IMMUNOHISTOCHEMICAL LOCALIZATION OF EPIDERMAL GROWTH FACTOR RECEPTOR AND C-erbB-2 ONCOGENE PRODUCT IN DEVELOPING HUMAN PLACENTA

Cytologic locailzation of epidermai growth factor receptor (EGF-R) and C-erbB2oncogene product in normal developing placenta ovas studied by avidin/biotin immunoperoxidase techniques.Both proteins were predominantly expressed in the villous syncytiotrophoblasts but not in the cytotrophoblasts.The immunoreactive intensity for EGF-R decreased with the development of pregnancy.Concerning the intermediate trophoblasts in cell islands and cell columns,both proteins were more easily detected in the cells distal to the villous stroma than in the juxtastromal cells.These findings suggest that EGF-R and C-erbB-2 may play a significant role in the induction and regulation of differentiated trophoblast function

Study of differential polymerase chain reaction of C-erbB-2 oncogene amplification in gastric cancer

AIM To study the significance of C-erbB-2 oncogene amplification in gastric cancer.METHODS C-erbB-2 oncogene amplification was examined by using differential polymerase chain reaction (dPCR) in surgical and endoscopic specimens of 83 cases of gastric cancer and 101 metastatic lymph nodes.RESULTS C-erbB-2 amplification was found in 28.9% (24/ 83) surgical specimens and 20.5% (17/ 83) endoscopic ones of gastric cancer patients. The amplification was significant in both types of specimens of advanced cancer cases (P＜0.05) and surgical specimens with lymph node metastasis (P＜0.01). The incidence of C-erbB-2 amplification in lymph nodes with metastasis was higher than in primary sites (surgical specimens, P＜0.05). The patients with amplification tumors had poorer 5-year survival rates than those with unamplification ones in the early cancers and well to moderately differentiated adenocarcinomas (P＜0.05). The same surgical samples were tested again by Southern blot hybridization to ascertain C-erbB-2 amplification, and the positive rate of C-erbB-2 amplification (15.7%) was lower than that of dPCR (28.9%, P＜0.05).CONCLUSION Examining C-erbB-2 amplification by dPCR is a quick, simple, reliable and independent method, and is helpful in predicting prognosis and metastatic potential of gastric cancer.

Expression of c-erbB-2 oncogene protein, epidermal growth factor receptor, and TGF-β1 in human pancreatic ductal adenocarcinoma

Objective: To detect the relations of c-erbB-2 onco-gene protein, epidermal growth factor receptor (EG-FR) and transforming growth factor-β1 (TGF-β1)to the progression or metastasis of pancreatic carci-noma.Methods: Using streptavidinbiotin complex (SABC)method, c-erbB-2 oncongene protein, we examinedimmunohistochemically EGFR and TGF-β1 expres-sions in wax-tissue sections from 10 individuals withnormal pancreas (NP), 13 patients with chronic pan-creatitis (CP) and 36 patients with pancreatic ductaladenocarcinoma (PC).Results: The positive expression rates of c-cerbB-2oncogene protein, EGFR and TGF-β1 in the NP, CPand PC groups were 0, 0, 10%; 7.7%, 7.7%,7.7%; and 41.7%, 50.0%, 44.4%, respectively.The positive expression rates of the three specific pro-teins increased more significantly in the PC groupthan in the NP and CP groups (P【0.05). The indi-vidual expression of c-erbB-2, EGFR and TGF-β1was not related to the age and sex of the patients aswell as the site, size and histopathological grade oftumors (P】0.05), but to the clinical stage of tumors(P【0.01). The coexpression rate of the three pro-teins was 27.8 % (10/36). This coexpression in thePC group was correlated with the histopathologicalgrades and clinical stages of tumors (P【0.01).Conclusion: Detection of c-erbB-2 oncogene protein,EGFR, and TGF-β1 expressions in pancreatic tissueis helpful to judge the malignancy, progression, andmetastasis of PC.

Dual fluorescence in situ hybridization in detection of HER-2 oncogene amplification in primary hepatocellular carcinoma

BACKGROUND: Molecular cytogenetics of oncogene HER-2 amplification in primary hepatocellular carcinoma (HCC) is still unknown. The aim of this study was to in vestigate the frequency of HER-2 oncogene amplification in primary HCC and its relations to clinicopathological pa rameters and prognosis. METHODS: Forty-two surgical samples from patients with primary HCC were detected for their HER-2 oncogene am plification. The number of chromosome 17 and their ratio were tested by dual fluorescence in situ hybridization (FISH) technique, and then the correlations between HER-2 amplification, clinicopathological characteristics and prog nosis were analyzed statistically. RESULTS: HER-2 oncogene amplification was detected in 9 (21.4%) of the 42 primary HCCs, including 4 patient with high copy (HC) (9.5%) and 5 patients with low copy (LC) (11.9%). HER-2 amplification was associated signifi cantly with tumor size and postoperative survival time o HCC patients (P<0.05), and the presence of HER-2 gene amplification was correlated with postoperative relapse (P— 0.257), but not related to sex, age, AFP level, HBV infec tion, histopathological grading and clinical staging of HCC patients (P>0.05). The HER-2 oncogene copy was exa mined in 31 (73.8%) of the 42 primary HCCs, consisting of 9 patients with HER-2 amplification (21.4%) and 22 pa tients with aneuploidy (52.4%). No significant relation were observed between the HER-2 oncogene copy, patien sex, tumor size, histopathological grading, clinical stag ing, postoperative relapse and survival time (P >0.05); bu the HER-2 oncogene copy was correlated significantly to age, AFP level and HBV infection (P <0.05). CONCLUSIONS: There are a lower frequency of HER-2 oncogene amplification and a higher frequency of chromo- some 17 aneuploidy in primary HCC. HER-2 oncogene amplification may be involved in the development and pro- gression of large HCC in some patients, and seems to be a valuably independent prognostic factor predicting the re- currence and poor survival in patients with large HCC.

Expression of bcl-2 oncogene in gastric precancerous lesions and its correlation with syndromes in traditional Chinese medicine

AIM: To observe the protein and mRNA expression of bcl-2 oncogene in gastric precancerous lesions (GPL) and to analyze its correlation with syndromes in traditional Chinese medicine (TCM). METHODS: Sixty-seven patients with GPL confirmed by gastroscopy and pathology were studied,including 39 cases of moderate gastric mucosal dysplasia,19 cases of severe gastric mucosa dysplasia, 9 cases of incomplete colon metaplasia. In syndrome differentiation of TCM,17 cases belonged to the syndrome of qi and yin deficiency of the spleen and stomach complicated by qi stagnation, 21 cases belonged to the syndrome of qi and yin deficiency of the spleen and stomach complicated by stomach heat, 29 cases belonged to the syndrome of qi and yin deficiency of the spleen and stomach complicated by blood stasis. Protein and mRNA expression of bcl-2 oncogene were detected by labeled streptavidin biotin (LSAB) immunohist-ochemistry and in situ hybridization respectively. RESULTS: Abnormal expression of protein and mRNA on bcl-2 oncogene was found in GPL,which increased gradually with the course of lesions. In moderate and severe gastric mucosal dysplasia and incomplete colon metaplasia,there was no difference in the expression of bcl-2 oncogene (P>0.05).In different accompanying syndromes, the expression of protein and mRNA on bcl-2 oncogene increased gradually in the following order: deficiency of both qi and yin of the spleen and stomach accompanying qi stagnation→stomach heat→blood stasis. In GPL, compared with accompanying blood stasis, there was an obvious difference in the expression of bcl-2 oncogene between the syndrome of qi and yin deficiency of the spleen and stomach and accompanying stomach heat, so did accompanying qi stagnation (the level of protein: X2=8.45, P<0.05;the level of mRNA: X2=7.35, P<0.05). CONCLUSION: Apoptosis-associated bcl-2 oncogene is abnormally expressed in GPL,which correlates with different accompanying syndromes in TCM.

Identification of APEX2 as an oncogene in liver cancer

BACKGROUND DNA damage is one of the critical contributors to the occurrence and development of some cancers.APEX1 and APEX2 are the most important molecules in the DNA damage,and APEX1 has been identified as a diagnostic and prognostic biomarker in liver hepatocellular carcinoma(LIHC).However,the expression of APEX2 and its functional mechanisms in LIHC are still unclear.AIM To examine the expression of APEX2 and the potential mechanism network in LIHC.METHODS We conducted a pan-cancer analysis of the expression of APEX1 and APEX2 using the interactive TIMER tool.GEO datasets,including GSE14520,GSE22058,and GSE64041,were used to compare the APEX2 expression level in tumor tissues and adjacent non-tumor tissues.Then,we calculated the 5-year survival rate according to the web-based Kaplan-Meier analysis.We included the TCGA liver cancer database in GSEA analysis based on the high and low APEX2 expression,showing the potential mechanisms of APEX2 in LIHC.After that,we conducted Pearson correlation analysis using GEPIA2.Next,we performed quantitative polymerase chain reaction(qPCR)assay to examine the APEX2 levels in normal liver cell line LO2 and several liver cancer cell lines,including HepG2,Huh7,SMMC7721,and HCCLM3.APEX2 in HCCLM3 cells was knocked down using small interfering RNA.The role of APEX2 in cell viability was confirmed using CCK-8.Dualluciferase reporter assay was performed to examine the promoter activity of CCNB1 and MYC.RESULTS APEX1 and APEX2 are both highly expressed in the tumor tissues of BLCA,BRCA,CHOL,COAD,ESCA,HNSC,LIHC,LUAD,LUSC,READ,and STAD.APEX2 overexpression in LIHC was validated using GSE14520,GSE22058,and GSE64041 datasets.The survival analysis showed that LIHC patients with high expression of APEX2 had a lower overall survival rate,even in the AJCC T1 patients.High level of APEX2 could indicate a lower overall survival rate in patients with or without viral hepatitis.The GSEA analysis identified that kinetochore and spindle microtubules are the two main cellular components of APEX2 in GO Ontology.APEX2 was also positively associated with molecular function regulation of chromosome segregation and DNA replication.The results of KEGG analysis indicated that APEX2 expression was positively correlated with cell cycle pathway and pro-oncogenic MYC signaling.Pearson correlation analysis showed that APEX2 had a significant positive correlation with CCNB1 and MYC.APEX2 level was higher in liver cancer cell lines than in normal liver LO2 cells.Small interfering RNA could knock down the APEX2 expression in HCCLM3 cells.Knockdown of APEX2 resulted in a decrease in the viability of HCCLM3 cells as well as the expression and promoter activity of CCNB1 and MYC.CONCLUSION APEX2 is overexpressed in LIHC,and the higher APEX2 level is associated with a worse prognosis in overall survival.APEX2 is closely involved in the biological processes of chromosome segregation and DNA replication.APEX2 expression is positively correlated with the pro-oncogenic pathways.Knockdown of APEX2 could inhibit the cell viability and CCNB1 and MYC pathways,suggesting that APEX2 is an oncogene in LIHC,which could be a potential pharmaceutic target in the anti-tumor therapy.

THE EXPRESSIONS OF HBV X GENE AND ets-2, IGF-Ⅰ, c-myc AND N-ras ONCOGENES IN HUMAN HEPATOCELLULAR CARCINOMA AND TUMOR-ADJACENT TISSUES

The expressions of HBV X gene and ets-2, IGF-I, c-myc and N-ras were studied in 7 pairs of human primary hepatocellular carcinoma (PHC) and tumor-adjacent tissues, using RNA hybridization and im-munoblot methods. The results showed that specific 17 and 28 kD HBV X gene products (HBxAg) were existed in a portion of PHC and tumor-adjacent tissues. The 17 kD HBxAg was detected in the sera of 3 patients who also had 17 kD HBxAg in their liver tissues. Multiple expressions of oncogenes such as ets-2, c-myc and N-ras were observed in PHC and tumor-adjacent tissues that had HBxAg expressed, indicating HBxAg might function as a transactivator in the course of intracellular proto-oncogene activation. It is also observed that in some tumor-adjacnet tissues the expressions of ets-2, c-myc and N-ras were higher than those in corresponding PHC. The relationship of HBxAg to the expression of est-2, IGF-Ⅱ, c-myc and their possible roles in the carcinogenesis of PHC are discussed.

Correlation of Kif2a and HPK1 expression in breast cancer with the oncogene and drug resistance gene expression

Objective: To investigate the correlation of Kif2a and HPK1 expression in breast cancer with the oncogene and drug resistance gene expression. Methods: A total of 91 patients with breast cancer and 85 patients with breast adenoma who accepted surgical treatment in our hospital between August 2016 and February 2018 were selected, and the breast cancer tissues and breast adenoma tissues were collected respectively as the research samples. Fluorescence quantitative PCR method was used to detect the expression of Kif2a and HPK1 genes as well as oncogenes and drug resistance genes in sample tissues, and Pearson test was used to evaluate the inner link of Kif2a and HPK1 gene expression in breast cancer tissue with oncogene and drug resistance gene expression. Results: Kif2a mRNA expression in breast cancer tissues was higher than that in breast adenoma tissues whereas HPK1 mRNA expression was lower than that in breast adenoma tissues;oncogenes DEK, iASPP-SV, Stat3, MDM2 and Fra-1 mRNA expression were higher than those in breast adenoma tissues;drug resistance genes ESR1, MDR1, P-gp, MRP1 and GST- mRNA expression were higher than those in breast adenoma tissues whereas BCRP mRNA expression was lower than that in breast adenoma tissues. Correlation analysis showed that the Kif2a and HPK1 gene expression in breast cancer tissues were directly correlated with the expression of oncogenes and drug resistance genes. Conclusion: Kif2a gene is abnormally highly expressed whereas HPK1 gene is abnormally lowly expressed in breast cancer tissues, and they are involved in the regulation of oncogene and drug resistance gene expression.

乳腺癌MRI形态学表现与C-erbB-2表达的相关性研究

目的 探讨乳腺癌MRI形态学表现与C erbB 2癌基因的相关性。方法 对 78例乳腺癌和 42例乳腺纤维腺瘤患者术前行乳腺MR扫描 ,分析乳腺癌的MRI形态学表现。术后标本行免疫组织化学染色测定肿瘤细胞C erbB 2的表达情况 ,并分析与相应病灶MRI表现的关系。结果 乳腺癌MRI多表现为边缘形态不规则或毛刺状边缘、边界模糊、瘤内有坏死。乳腺癌内部坏死与癌细胞C erbB 2阳性表达呈显著正相关 (r=0 .2 7,P <0 .0 5 ) ;而边界模糊、毛刺状边缘与癌细胞C erbB 2表达情况无显著相关性 (r =0 .11,r=-0 .13 ,P >0 .0 5 )。结论 乳腺癌MRI形态学表现与分子生物学指标C erbB 2之间存在一定的相关性。乳腺癌的MRI表现从一定程度上反映了癌细胞的生物学行为和预后 ,为临床治疗方案的选择提供客观依据。

乳腺癌ER、PR、c-erbB-2和nm23表达的相关性及临床病理意义

目的研究乳腺癌癌基因c-erbB-2、抑癌基因nm23和雌激素(ER)、孕激素受体(PR)的表达及意义。方法应用免疫组化SP法检测126例浸润性乳腺癌c-erbB-2、nm23及雌、孕激素受体的表达。结果①ER的表达与癌组织分化、肿瘤TNM分期及肿瘤大小呈负相关,小叶癌ER阳性率高于导管癌,而与患者年龄及淋巴结转移无显著相关性。②PR的表达与癌组织分化、肿瘤TNM分期呈负相关,与肿瘤大小、肿瘤类型、患者年龄及淋巴结转移无显著相关性。③c-erbB-2表达与肿瘤TNM分期、组织学分级、肿瘤大小及淋巴结转移呈正相关,与患者年龄、肿瘤类型无显著相关性。④乳腺癌Ⅰ期nm23表达的阳性率及阳性强度明显高于Ⅱ、Ⅲ期癌,nm23表达与组织学分级、淋巴结转移呈负相关,而与肿瘤大小及类型无显著相关性。⑤ER与PR表达呈正相关;nm23表达与ER、PR表达呈正相关,与c-erbB-2表达呈负相关;癌组织c-erbB-2与ER表达呈负相关,与PR表达无显著相关性。结论ER、PR、c-erbB-2及nm23的联合检测能够较好地反映乳腺癌病理生物学特征。

c-erbB-2、VEGF和组织蛋白酶D在胃癌中的表达及其相关性

目的 :探讨癌基因c erbB 2、血管内皮生长因子 (VEGF)和组织蛋白酶D(Cath D)在胃癌中的表达及其与胃癌生物学行为的关系。方法 :采用免疫组织化学 (S P)法 ,检测了 10 2例胃癌手术标本中c erbB 2、VEGF及Cath D的表达 ,同时观察了网状纤维分布与c erbB 2、Cath D之间的关系 ,并将检测结果与跟踪随访资料进行了综合分析。结果 :10 2例胃癌组织中c erbB 2表达阳性率为 38 2 4 % (39/ 10 2 ) ,与胃癌浸润深度 (P <0 0 5 )、淋巴结转移 (P <0 0 5 )密切相关 ;VEGF表达阳性率为 5 0 %(5 1/ 10 2 ) ,与胃癌浸润深度 (P <0 0 1)、生长方式 (P <0 0 1)、淋巴结转移 (P <0 0 1)密切相关 ;Cath D表达阳性率为81 37% (83/ 10 2 ) ,与胃癌浸润深度 (P <0 0 5 )、生长方式 (P <0 0 5 )、淋巴结转移 (P <0 0 5 )及脉管内有无癌栓 (P <0 0 5 )有关。对生存期分析显示 :Cath D、VEGF、c erbB 2阳性患者预后差 ,5年生存率低于阴性表达患者。结论 :c erbB 2、VEGF及Cath D与胃癌的生长、浸润、转移、预后有密切关系 。

Ki67、P53、VEGF和C-erbB-2在乳腺癌组织中表达的相关性研究及其临床意义

背景与目的:细胞增殖抗原标记物(Ki67)为细胞增殖的一个重要生物学指标。本研究旨在探讨Ki67、P53、VEGF和C-erbB-2在乳腺癌组织中的表达及其与临床病理因素的相关性。方法:用免疫组化方法检测151例乳腺癌组织中Ki67和其他生物学指标的表达,并与临床病理因素进行相关性分析。结果:Ki67在乳腺癌组织中的阳性率为74.8%(113/151)。Ki67表达与乳腺癌临床分期有关(P<0.05),而与患者年龄、肿瘤大小、淋巴结转移状况无显著性相关(P>0.05);Ki67表达与P53、C-erbB-2表达呈正相关(P<0.05),而与VEGF表达无显著性相关;Ki67和VEGF的共表达与肿瘤大小和临床分期有关(P<0.05)。结论:Ki67阳性表达可作为评价乳腺癌发生、发展的生物学指标,联合VEGF检测更有助于乳腺癌临床分期的判断。

人乳头状瘤病毒HPV-CIP5及癌基因c-erbB-2与宫颈癌的关系

目的：研究人乳头状瘤病毒ＨＰＶ－ＣＩＰ５及癌基因ｃ－ｅｒｂＢ－２与宫颈癌的关系。方法：应用免疫组化ＳＰ法对宫颈鳞癌７６例、腺癌２２例、宫颈上皮内瘤变ｃｅｒｖｉｃａｌｉｎｔｒａｅｐｉｔｈｅｌｉａｌｎｅｏｐｌａｓｉａ（ＣＩＮ）１０例及正常子宫颈粘膜２０例行ＨＰＶ－ＣＩＰ５及ｃ－ｅｒｂＢ－２染色。结果：上述各组织ＨＰＶ－ＣＩＰ５阳性率分别为７２４％（５５／７６）、４０９％（９／２２）、８０％（８／１０）、３５％（７／２０），其中鳞癌及ＣＩＮ中明显高于正常宫颈组织的表达（Ｐ＜００１），腺癌与正常宫颈组织表达无明显差异（Ｐ＞００５）；各组织中ｃ－ｅｒｂＢ－２阳性率分别为５２６％（４０／７６）、５９１％（１３／２２）、２０％（２／１０）、１５％（３／２０），其中鳞癌、腺癌中明显高于正常宫颈组织中表达（Ｐ＜００１）；在鳞癌ＨＰＶ－ＣＩＰ５与ｃ－ｅｒｂＢ－２同时表达３８例，占５０％（３８／７６），即４０例ｃ－ｅｒｂＢ－２阳性患者中有３８例ＨＰＶ－ＣＩＰ５同时呈现阳性；在腺癌ＨＰＶ－ＣＩＰ５与ｃ－ｅｒｂＢ－２同时表达８例，占３６３％（８／２２），即：９例ＨＰＶ－ＣＩＰ５阳性患者中有８例ｃ－ｅｒｂＢ－２同时呈现?

乳腺癌C-erbB-2癌基因与雌激素和孕激素受体的关系及其意义

目的 探讨乳腺癌C -erbB - 2癌基因与雌激素和孕激素受体的关系及其意义。方法 采用免疫组化方法 (二步法 ) ,检测 83例乳腺癌组织中C -erbB - 2、ER、PR的表达。结果 C -erbB - 2、ER、PR在乳腺癌组织中表达阳性率为 5 7 83%、71 0 8%、6 6 2 7%。C -erbB - 2表达 :在ER、PR阴性组高于ER、PR阳性组 (P <0 0 5 ) ;在淋巴结转移组的乳腺癌高于淋巴结未转移组 (P <0 0 5 )。结论 C -erbB - 2与ER、PR联合检测 ,对于乳腺癌患者术后选择个性化化疗具有指导意义 ,也是衡量预后的重要指标。

乳腺癌组织中C-erbB-2、nm23基因的表达及其预后的关系

目的探讨乳腺癌组织中C-erbB-2基因和nm23基因的表达与预后的关系。方法采用免疫组织化学S-P法检测298例乳腺癌C-erbB-2、nm23基因表达情况并与乳腺癌病理类型、发病年龄、临床分期、腋淋巴结转移情况及5a生存率之间的关系进行分析。结果C-erbB-2基因阳性率36.24%(108/298),nm23基因阳性率为58.05%(173/298);C-erbB-2和nm23基因的表达与肿瘤病理类型、发病年龄、临床分期无明显相关性(P>0.05);C-erbB-2基因表达与腋淋巴结转移呈正相关,与5a生存率呈负相关,nm23基因的表达与腋淋巴结转移呈负相关,与5a生存率呈正相关(P<0.05);C-erbB-2基因表达与nm23基因表达两者之间明显负相关(P<0.05)。结论联合检测乳腺癌组织中C-erbB-2和nm23基因表达可能成为预测、评估乳腺癌患者临床预后的标记物。

青年和绝经后女性乳腺癌c-erbB-2、p53、ER和PR受体表达及意义

目的 探讨青年和绝经后女性乳癌c erbB 2、p53、ER、PR的表达及意义。方法 采用SP法检测青年组 (13 1例 )与绝经组 (13 6例 )乳癌组织中各指标的表达及其与临床分期、腋淋巴结 (ALN )转移、3年无病生存率 (DFS)之间的关系。结果 c erbB 2阳性与临床分期、ALN转移相关 (P <0 .0 5) ,c erbB 2阳性者 3年DFS低于阴性者 (P <0 .0 5)。青年组c erbB 2、p53阳性率高、ER阳性率低 (P <0 .0 1) ,3年DFS低于绝经组 (P <0 .0 5)。结论 c erbB 2表达是乳腺癌预后重要指标 ,青年乳腺癌c erbB 2、p53阳性率高 ,ER阳性率低 ,3年DFS低 。

子宫内膜腺癌C-erbB-2COX-2过度表达的相关性分析

目的:研究C-erbB-2、COX-2在子宫内膜增生性病变和子宫内膜腺癌中的表达特点及其相关性。方法:应用免疫组织化学S-P法检测了20例正常增生期子宫内膜、23例单纯性子宫内膜增生、21例复杂性子宫内膜增生、43例非典型性子宫内膜增生、25例子宫内膜腺癌中C-erbB-2、COX-2的表达。结果:C-erbB-2和COX-2在各实验组中的阳性表达率:单纯性增生组为4.5%和9.1%,复杂性增生组为4.8%和14.3%,低级别非典型增生组为30.0%和25.0%,高级别非典型增生组为60.9%和52.4%,腺癌组为92.0%和91.7%;C-erbB-2、COX-2在各实验组间差异均有显著性(P=0.000)。C-erbB-2与COX-2在各组的表达水平呈显著正相关关系(P<0.01)。结论:C-erbB-2、COX-2可能在子宫内膜癌的发生发展中发挥重要的协同作用,两者联合检测对子宫内膜腺癌及癌前病变的鉴别诊断有较高的诊断价值。

胃粘膜癌变过程中幽门螺杆菌感染与p53,c-erbB-2基因表达的研究

目的探讨胃粘膜癌变过程中幽门螺杆菌（Ｈｅｌｉｃｏｂａｃｔｅｒｐｙｌｏｒｉ，Ｈｐ）感染与ｐ５３，ｃｅｒｂＢ２基因表达的关系．方法浅表性胃炎１６例，肠上皮化生２２例，异型增生１４例，早期胃癌１８例及进展期胃癌４０例作为研究对象．用ＷａｒｔｈｉｎＳｔａｒｙ银染色法检测Ｈｐ，用免疫组化Ｓｐ法检测ｐ５３和ｃｅｒｂＢ２的基因表达产物．结果Ｈｐ，ｐ５３，ｃｅｒｂＢ２在浅表性胃炎的检出率各为５００％，００％，００％；在肠上皮化生的检出率各为５９１％，２２７％，１３６％；在异型增生的检出率各为８５７％，６４３％，２８６％；在早期胃癌的检出率各为１６７％，３３３％，１１１％；在进展期胃癌的检出率各为５０％，５２５％，５５０％；在癌旁粘膜的Ｈｐ检出率为８６７％；在癌前病变中，Ｈｐ阳性组的ｐ５３，ｃｅｒｂＢ２表达率均高于Ｈｐ阴性组．结论Ｈｐ感染参与了胃癌前病变的发生与发展；Ｈｐ感染可引起野生型ｐ５３基因失活和ｃｅｒｂＢ２基因激活，从而导致胃粘膜的癌变．

survivin在乳腺癌中的表达及其与Ki-67和c-erbB-2表达的关系

目的观察凋亡抑制蛋白survivin在乳腺癌组织中的表达,及其与c-erbB-2、Ki-67增殖指数的相关性及临床病理意义。方法应用免疫组织化学SP法检测survivin在正常乳腺组织(20例)和乳腺癌组织(96例)中的表达以及Ki-67、c-erbB-2在乳腺癌组织中的表达。结果 survivin阳性表达乳腺癌的Ki-67增殖指数(35.32±21.28)%明显高于survivin阴性者(20.42±11.34)%,survivin表达与肿瘤细胞增殖呈正相关(P<0.01);survivin在乳腺癌组织中的阳性表达率为70.83%(68/96),正常乳腺组织未见survivin表达;survivin蛋白的表达与c-erbB-2的表达呈正相关(P<0.01);sur-vivin蛋白的表达与临床分期、淋巴结转移和5年生存率有关(P<0.05),与年龄、是否绝经、肿瘤大小和组织学分级均无关。结论 survivin不仅参与凋亡的调控,还促进了细胞增殖,在乳腺癌发生、发展中起重要作用,过度表达提示预后不良。