的卵巢组织进行C -erbB - 2和P5 3蛋白表达的检测。结果　①在卵巢恶性肿瘤、交界性肿瘤、良性肿瘤之间C -erbB - 2的表达差异有显著性 (P <0 0 5 ) ;C -erbB - 2的表达率及表达强度与组织分化程度有显著相关性 (P <0 0 5 ) ,C -erbB - 2的过度表达见于恶性程度高 ,组织分化差的肿瘤中。②在卵巢恶性肿瘤、交界性肿瘤、良性肿瘤之间P5 3的表达差异有显著性 (P <0 0 1 ) ;其表达强度与组织分化程度及临床分期有显著相关性 (P <0 0 5 )。在恶性程度较高 ,组织分化差 ,较晚期的肿瘤P5 3的表达较强。结论　癌基因C -erbB -2及抑癌基因P5 3在卵巢癌组织中广泛存在 ,并与其临床病理指标之间有一定的相关性 ,提示这些基因在卵巢癌的发生发展中起一定作用。对各基因之间复杂的相互作用 ,协同作用有待进一步研究     

细胞周期素D1蛋白在卵巢上皮性肿瘤中的表达及其意义

目的　研究细胞周期素D1(cyclinD1)在卵巢上皮性肿瘤中的表达及意义。方法　 1997～ 2 0 0 0年采用免疫组织化学SP法 ,检测恶性卵巢上皮性肿瘤、交界性肿瘤、良性肿瘤、正常卵巢组织cyclinD1的表达。结果　在恶性卵巢上皮性肿瘤 ,良性肿瘤 ,正常卵巢组织之间cyclinD1的表达差异有显著性 (P <0 0 1)。cyclinD1的表达率与组织分化程度和临床分期有显著相关性 (P <0 0 5 ) ,cyclinD1的过度表达见于组织分化差 ,肿瘤发病的晚期。结论　cyclinD1在卵巢癌组织中广泛存在 ,并与组织分化 ,临床分期有一定相关性 ,提示该基因在卵巢癌的发生、发展中起一定作用     

肺耐药蛋白在上皮性卵巢癌中的表达及临床意义

目的 :探讨肺耐药蛋白 (lungresistanceprotein ,LRP)在原发性上皮性卵巢癌(POEC)组织中的表达及其临床意义。方法 :采用免疫组化SP法检测POEC 6 4例、经化疗后二次手术癌组织 2 3例以及良性卵巢肿瘤 2 1例石蜡标本中LRP的表达 ,并分析 6 4例POEC患者的临床病理资料。结果 :6 4例POEC组织中LRP阳性表达 5 3例 ,阳性率82 .8% ;2 3例化疗后癌组织中LRP阳性表达 2 3例 ,阳性率 10 0 % ;2 1例良性卵巢上皮性肿瘤中LRP阳性表达 7例 ,阳性率 33.3%。POEC中LRP的阳性表达率与良性肿瘤中表达率差异有高度显著性 (P <0 .0 1) ;化疗后癌组织中LRP的阳性表达率与初治POEC中的表达率差异有显著性 (P <0 .0 5 )。POEC组织中LRP的表达与患者年龄、组织学类型、细胞分级、临床分期和术后肿瘤残存灶大小无关 (P >0 .0 5 ) ;POEC患者LRP阳性表达组近期化疗疗效明显低于阴性表达组 (P <0 .0 5 ) ;但POEC患者LRP表达与患者术后生存时间无关 (P >0 .0 5 )。结论 :LRP在POEC组织中有较恒定的表达 ,化疗可增加POEC组织LRP表达 ,检测LRP可预测化疗近期疗效 ,指导临床化疗方案的选择。     

细胞周期素Dl与p53蛋白在卵巢上皮性肿瘤的表达及意义

目的：探讨细胞周期素D1(CyclinD1)与p53蛋白在卵巢上皮性肿瘤的表达及意义。方法：1990--1995年应用免疫组化法对40例恶性卵巢上皮性肿瘤及20例良性卵巢上皮性肿瘤组织进行CyclinD1与p53蛋白检测。结果：良性卵巢上皮性肿瘤CyclinD1阳性表达为10．0％，而恶性卵巢上皮性肿瘤CyclinD1阳性表达为37．5％。良性卵巢上皮性肿瘤p53阳性表达为15．0％，恶性卵巢上皮肿瘤p53阳性表达为47．5％。CyclinD1在卵巢上皮癌Gl与G2、G3中的阳性表达统计学差异有显著性(P＜0．05)，p53蛋白在早期卵巢上皮癌与晚期卵巢上皮癌组织中的阳性表达，统计学差异有显著性(P＜0．05)，p53蛋白的阳性表达在卵巢癌G1与G2、G3比较差异有显著性(P＜0．05)。CyclinD1过表达的细胞同时也有p53的过表达。结论：CyclinD1与p53蛋白在卵巢上皮性肿瘤的共同表达可能是促进卵巢上皮性肿瘤发展的因素。     

HE4、Sp1在上皮性卵巢癌中的表达及其临床意义

目的探讨人附睾蛋白4(HE4)和转录因子Sp1在卵巢癌中的表达及其临床价值。方法应用免疫组化法检测40例卵巢癌和20例卵巢上皮性良性卵巢肿瘤组织中HE4、Sp1的表达。结果 HE4在卵巢癌中的阳性表达率(80.00%)明显高于良性上皮性肿瘤(20.00%),差异有统计学意义(P0.01);HE4在各种病理类型卵巢癌中均表达,在浆液性卵巢癌中表达率最高(92.59%),其次为子宫内膜样癌(71.43%);HE4在中低分化卵巢癌阳性表达率(85.71%)高于高分化者(40.00%),差异有统计学意义(P0.05),而与卵巢癌FIGO分级及是否伴有淋巴结转移无明显相关性。Sp1在卵巢癌中的阳性表达率(42.50%)高于良性上皮性肿瘤组(15.00%),差异有统计学意义(P0.05);Sp1在浆液性癌、黏液性癌、内膜样癌中均有表达,表达率差异无统计学意义(P0.0 5);Sp1在晚期卵巢癌中表达阳性率(57.14%)高于早期卵巢癌(26.32%),中低分化组中阳性率(48.57%)高于高分化组(0.00%),差异均有统计学意义(P0.05),但与淋巴转移情况无关。HE4及Sp1在上皮性卵巢癌组织中的表达呈正相关(r=0.496,P0.05)。结论 HE4、Sp1与卵巢癌的发生、发展关系密切,HE4及Sp1有望成为卵巢癌诊断、治疗的新靶点。     

凋亡抑制基因survivin在卵巢上皮性癌组织中的表达及其与bcl-2、bax蛋白表达的关系

目的　探讨凋亡抑制基因survivin在卵巢上皮性癌中的表达 ,及其与bcl 2、bax蛋白表达的相关性。方法　应用逆转录聚合酶链反应 (RT PCR)技术 ,检测 35例卵巢上皮性癌组织中survivin基因的表达 ;应用免疫组织化学链霉亲和素 生物素 过氧化物酶复合物 (SABC)方法 ,检测bcl 2及bax蛋白的表达 ,并与卵巢上皮性交界性肿瘤、良性卵巢肿瘤及正常卵巢组织各 10例进行对照。结果　卵巢上皮性癌、交界性肿瘤组织中 ,survivin基因的表达率分别为 83%及 80 % ,显著高于良性卵巢肿瘤及正常卵巢组织的表达率 2 0 %及 0 % (P均 <0 .0 5 )。survivin基因表达与卵巢上皮性癌的临床分期、病理学类型、组织学分级及淋巴结转移无相关性 (P均 >0 .0 5 )。survivin基因表达与bcl 2蛋白表达呈正相关 (P <0 0 1) ,而与bax蛋白表达呈负相关 (P <0 .0 5 )。结论　survivin基因可通过抑制癌细胞凋亡 ,对卵巢上皮性癌的发生和发展起作用 ;survivin基因可能与凋亡相关基因bcl 2、bax ,在卵巢上皮性癌的发展中分别起协同和拮抗作用。     

Evidence for local production of inhibin A and activin A in patients with ovarian endometriosis

OBJECTIVE: To evaluate the expression of inhibin A and activin A in ovarian endometriosis. DESIGN: Uncontrolled cross-sectional study and controlled prospective in vitro study. SETTING: Academic health centers in Siena, Udine, Sassari, and Milan, Italy. PATIENT(S): A group of women (n = 19) who underwent laparoscopic excision of ovarian endometriotic cysts. INTERVENTION(S): Specimens of serum, peritoneal fluid, and cystic fluid, ovarian tissue for immunohistochemistry, and endometriotic cells for primary culture were collected. Cell cultures were also prepared from proliferative endometrium of women without endometriosis. MAIN OUTCOME MEASURES: Dimeric inhibin A and activin A concentrations in biological fluids; immunostaining of alpha and betaA subunits in ovarian endometrioma; alpha and betaA gene expression in cultured endometriotic cells compared with normal endometrium. RESULT(S): Inhibin A and activin A concentrations in the cystic fluid were slightly higher than in peritoneal fluid and significantly higher than in serum (P<.05). Immunoreactive alpha and betaA subunits were strongly expressed both in the epithelial and stromal components of ovarian endometrioma. The relative abundance of betaA mRNA was significantly decreased in endometriotic cells compared with eutopic stromal cells. CONCLUSION(S): The results of the present study provide evidence for a local production and secretion of inhibin A and activin A in ovarian endometriotic cysts.     

Serum inhibin, activin and follistatin in postmenopausal women with epithelial ovarian carcinoma

Objective To investigate the role of serum inhibin A, inhibin pro-αC immunoreactivity, activin A, and follistatin in postmenopausal women with epithelial ovarian cancer.
Design Case-control study.
Sample Serum samples from 27 postmenopausal women with epithelial ovarian cancer and 54 controls from the general population participating in an ovarian cancer screening trial.
Results Women with epithelial ovarian cancer had significantly higher serum levels of pro-αC immunoreactivity (   P = 0.03  ), activin A (   P = 0.004  ) and follistatin (   P = 0.04  ), but not inhibin A (   P = 0.13  ). Using the 90th centile in the control group as the cut off, pro-αC levels were elevated in 41% of women with epithelial ovarian cancer, while inhibin A was elevated in only 15%. Using the 95th centile as the cut off, serum pro-αC was elevated in only 11% of women with epithelial ovarian cancer (3/27), while activin A was elevated in 48% (11/23). Follicle stimulating hormone levels were significantly lower in women with epithelial ovarian cancer (   P = 0.01  ). Although, inhibin-related peptides can modulate follicle stimulating hormone levels, there was no correlation between inhibin A, pro-αC immunoreactivity, activin A or follistatin and follicle stimulating hormone.
Conclusion These data demonstrate that though there is preferential secretion of precursor forms of the α subunit rather than dimeric inhibin A by epithelial ovarian cancer, pro-αC is unlikely to be a useful tumour marker. Activin A is more commonly elevated in postmenopausal women with epithelial ovarian cancer and its role as a tumour marker in the diagnosis and screening of epithelial ovarian cancer warrants further evaluation.     

Inhibin subunits mRNA expression level in human placenta from normal and Down's syndrome pregnancies

In order to study the mechanisms leading to increased inhibin A and activin A in maternal serum with advancing gestation and increased inhibin A in Down's syndrome pregnancy, the mRNA expression level of inhibin and activin subunits was quantitatively studied in human placenta using Northern blot and semiquantitative RT-PCR analysis. The corresponding protein level was also determined by specific ELISAs for inhibin A, inhibin B, activin A and inhibin pro alphaC in placental extracts. Normal placenta (n=27) showed a slight significant increase in alpha and betaA subunit mRNA levels in term pregnancy, with no change of the corresponding protein level. Placenta from Down's syndrome pregnancies (n=6) did not differ from controls in either mRNA expression or corresponding protein levels. In conclusion, there is a dissociation between inhibin and activin subunit mRNA levels and the corresponding protein levels in maternal serum, and Down's syndrome inhibin A increase is not explained by mRNA expression upregulation. In an additional study, ovarian cortex tissue from term pregnancies (n=3) were examined. Only the alpha subunit mRNA was expressed, at a higher level than in the placenta, suggesting that ovary could be a source of inhibin pro alphaC during pregnancy.     

Serum inhibin B correlates with successful ovulation in infertile women

Purpose : To investigate whether inhibin B and activin A serum and follicular fluid levels in infertile women undergoing induction of superovulation correlate with successful ovulation. Methods : Infertile women (n = 16) (30–43 years of age) undergoing induction of superovulation for assisted reproduction were studied. A blood sample was collected before and days 3, 8, and 12 during the induction of superovulation. A follicular fluid sample at the time of ovarian pick up was also collected. Serum and follicular fluid were assayed for inhibin B, activin A, and estradiol. Results : According to the successful follicular development women were divided in two groups: (A) responders (n = 10) and (B) poor responders (n = 6). Women of group A showed mean follicular fluid inhibin B levels higher than in group B (P = 0.001), while no significant difference for activin A levels was found. During induction of superovulation serum activin A levels did not change in both groups of women, while inhibin B and estradiol levels significantly increase only in responder women (P < 0.001). Serum inhibin B and estradiol levels correlated with follicles developed 10 mm (P = 0.000). Conclusions : Serum inhibin B is an effective marker of follicular development in infertile women undergoing induction of superovulation, and may represent a further marker for ovarian follicular capacity.     

Tissue immunoexpression and messenger ribonucleic acid localization of inhibin/activin subunit in human epididymis

OBJECTIVE: To determine the expression of inhibin betaA and betaB subunits and follistatin and the ability of human epididymal epithelium to synthesize these molecules. DESIGN: The main aim of this study was to investigate the expression of inhibin alpha, betaA, and betaB-subunits and follistatin in human epididymis with immunohistochemistry, in situ hybridization, and Western blotting in adult life. SETTING: Academic university hospital. PATIENT(S): Epididymes were obtained from 10 men undergoing routine vasectomy or surgery for benign disease at the Royal Hallamshire Hospital, Sheffield, United Kingdom. MAIN OUTCOME MEASURE(S): Immunoexpression of activin betaA and betaB subunits and follistatin proteins and mRNA in human caput and cauda epididymis. RESULT(S): Positive immunoexpression for activin betaA and betaB subunits and follistatin were detected in different parts of the epididymis epithelium. Western blotting under a reducing condition detected a 28-kd band (possibly corresponding to the activin dimer). In situ hybridization indicated positive mRNA localization signal in both caput and cauda epididymal epithelium. CONCLUSION(S): Activins betaA and betaB subunits, but not inhibin alpha subunit, were detected in epididymal epithelium. These finding suggest that activins might have a role in the processes of sperm maturation and sperm fertilizing capability during transit and storage.     

磷脂酰肌醇3激酶在卵巢上皮性癌组织中的表达及其抑制剂对卵巢上皮性癌细胞生长抑制作用的研究

目的 探讨细胞信号转导信使磷脂酰肌醇3激酶(PI3K)在卵巢上皮性癌(卵巢癌)组织中的表达及其意义;并探讨PI3K抑制剂LY294002联合顺铂对卵巢癌细胞株的生长抑制作用.方法 应用蛋白印迹法和RT-PCR技术检测正常卵巢组织(正常组,20份)、卵巢良性上皮性肿瘤组织(良性组,6份)、卵巢交界性上皮性肿瘤组织(交界性组,6份)和卵巢癌组织(卵巢癌组,39份)中PI3K p85亚单位蛋白和mRNA的表达.将SKOV3细胞分为对照组(只加培养液)、LY294002组(加1、10、30、50、100 μmol/L LY294002)、顺铂组(加0.33、1.25、2.5、5、10 μmol/L顺铂)和联合组(加50 μmol/L LY294002+10 μmol/L顺铂),四甲基偶氮唑蓝还原法测定不同浓度的LY294002及顺铂对SKOV3细胞的生长抑制作用.结果 (1)PI3K p85亚单位蛋白的表达阳性率:正常组和良性组均为0,交界性组为2/6,卵巢癌组为85%(33/39),正常组、良性组、交界性组分别与卵巢癌组比较,差异均有统计学意义(P＜0.01).(2)PI3K p85亚单位mRNA的表达水平:正常组为0.178±0.102,良性组为0.643±0.112,交界性组为0.847±0.058,卵巢癌组为1.689±0.423,正常组、良性组、交界性组分别与卵巢癌组比较,差异均有统计学意义(P＜0.01).卵巢癌组织中,PI3K p85亚单位蛋白表达阳性率及mRNA的表达水平,不同年龄、病理类型间比较,差异均无统计学意义(P＞0.05);而不同病理分化程度、手术病理分期间比较,差异均有统计学意义(P＜0.05).(3)LY294002及顺铂呈剂量依赖性地抑制SKOV3细胞的生长.LY294002组(50 μmol/L)、顺铂组(10 μmol/L)、联合组SKOV3细胞的抑制率分别为(46.0±2.0)%、(44.4±3.2)%、(57.1±4.1)%,联合组SKOV3细胞的抑制率高于LY294002组及顺铂组(P＜0.01).结论 PI3K p85亚单位在卵巢癌组织中呈高表达,与病理分化程度、手术病理分期有关.LY294002与顺铂联合用药对卵巢癌细胞生长的抑制具有协同效应.     

卵巢癌临床和生物学预测因子研究

目的 :研究影响卵巢癌患者预后的临床和生物学因素。方法 :回顾分析卵巢癌患者 88例的临床资料 ,并检测肿瘤组织上皮中血管内皮生长因子 (VEGF)和胸苷磷酸化酶 (TP)的表达及肿瘤间质内微血管密度 (MVD) ,应用Cox比例风险模型评估临床因素包括年龄、临床分期、组织学类型、细胞分化级别、术后残余癌灶及生物学因子 :VEGF、TP、MVD与总生存期 (OS)和无进展生存期 (PFS)之间的相关性。结果 :(1)患者的年龄、临床分期和术后癌灶大小显著影响其生存期的长短 ;(2 )Cox模型未发现VEGF、TP和MVD与OS和PFS之间的相关性 ;(3)低分化 (G3、G4 )肿瘤细胞中VEGF的表达显著高于高分化(G1、G2 )者。结论 :(1)年龄、临床分期和术后残余癌灶是三个独立的临床预测因子 ,表明早期诊断和适宜治疗极为重要 ;对老年患者应密切监护 ;(2 )低分化肿瘤细胞比高分化肿瘤细胞具有更恶的基因型和表现型 ,更易诱导间质内微血管生成 ,促进肿瘤的复发、转移和快速生长 ,提示抗微血管生成治疗肿瘤的可行性     

Effect of activin A on tumor necrosis factor-alpha/intercellular adhesion molecule-1 pathway in endometrial stromal cells

OBJECTIVE[S]: Activin A and inhibin A are growth factors expressed by human endometrium involved in the control of endometrial functions. In the present study we investigated the effects of activin A and inhibin A in modulating the tumor necrosis factor (TNF)-alpha/intercellular adhesion molecule (ICAM)-1 system in cultured human endometrial stromal cells. STUDY DESIGN: Endometrial samples were obtained from 34 reproductive age women undergoing laparoscopy for benign ovarian cysts or infertility. Endometrial stromal cells were cultured and soluble ICAM-1 and TNF-alpha were measured in cell-free supernatants following treatment with or without activin A or inhibin A. Cell surface ICAM-1 was assayed by flow cytometry by staining endometrial cells with specific monoclonal antibodies. RESULTS: Activin A and inhibin A did not influence either the expression of cell surface ICAM-1 or soluble ICAM-1 shedding by cultured endometrial cells. On the other hand, TNF-alpha secretion significantly increased in presence of activin A but not of inhibin A. CONCLUSIONS: Since TNF-alpha modulates several endometrial processes such as menstruation, proliferation, apoptosis, implantation and decidualization, an effect of activin A in the physiological control of endometrium is further supported by the present data.     

应用组织芯片技术分析卵巢癌组织中Bit1基因的表达

目的:研究B it1基因在正常卵巢组织和不同病理分级的卵巢癌组织中的表达。方法:应用组织芯片技术,通过免疫组织化学方法检测82例卵巢癌标本和78例正常卵巢组织标本中B it1基因的表达。结果:B it1基因在卵巢癌和正常卵巢组织中的弱阳性及阳性表达率分别为100%和33.3%,差异有统计学意义(P<0.01);B it1基因在不同病理分级的卵巢癌组织中的阳性表达率分别为:Ⅰ级,53.1%;Ⅱ级,28.1%;Ⅲ级,7.1%。统计学分析表明,B it1基因在Ⅰ级与Ⅱ级或Ⅲ级的卵巢癌组织中的表达存在显著的统计学差异(P=0.042,0.003),而在Ⅱ级和Ⅲ级中的表达则无统计学差异(P=0.143)。结论:B it1基因在正常卵巢组织中的表达明显低于卵巢癌组织,而且卵巢癌组织中B it1基因的表达与病理分级密切相关。