Decreased expression of BTG3 was linked to carcinogenesis, aggressiveness, and prognosis of ovarian carcinoma

B-cell translocation gene 3 (BTG3) is a member of the BTG family which inhibits cell proliferation, metastasis, and angiogenesis, and also regulates cell-cycle progression and differentiation in a variety of cell types. However, there is no study to analyze BTG3 expression in epithelial ovarian carcinoma (EOC). Here, we investigated the expression of BTG3 in EOC carcinogenesis and subsequent progression. BTG3 mRNA expression was detected by real-time RT–PCR in ovarian benign and malignant tumors. The expression of BTG3 protein was examined by immunohistochemistry on tissue microarrays containing ovarian normal tissue, benign and borderline epithelial ovarian tumors, and EOCs. Relationships of BTG3 with both EOC clinicopathology and prognosis were analyzed statistically. The expression of BTG3 protein was also evaluated in ovarian normal tissue, benign tumors, and EOCs by western blot. The BTG3 mRNA expression level was higher in ovarian normal tissue and benign tumors than that in borderline, primary, and metastatic carcinoma (p?<?0.05), and was negatively correlated with dedifferentiation and FIGO staging of EOC (p?<?0.05). Using western blot, BTG3 protein was found lower in EOCs compared to the normal and benign tumors (p?<?0.05), and poorly differentiated EOCs showed lower BTG3 expression than well-differentiated and moderately differentiated EOCs (p?<?0.05). Immunohistochemically, BTG3 protein expression was statistically lower in EOCs than normal tissue and benign tumors (p?<?0.05). EOC patients with low BTG3 protein expression showed a higher incidence of metastasis (p?=?0.020), poor differentiation (p?=?0.030), and shorter disease-free time and overall survival time (p?<?0.05). By using Cox’s proportional hazard model, BTG3 protein expression and FIGO staging were independent prognostic factors for both disease-free time and overall survival time of EOCs (p?<?0.05). It was suggested that down-regulated BTG3 expression might play roles in the pathogenesis and aggressiveness of EOC. BTG3 protein expression may be considered as a good marker to indicate the favorable prognosis of EOCs.     

Beclin 1 expression is an independent prognostic factor for gastric carcinomas

Beclin 1, an important autophagy-related protein in human cells, is involved in autophagy, differentiation, anti-apoptosis, and cancer progression, which is increased during periods of cell stress and extinguished during the cell cycle. In order to clarify the role of Beclin 1 in gastric carcinogenesis and subsequent progression, its expression was examined by immunohistochemistry and in situ hybridization (ISH) on tissue microarrays containing gastric carcinomas, adjacent non-neoplastic mucosa, and metastatic lymph node. Gastric carcinoma tissue and cell lines were studied for Beclin 1 expression by Western blot or RT-PCR, respectively. The results demonstrated that Beclin 1 was distinctively expressed in GES-1, AGS, BGC-823, GT-3 TKB, HGC-27, KATO-III, MGC-803, MKN28, MKN45, SCH, SGC-7901, or STKM-2 at both mRNA and protein levels. However, Beclin 1 mRNA was highly expressed in gastric carcinoma than matched mucosa by real-time PCR and ISH (P?<?0.05). Beclin 1 expression was negatively related to distant metastasis and poor prognosis of gastric carcinoma (P?<?0.05). Beclin 1 was highly expressed in male than female patients with gastric carcinoma (P?<?0.05). The 65-year-elder patients with gastric carcinoma had higher Beclin 1 expression than the younger ones (P?<?0.05). The diffuse-type carcinomas showed less Beclin 1 expression than intestinal- and mixed-type ones (P?<?0.05). In intestinal-type gastric carcinoma, Beclin 1 expression was inversely associated with venous invasion, lymph node metastasis, and tumor–node–metastasis (TNM) staging (P?<?0.05). Kaplan–Meier analysis indicated that Beclin 1 expression was positively linked to favorable prognosis of the patients with overall and intestinal-type carcinoma (P?<?0.05). Cox’s proportional hazard model indicated that venous invasion, lymph node metastasis, distant metastasis, TNM staging, and Beclin 1 expression were independent prognostic factors for gastric carcinomas (P?<?0.05). It was suggested that aberrant Beclin 1 expression is closely linked to pathogenesis, metastasis, and differentiation of gastric carcinoma. Beclin 1 expression might be employed to indicate the favorable prognosis of gastric carcinomas as an independent factor.     

Relationship among COX-2 protein expression,PGs levels and biologic behavior in ovarian carcinoma tissues

Recent epidemiological studies shows thatlong-term use of aspirin or other NSAIDs (non-steroidanti-inflammatory drugs, NSAIDs) reduces the risk ofcolon cancer development by 40% — 60%[1,2].Although the exact mechanisms of NSAIDs on cancerprevention have not been clarified, one of them maybe via the inhibition of COX-2 enzyme. In the presentstudy, we investigated the COX-2 protein,prostaglandin (PG)E2, 6-keto-PGF1α and thromboxane(TX)B2 by Western blot analysis and radio-immunoass…     

自噬基因Beclin1与上皮性卵巢癌发生、发展的相关性研究

背景与目的:有研究表明自噬的抑制与肿瘤的发生有关,沉默自噬基因Beclin1可导致多种恶性肿瘤的发生.本研究探讨Beclin1基因在上皮性卵巢癌发生、发展中的作用,并分析其过表达对人卵巢癌细胞株SKOV3体外生长的影响.方法:用免疫组化检测25例正常卵巢组织、25例良性上皮性卵巢肿瘤、19例交界性上皮性卵巢肿瘤及69例上皮性卵巢癌组织的Beclin1表达;构建真核表达载体pcDNA3.1/Beclin1,脂质体法分别将质粒pcDNA3.1/Beclin1、pcDNA3.1转染人卵巢癌细胞株SKOV3,用MTT法分析外源性Beclin1过表达对SKOV3增殖的影响,并用流式细胞仪检测凋亡情况.结果:正常卵巢组织和良性卵巢肿瘤组织中Beclin1表达的积分光密度(integrated optical density,IOD)值均较高,两者之间的差异无显著性(P＞0.05);交界性卵巢肿瘤组织中Beclin1的表达降低,而在上皮性卵巢癌中Beclin1表达的IOD值最低,与正常卵巢组织比较差异有显著性(P＜0.05).ocDNA3.1/Beclin1转染SKOV3细胞后细胞生长抑制率为(68.75±5.10)%,而pcDNA3.1转染组为(10.91±4.20)%,两者之间差异有显著性(P＜0.05).pcDNA3.1/Beclin1转染后72 h SKOV3细胞的凋亡率为19.07%,高于pcDNA3.1转染组和未转染组,差异有显著性(P＜0.05).结论:Beclin1在上皮性卵巢癌中的表达下调,可能与上皮性卵巢癌的发生、发展有关;自噬基因Beclin1的过表达可抑制人卵巢癌细胞SKOV3的增殖,并诱导其凋亡.     

Le^y抗原在卵巢上皮性肿瘤中的表达及意义

目的：探讨卵巢癌组织Le^y抗原的表达及其临床意义。方法：采用免疫组织化学SP法检测恶性、交界性、良性卵巢上皮肿瘤及正常卵巢组织中Le^y抗原的表达，并分析其与卵巢癌生物学特性之间的关系。结果：Le^y抗原在恶性卵巢上皮性癌中的阳性表达率为75．47％（40／53），明显高于交界性卵巢上皮性肿瘤（47．06％）及良性卵巢上皮性肿瘤（42．86％）（P均〈0．05）。正常卵巢组织中未检出Le^y抗原的表达。晚期卵巢上皮性癌的Le^y抗原的阳性表达率为84．21％，明显高于早期卵巢上皮性癌（53．33％），（P〈0.05）。结论：Le^y抗原与卵巢上皮性癌的发生、发展相关。Le^y抗原的表达可作为反映卵巢癌恶性潜能的一项新的指标。     

Expression and correlation of Lewis y antigen and TGF-β1 in ovarian epithelial carcinoma

Lewis y is a difucosylated oligosaccharide carried by glycoconjugates on the cell surface. Elevation of Lewis y is frequently observed in epithelial-derived cancers. This study aimed to detect the expression and clinical significance of the Lewis y antigen and TGF-β1 (transforming growth factor β1) in ovarian epithelial tumors, and to evaluate the correlation between them. Immunohistochemical staining was used to detect the expression of Lewis y antigen and TGF-β1 in 60 cases of ovarian epithelial malignant tumors, 20 cases of borderline ovary tumors, 20 cases of benign ovary tumors and 10 cases of normal ovarian tissues. An immunofluorescence double labeling method was also used to detect the correlation between Lewis y antigen and TGF-β1. The positive rates of Lewis y antigen in ovarian epithelial cancer tissues was 88.33%, significantly higher compared to those of borderline ovarian tumors (60.00%) (P<0.05), benign ovarian tumors (35.00%) (P<0.01) and normal ovarian tissues (0%) (P<0.01). Its expression was not associated with clinical parameters; the positive rates of TGF-β1 in ovarian epithelial cancers were 78.33%, significantly higher compared to those of benign ovarian tumors (65.00%) (P<0.05) and normal ovarian tissues (40.00%) (P<0.05); the positive rates of the TGF-β1 and Lewis y were not associated with metastasis of lymph nodes and histological types, differentiation degree and clinical stage (P>0.05). Expression of Lewis y antigen and TGF-β1 was significantly positively associated with epithelial carcinoma. Close correlation between Lewis y, TGF-β1 and ovarian cancer was observed. Altered expression of Lewis y antigen may cause changes in TGF-β1 expression. Lewis y can increase the growth of ovarian cancer cells and the invasion ability by promoting TGF-β1 abnormal expression and by promoting angiogenesis and a change in its signal transduction pathway. This study provides theoretical evidence for the development of ovarian cancer biological treatments.     

Alteration of BRCA-1 tumor suppressor gene expression in serous and mucinous ovarian neoplasms in the benign-borderline-malignant pathway

Alteration of expression of the tumor suppressor gene BRCA-1 has been widely studied in breast and ovarian carcinoma. However, pattern of this alteration in the benign-borderline-carcinoma sequence in serous and mucinous ovarian neoplasms have not yet fully described. Tissue sections from 214 formalin-fixed paraffin-embedded ovarian specimens were stained immunohistochemically with BRCA-1 antibody. Specimens were 10 normal ovarian surface epithelium, 10 fallopian tube epithelium, 70 benign adenoma (50 serous and 20 mucinous), 28 borderline (13 serous and 15 mucinous), 78 carcinoma (58 serous and 20 mucinous), and 18 metastatic deposit (13 serous and 5 mucinous). Expression was evaluated into 0, +1, +2, and +3. Score +3 staining similar to normal tissues was considered normal and other scores were considered altered expression. Strong expression was seen in all normal epithelium specimens. Altered expression was seen in 34 serous neoplasms; 17 of 50 (34%) of benign cystadenomas, 6 of 13 (46%) of borderline tumors, 43 of 58 (74%) of primary carcinoma, and in 8 of 13 (62%) of metastatic carcinoma. This alteration was significantly associated with higher histopathologic grade (P = 0.049), presence of necrosis (P = 0.0001), and higher proliferation rate (P = 0.001). In mucinous neoplasms; altered BRCA-1 was detected in 25 specimens; 7 of 20 (41%) of benign cystadenomas, 5 of 15 (33%) of borderline neoplasms, 9 of 20 (45%) of primary carcinoma, and 4 of 5 (80%) of the metastatic deposits. This alteration was not associated with any of the clinicopathologic tumor characteristics. In conclusion, alteration of BRCA-1 expression is more frequent in serous than in mucinous carcinomas and is associated with tumors of higher grades and high proliferation rate.     

Expression and Significance of RKIP and E-cadherin in Lung Squamous Cell Carcinoma

The purpose of this study was to investigate the expression of Raf kinase inhibitor protein (RKIP) and epithelial cadherin (E-cadherin) in lung squamous cell carcinoma tissue and its correlation with the clinical pathology of lung squamous cell carcinoma. RKIP and E-cadherin mRNA (by RT-PCR) and protein (by western blotting) levels were monitored in carcinoma tissues and surrounding normal tissues from 86 lung squamous cell carcinoma cases, and their positive rates were calculated. The rates of positive RKIP and E-cadherin mRNA expression were significantly lower in lung squamous cell carcinoma than in the surrounding normal tissues (P?<?0.05). The positive expression rates were significantly lower in those with lymph node metastasis than in those without (P?<?0.05). The lower the degree of tumor differentiation, the lower the E-cadherin mRNA positive expression rate (P?<?0.05). The rates of positive RKIP and E-cadherin mRNA expression were significantly lower in patients at advanced (III, IV) stages than in patients at early (I, II) stages (p?<?0.05); this rate, however, was independent of gender, age, and tumor size (P?>?0.05). The protein levels of RKIP and E-cadherin were significantly lower in lung squamous cell carcinoma than in the surrounding normal tissues (P?<?0.05). The levels were significantly lower in patients with lymph node metastasis than in those without it (P?<?0.05). The lower the degree of tumor differentiation, the lower the protein level of E-cadherin (P?<?0.05). Both RKIP and E-cadherin are tumor suppressors, their low expression levels may be associated with initiation, invasion and/or metastasis, as well as with the inhibition of lung squamous cell carcinoma differentiation.     

微管相关蛋白LC3和自噬基因Beclin1在上皮性卵巢癌中的表达及其意义

背景与目的:有研究表明自噬活性的改变与肿瘤的发生、发展有关。诱导自噬性细胞死亡已经成为杀死肿瘤细胞的新策略。本研究检测微管相关蛋白LC3和自噬基因Beclin1在不同卵巢肿瘤组织中的表达情况,探讨其与上皮性卵巢癌发生、发展的相关性及意义。方法:用免疫组化法检测25例良性卵巢肿瘤、25例交界性卵巢肿瘤及75例上皮性卵巢癌组织的LC3和Beclin1表达,并结合临床病理因素进行分析。结果:良性肿瘤组LC3和Beclin1的阳性率(100%、100%)和交界性卵巢肿瘤组LC3和Beclin1的阳性率(96%、84%)都明显高于上皮性卵巢癌组(57%、57%),且差异具有统计学意义(P均<0.001)。LC3在上皮性卵巢癌中的表达与FIGO分期和肿瘤分化程度相关(P=0.017;0.001)。Beclin1表达与上皮性卵巢癌患者FIGO分期相关(P=0.04)。LC3和Beclin1在卵巢上皮癌中的表达无相关性(P=0.875)。结论:LC3和Beclin1在上皮性卵巢癌中的表达下调,自噬活性的改变可能与上皮性卵巢癌的发生、发展相关。     

RhoC is a major target of microRNA-93-5P in epithelial ovarian carcinoma tumorigenesis and progression

Background

An increasing amount of evidence has revealed that microRNAs regulate various biological processes, including cell differentiation, cell proliferation, apoptosis, drug resistance, and fat metabolism. Studies have shown that miR-93’s targetome in cancer has not been fully defined. Moreover, the role of miR-93 in epithelial ovarian carcinoma (EOC) remains largely unknown.

Methods

MIR-93 mRNA expression in normal ovarian tissue, benign tumors, borderline tumors, primary ovarian carcinomas, and metastatic omentum was quantified. The ovarian carcinoma cell lines OVCAR3, SKOV3/DDP, and HO8910-PM were transfected with miR-93-5P, after which cell phenotype and expression of relevant molecules were assayed. Dual-luciferase reporter assay and a xenograft mouse model were used to examine miR-93 and its target gene RHOC (Ras homolog gene family member C).

Results

MIR-93 mRNA expression was significantly lower in ovarian carcinomas and borderline tumors than in normal ovarian tissues (p < 0.05), and was lower in metastatic omentum than in relative primary ovarian carcinomas (p < 0.05). MIR-93 mRNA expression was also negatively associated with differentiation (well vs. poor and moderate) and International Federation of Gynecology and Obstetrics staging (FIGO stage I/II vs. stage III/IV) in ovarian carcinoma (p < 0.05), besides, miR-93 was higher expressed in mucinous adenocarcinoma than the other types (p < 0.05). MiR-93-5P overexpression reduced proliferation (p < 0.05); promoted G₁ or S arrest and apoptosis (p < 0.05); suppressed migration and invasion (p < 0.05); and reduced RhoC, P70S6 kinase, Bcl-xL, matrix metalloproteinase 9 (MMP9) mRNA or protein expression; conversely, it induced P53 and cleaved PARP expression (p < 0.05). Dual-luciferase reporter assay indicated that miR-93 directly targeted RhoC by binding its 3′ untranslated region. MiR-93-5P transfection also suppressed tumor development and RhoC expression (determined by immunohistochemistry) in vivo in the xenograft mouse model (p < 0.05).

Conclusions

This is the first demonstration that miR-93-5P may inhibit EOC tumorigenesis and progression by targeting RhoC. These findings indicate that miR-93-5P is a potential suppressor of ovarian cellular proliferation. The involvement of miR-93-5P–mediated RhoC downregulation in inhibiting EOC aggressiveness may provide extended insight into the molecular mechanisms underlying cancer aggressiveness.     

卵巢癌中EIF-5A2 基因表达与临床意义*

目的:探讨真核翻译起始因子5A2（EIF-5A2）基因在卵巢上皮性肿瘤中的表达及其临床意义。方法:运用免疫组化和荧光原位杂交方法,结合组织芯片技术,检测EIF-5A2 基因在50例卵巢腺瘤、50例卵巢交界性肿瘤和150 例卵巢癌中的表达,分析其与肿瘤临床病理学参数之间的相关性。结果:免疫组化检测结果,分别有6.4% 的卵巢良性腺瘤、28.3% 的交界性肿瘤和56.6% 的卵巢癌出现EIF-5A2 蛋白的过度表达。在卵巢癌中,EIF-5A2 蛋白表达与肿瘤的组织学Silverberg 氏分级和临床FIGO分期均有显著的相关性（P<0.05）,其中70.0% 的高级别（G3 级）的卵巢癌出现EIF-5A2 蛋白的过度表达,明显高于G1/G2 级的卵巢癌（49.5%）;在FIGO分期中,65.6% 的临床晚期（Ⅲ/Ⅳ期）卵巢癌呈EIF-5A2 蛋白过度表达,明显高于Ⅰ/Ⅱ期的肿瘤（38.3%）。 另外,EIF-5A2 蛋白过度表达与卵巢癌细胞增殖（Ki-67的表达水平）显著正相关（P<0.01）,大多数（72.8%）EIF-5A2 蛋白过度表达的卵巢癌中出现Ki-67蛋白高表达,而多数（66.1%）EIF-5A2 蛋白正常表达的卵巢癌则呈Ki-67蛋白低表达。荧光原位杂交结果显示,只有13.8% 的卵巢癌出现EIF-5A2 基因扩增;卵巢交界性肿瘤和良性腺瘤中均未观察到EIF-5A2 基因的扩增。结论:EIF-5A2 蛋白过度表达可能通过促进肿瘤细胞增殖的效应,在卵巢上皮性肿瘤的发生发展中起重要作用,而且与卵巢癌的恶性组织学表型和浸润转移密切相关。      

间皮素mRNA及蛋白在卵巢癌中的表达及分析

目的 研究间皮素(MESO)在卵巢癌中的表达及意义.方法 用逆转录聚合酶链反应(RT-PCR)技术和免疫组化方法分别检测卵巢肿瘤和正常卵巢组织中MESO mRNA及其蛋白水平.结果MESO mRNA和蛋白在上皮性卵巢癌(1.4005 ±0.4646,2.7857±2.2712)和交界性卵巢肿瘤(1.0650 ±0.3100,2.9167 ±2.391)中的表达水平高于良性卵巢肿瘤(0.6463±0.2419,1.2500 ±1.6125)和正常卵巢组织(0.6439 ±0.2729,0.9167 ±1.2401),差异有统计学意义(P＜0.05);MESOmRNA和蛋白在浆液性卵巢癌(1.5255 ±0.4151,3.3036 ±2.6141)和子宫内膜样癌(1.5250 ±0.5419,3.0000 ±2.3094)中的表达水平高于黏液样癌(1.0675±0.3149,1.0556 ±1.9242),差异有统计学意义(P＜0.05);临床Ⅲ、Ⅳ期MESO表达水平(1.5100 ±0.4142,3.6087 ±3.3959)高于Ⅰ、Ⅱ期(1.1190 ±0.4909,1.7895 ±2.6320),差异有统计学意义(P＜0.05).MESO表达水平与病理分级有关(P＜0.05),而与患者年龄和血清CA125水平无关(P＞0.05).结论 MESO mRNA及蛋白在卵巢癌和交界性肿瘤组表达增高,MESO可能参与卵巢癌的黏附转移.     

GLUT-1和DNA-PKcs在卵巢浆液性肿瘤组织中的表达及其意义

背景与目的:已知肿瘤细胞生长所需能量是通过葡萄糖转运体蛋白1(glucose transporter protein 1,GLUT-1)完成的葡萄糖代谢来提供的.另外,参与基因损伤修复的催化亚单位--DNA蛋白激酶(DNA-dependent protein kinase catalytic subunit,DNA-PKcs)在肿瘤形成中也起着非常重要的作用.本研究旨在探讨GLUT-1和DNA-PKcs在卵巢浆液性肿瘤组织中的表达及其与肿瘤生物学行为的关系和意义.方法:免疫组化方法检测80例卵巢浆液性肿瘤组织中GLUT-1、DNA-PKcs的表达,分析其异常表达与临床病理参数之间的相关性.以正常卵巢组织20例为对照.结果:正常卵巢组织GLUT-1表达全阴性,DNA-PKcs表达全阳性.GLUT-1在良性、交界性、恶性卵巢浆液性肿瘤中的表达呈增高的趋势,与卵巢浆液性肿瘤的发生发展呈正相关(rs=0.943,P＜0.01);在恶性肿瘤中的阳性率(100%)明显高于交界性(55%).DNA-PKcs在良性、交界性和恶性卵巢浆液性肿瘤中的阳性率分别为95%、90%、60%,差异有统计学意义(P＜0.01).GLUT-1与DNA-PKcs的表达呈负相关(rs=-0.270,P＜0.01).GLUT-1表达与临床分期、腹腔种植、腹水、淋巴结转移均相关(P＜0.05);DNA-PKcs仅与临床分期和淋巴结转移相关(P＜0.05),与腹水、腹腔种植无关(P＞0.05).结论:GLUT-1的异常表达和DNA-PKcs的丢失与卵巢浆液性肿瘤恶变相关.     

P16 P15及VEGF蛋白在原发性卵巢癌中的表达及临床意义

  目的   探讨P16、P15及血管内皮生长因子(VEGF)在原发性卵巢癌中表达情况及其与临床病理特征的关系。   方法   采用免疫组织化学S-P法对170例原发性卵巢癌、60例交界性肿瘤及60例良性肿瘤组织进行P16、P15和VEGF蛋白检测。   结果   P16在卵巢癌的表达率为40.0%(68/170), 明显低于良性肿瘤组65.0%(39/60)和交界性肿瘤组56.7%(34/60)(P < 0.05);P15在卵巢癌组的阳性表达率为45.3%(77/170), 显著低于良性肿瘤组68.3%、交界性肿瘤组61.7%(37/60)(P < 0.05);VEGF在卵巢癌组的阳性表达率为71.2%(14/170), 明显高于良性肿瘤组45.0%(27/60)和交界性肿瘤组53.3%(32/60)(P < 0.05)。在卵巢癌组中, P16和P15表达呈正相关(r=0.294, P < 0.01), VEGF与P16和P15的表达呈负相关(r值分别为-0.461和-0.251, P < 0.01)。三者表达强度与肿瘤分化程度、临床分期、淋巴结转移有显著相关性, 肿瘤分化越低、临床分期越高、淋巴结转移者P16、P15阳性表达率越低(P < 0.05), VEGF阳性表达率越高(P < 0.05)。P16和P15的表达与有无脉管瘤栓无关, VEGF在有脉管瘤栓组的表达高于无脉管瘤栓组。   结论   P16和P15的低表达与VEGF蛋白高表达在卵巢癌的发展过程中可能起协同作用, 共同促进卵巢癌的恶性发展进程。      

Expression of Vascular Endothelial Growth Factor-C and Vascular Endothelial Growth Factor Receptor-3 in Ovarian Epithelial Tumors

Objective： To explore the role of vascular endothelial growth factor-C （VEGF-C） in the process of angiogenesis, lymphangiogenesis and lymphatic metastasis in epithelial ovarian tumors. Methods： In situ hybridization and immunohistochemical staining for VEGF-C were performed in 30 epithelial ovarian carcinomas, 9 borderline tumors and 26 benign tumors. Endothelial cells were immunostained with anti-VEGFR-3 pAb and anti-CD31 mAb, and VEGFR-3 positive vessels and microvessel density （MVD） were assessed by image analysis. Results： VEGF-C mRNA and protein expression were detected in cytoplasm of carcinoma cells. VEGF-C mRNA and protein expression in ovarian epithelial carcinomas were significantly higher than those in borderline tumors and benign tumors （P〈0.05 or P〈0.01）. In ovarian epithelial carcinomas, VEGF-C protein expression, VEGFR-3 positive vessels and MVD were significantly higher in the cases of clinical stage Ⅲ-Ⅳ and with lymph node metastasis than those of clinical stage Ⅰ-Ⅱ and without lymph node metastasis respectively （P〈0.05 or P〈0.01）. VEGFR-3 positive vessels and MVD were significantly higher in VEGF-C protein positive tumors than negative tumors （P〈0.05）. VEGFR-3 positive vessels was significantly correlated with MVD（P〈0.01）. Conclusion： VEGF-C might play a role in lymphatic metastasis via lymphangiogenesis and angiogenesis in epithelial ovarian tumors, and VBEGF-C could be used as a biologic marker of metastasis in ovarian epithelial tumors.     

FISH技术检测卵巢上皮性肿瘤组织CCND1表达及临床意义

目的:探讨荧光原位杂交技术(FISH)检测卵巢上皮性肿瘤中CCND1基因的表达及其临床意义.方法:应用FISH技术检测45例卵巢正常组织和113例卵巢上皮性肿瘤中CCND1基因的表达.结果:CCND1基因在正常卵巢组织、卵巢良性肿瘤、交界性肿瘤及恶性肿瘤中的扩增表达率分别为11.1％、33.3％、43.5％和66.1％,恶性组的表达扩增率明显高于其他组,差异有统计学意义,P＜0.01;卵巢上皮性癌组织中CCND1基因的表达扩增率与病理分级、临床病理分期及癌组织转移明显相关,差异有统计学意义(P＜0.05),但与年龄、病理学类型无相关性,P＞0.05.结论:CCND1基因的扩增在卵巢肿瘤的发生发展中起重要作用,且与卵巢癌的病理分级、临床分期及癌组织的转移有关,可用以预测肿瘤患者的预后.