Expression and significance of proapoptotic gene Bax in gastric carcinoma

AIM To study the expression of proapoptotic gene Bax in human gastric carcinoma and its significance. METHODS Using immunohistochemistry methods, the Bax protein expression in 57 specimens of gastric carcinoma and its relationship with clinical status and pathomorphological parameters were observed. RESULTS Thirty three (57 89%) cases were positive for Bax protein staining which was mainly located in the cytoplasm of tumor cells. The rate of Bax protein expression was not correlated with the tumor size, lymph node metastasis, depth of invasion, clinical stages of tumors and age and sex of patients ( P >0 05), but strongly associated with the morphological type and differentiation degree of tumors. It was significantly higher in intestinal type and well/moderately differentiated gastric carcinoma than in diffuse type and poorly differentiated gastric carcinoma ( P <0 05 and P <0 01). CONCLUSION The proapoptotic gene Bax is differentially expressed in most of gastric carcinoma and may take part in the modulation of apoptosis in gastric carcinoma. The expression of Bax might be associated with the occurrence of intestinal type gastric carcinoma and the differentiation of gastric carcinoma.

Microsatellite instability,MMR gene expression and proliferation kinetics in colorectal cancer with famillial predisposition

INTRODUCTIONGenetic instability is a conunon property of manyhuman cancers,including those of HNPCC.A novel form of genetic instability involving somaticalterations,such as deletions and insertions insimple repeated sequences,has been found.Microsatellitcs are relatively short runs of tandemlyrepeated sequences scattered throughout

Effects of endotoxin on expression of ras, p53 and bcl-2 oncoprotein in hepatocarcinogenesis induced by thioacetamide in rats

AIM To evaluate the relationship between expression of ras, p53, bcl 2 gene products, and hepatocarcinogenesis since endotoxemia produced from lipopolysaccharide admi nistration and/or the hypophagocytic state of splenectomy significantly accelerated hepatocarcinogenesis induced by thioacetamide. 〖WTH4〗METHODS〓〖WTXFZ〗The hepatocarcinoma model was induced by oral intake of 0 03% thioacetamide for six months. During the induction of hepatocarcinoma model, rats were additionally treated with splenectomy and/or lipopolysaccharide administration. The techniques of flow cytometry, immunohistochemistry and immunoelectronmicroscopy were applied to quantitative analysis of the expression of oncogene proteins. RESULTS In this model system, overexpression of ras p21 protein mainly occurred on precancerous cell population or in early stage of hepatocyte transformation. And the levels of ras p21 declined when nuclear DNA aneuploid increased. Expression of bcl 2 protein slowly and steadily rose with more hepatocytes staying in S+G2M phases as the hepatocarcinoma became more malignant. P53 was moderately expressed during the hepatocarcinogenesis. There was no statistical correlation between endotoxemia levels and the changes of ras, p53 and bcl 2 gene products. CONCLUSION Over expression of oncogene ras p21 was likely to be a precursor of the premalignant hepatocytes and it might be responsible for the initiation of hepatocarcinogenesis. Bcl 2 protein expression is proportional to the severity of the malignancies. P53 may be a key pathway on the transformation and development of hepatocarcinoma. This study confirmed the hypothesis that there are multiple genes and multiple steps involved in hepatocarcinogenesis. Expressions of oncogene proteins reflected the properties of the premalignant and malignant cells, but not directly related to endotoxemia statistically.[JP]

Expression of gap junction genes connexin 32,connexin 43 and their proteins in hepatocellular carcinoma and normal liver tissues

AIM To investigate the significance andmechanism of cx32 mRNA,cx43 mRNA and theirproteins in hepatocarcinogenesis.METHODS Sixty-one cases of HCC and 14cases of normal liver tissues were detected byimmunohistochemical and in situ hybridization(ISH)methods.RESULTS In HCC grades Ⅰ,Ⅱ,Ⅲ and normalliver tissues,the positive rates of Cx32 proteinwere 55.6%,42.1%,18.2% and 92.9%,respectively.The detection rates of Cx43 proteinwere 44.4%,26.3%,12.1% and 78.6%,respectively.There was significant difference inCx32 and Cx43 protein between HCC and normalliver tissues(P【0.01).ISH the positive rates ofcx32 mRNA shown by ISH in HCC grades Ⅰ,Ⅱ,Ⅲ and normal liver tissues were 88.9%,84.2%,87.9% and 92.9%,respectively.Those of cx43mRNA were 77.8%,78.6%,78.8% and 85.7%,respectively.There was no statistical differencein the positive rates of cx32 mRNA and cx43mRNA between HCC and normal liver tissue(P】0.05).CONCLUSION The aberrant location of Cx32and Cx43 proteins could be responsible forprogression of hepatocarcinogenesis,and thedefect of cx genes in post-translationalprocessing might be the possible mechanism.

Expression of nm23 gene in hepatocellular carcinoma tissue and its relation with metastasis

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Analysis of N-ras gene mutation and p53 gene expression in human hepatocellular carcinomas

IM To study the relationship between Nras gene mutation and p53 gene expression in the carcinogenesis and the development of human hepatocellular carcinomas (HCC).METHODS The Nras gene mutation and the p53 gene expression were analyzed in 29 cases of HCC by polymerase chain reactionsingle strand conformation polymorphism (PCRSSCP) and immunohistochemistry.RESULTS Thirteen cases of HCCs were p53 positive (448%), which showed a rather high percentage of p53 gene mutation in Guangxi. The aberrations at Nras codon 2-37 were found in 7931% of HCCs and 8077% of adjacent nontumorous liver tissues. More than 2 point mutations of Nras gene were observed in 22 cases (7586%). Twelve cases (4137%) of HCCs showed both Nras gene mutation and p53 gene expression.CONCLUSIONS Nras gene and p53 gene may be involved in the carcinogenesis and the development of HCC. That 38% of HCCs with Nras gene mutation did not express p53 protein indicates that some other genes or factors may participate in the carcinogenesis and the development of HCC.

KAI1/CD82 gene expression in benign prostatic hyperplasia and late-stage prostate cancer in Chinese

Aim: To evaluate KAII/CD82 expression in Chinese patients with benign prostatic hyperplasia (BPH) and late-stage carcinoma of prostate (CaP). Methods: Thirty Chinese patients with benign prostatic hyperplasia and 34 withCaP (adenocarcinoma clinical stage C and D) were analyzed by means of immunohistochemical methods. Results:The KAII/CD82 expression in BPH tissue was all positive, which was uniformly located on the glandular cell mem-brane at the cell-to-cell borders, but KAII/CD82 expression in metastasis CaP tissues was either significantly lower thanthat of BPH or negative, and the immunostaining pattern was not continuous. In late-stage CAP KAII/CD82 expressionwas correlated inversely to the pathological grade ( P < 0.05), but not to clinical stage ( P > 0.05). Conclusion:The authors believe that decreased and negative KAII/CD82 expression in late-stage CaP may be related to tumor pro-gression and metastasis, and appears to be a prognostic marker.

The expression of c-src gene in the carcinogenesis process of human cardia adenocarcinoma

AIM To investigate the activation, expression of c src gene and its role in the carcinogenetic process of human cardia adenocarcinoma (CA). METHODS Fifty six cases of CA, 34 cases of normal, 36 cases of protiferative epithelia adjacent to carcinoma, and 20 cases of lymph node metastases of CA were studied for PP60 c src , the expression product of c src gene immunohistochemically by using the specific monoclonal antibody, Mab327. RESULTS The positive rates of PP60 c src in the normal epithelia, protiferative epithelia, CA and lymph node metastases were 29 4% (10/*!34), 94 4% (34/*!36), 71 4% (40/*!56) and 60 0% (12/*!20) , respectively, among them, the differences of the positive rates were statistically significant ( P <0 01) . The expression levels of PP60 c src in CA and proliferative epithelia were significantly higher than that in the normal epithelia ( P <0 01) . The PP60 c src positive rates in the papillary, tubular, poorly differentiated and mucous adenocarcinoma were 75 0% (6/*!8) , 81 8% (18/*!22) , 50 0% (10/*!20) and 100 0% (6/*!6) , respectively, whereas those of tubular and mucous adenocarcinomas were significantly higher than those of papillary and poorly differentiated adenocarcinomas ( P <0 05) , and the PP60 c src expression levels of tubular and mucous adenocarcinomas were also significantly higher than those of papillary and poorly differentiated adenocarcinomas ( P <0 01) . CONCLUSION The activation and expression of c src gene are associated with the initiation and development of human CA; the protein amount of PP60 c src increased during the process of carcinogenesis; and PP60 c src expression is also related to lymph node metastases.

MULTIPLE GENETIC EXPRESSION ABNORMALITIES IN GASTRIC CANCER

By means of immunohistological technique, theexpressions of p53, c-erbB-2, EGFR and ras wereexamined on the adjacent sections of 75 cases of gastriccancer (GC), and their clinicopathological and prognosticsignificance were studied. Results: 1) Overexpressionsof p53 and c-erbB-2 were early and late sign of malignantchange of gastric mucosa, respectively: EGFR and rashad close association with the degree of malignancy ofGC. 2) The expression of ras had positive relationshipwith the expression of EGFR, and negative relationshipwith c-erbB-2.3). The multivariate analysis of Cox modelof GC showed only DNA ploidy, expression of EGFR,lymph node metastasis and distant metastasis wereindependent prognostic factors of GC.

老年女性乳癌组织中Bcl-2蛋白表达及临床意义

目的探讨B细胞淋巴瘤-2(Bcl-2)在老年女性乳癌组织中的表达及其与病人临床病理特征和预后的关系。方法采用免疫组织化学方法检测92例老年女性乳癌组织中Bcl-2蛋白的表达,分析Bcl-2蛋白在老年女性乳癌组织中表达与病人临床病理特征及预后的关系。结果Bcl-2蛋白在老年女性乳癌组织中的阳性表达率为80.4%。Bcl-2的表达与肿瘤大小、淋巴结转移、TNM分期、组织学分级和脉管瘤栓相关(χ^(2)=4.459~11.607,P<0.05)。分子特征分析结果显示,Bcl-2表达与病人的雌激素受体、人表皮生长因子受体-2表达和分子分型相关(χ^(2)=14.572~19.390,P<0.05)。生存分析显示,Bcl-2的表达与病人无进展生存率及总生存率无关(P>0.05)。结论检测Bcl-2蛋白的表达对于判断老年女性乳癌预后和指导治疗具有临床参考价值。

Multiple genetic alterations and behavior of cellular biology in gastric cancer and other gastric mucosal lesions:H.pylori infection,histological types and staging

AIM To investigate the expression of multiplegenes and the behavior of cellular biology ingastric cancer（GC）and other gastric mucosallesions and their relations to Helicobacter pylori（H.pylori）infection,tumor staging andhistological subtypes.METHODS Three hundred and twenty-sevenspecimens of gastric mucosa obtained viaendoscopy or surgical resection,and ABCimmunohistochemical staining were used todetect the expression of p53,p16,Bcl-2 andCOX-2 proteins.H.pylori was determined byrapid urea test combined with pathologicalstaining or14C urea breath test.Cellular image analysis was performed in 66 patients withintestinal metaplasia（IM）and/or dysplasia（Dys）.In 30 of them,both cancer and theparacancerous tissues were obtained at the timeof surgery.Histological pattern,tumor staging,lymph node metastasis,grading ofdifferentiation and other clinical data werestudied in the medical records.RESULTS p16 expression of IM or Dys wassignificantly lower in positive H.pylori chronicatrophic gastritis（CAG）than those withnegative H.pylori（CAG:54.8% vs 88.0%,IM:34.4% vs 69.6%,Dys:23.8% vs 53.6%,allP【0.05）,Bcl-2 or COX-2 expression of IM orDys in positive H.pylori cases was significantlyhigher than that without H.pylori（Bcl-2:68.8%vs23.9%,90.5% vs 60.7%;COX-2:50.0% vs10.8%,61.8% vs 17.8%;all P【0.05）.Themean number of most parameters of cellularimage analysis in positive H.pylori group wassignificantly higher than that in negative H.pylori group（Ellipser:53±14,40±12μm,Area1:748±572,302±202 μm2,Area2:3050±1661,1681±1990 μm2,all P【0.05;Ellipseb:79±23,58±15 μm,Ratio1:22%±5%,13%±4%,Ratio2:79%±17%,53%±20%,all P【0.01）.There was significant correlation between Bcl-2and histologic pattern of gastric carcinoma,andbetween COX-2 and tumor staging or lymph nodemetastasis（Bcl-2:75.0% vs 16.7%;COX-2:76.0% vs 20.0%,79.2% vs 16.7%;allP【0.05）.CONCLUSION p1l6, Bcl-2, and COX-2 but not p53 gene may play a role in the early genesis/ progression of gastric carcinoma and are associated with H. pylori infection. p53 gene is relatively late event in gastric tumorigenesis and mainly relates to its progression. There is more cellular-biological behavior of malignant tumor in gastric mucosal lesions with H. pylori infection. Aberrant Bcl-2 protein expression appears to be preferentially associated with the intestinal type cancer. COX-2 seems to be related to tumor staging and lymph node metastasis.

Expression of B7 costimulation molecules by colorectal cancer cells reduces tumorigenicity and induces anti-tumor immunity

AIM To study the tumorigenicity of colorectal cancer cells transfected with B7 gene and the anti-tumor immunity induced by B7 gene modified colorectal cancer cells.METHODS B7 gene was transfected into mouse colon cancer cell line CMT93. The transfectants were selected in DMEM containing 800 mg/ L G418, and B7 molecules were detected by immunohistochemistry. Experiments in vivo include: ① 5×106 B7+ CMT93 cells were inoculated into the back of C57BL/ 6 mice subcutaneously to determine their tumorigenicity (n=4). As control, wild type CMT93 cells were inoculated the same as the experimental group (n=3). ② The mice primed by B7+ CMT93 cells whose tumors vanished were rechallenged with wild type CMT93 to observe the immune protection of these mice against the wild type CMT93 (n=4). Non-primed 4 native mice inoculated with wild type CMT93 were used as control. With in vitro cytotoxicity assay, the mice were immunized with B7+ CMT93 or the wild type CMT93 by intraperitoneal injection (n=4×2). The spleen cells and the abdominal cavity infiltrating lymphocytes were obtained and cultured for two days. Cytotoxicity of these cells against the B7 gene modified or wild type CMT93 was detected by MTT assay.RESULTS B7 high expression clones were obtained after the transfection of the B7 gene into CMT93 cells by electroporation. Immunohistochemistry results showed mainly membrance staining and partly cytoplasm staining in B7 gene transfected CMT93 cells. In vivo experiments: ① After the inoculation of the B7+ CMT93 cells into the back of C57BL/ 6 mice, they lost their tumorigenicity greatly (P＜0.01). All the small tumors growing in the early period in the experimental group vanished in one month, and the tumors in control group grew progressively. ② No tumors were found in all 4 mice primed by B7+ CMT93 cells after they were rechallenged with wild type CMT93. In the control group all mice had grown tumors (P＜0.05). In vitro cytotoxicity assay, the CTLs induced by B7+ CMT93 had a higher cytotoxity against the wild type CMT93 than that induced by wild type CMT93 (P＜0.05), and the cytotoxity of CTLs induced by B7+ CMT93 against B7+ CMT93 cells was higher than that against wild type CMT93 cells (P＜0.05).CONCLUSION The results suggest that the expression of costimulation B7 molecules by colorectal cancer cells can decrease their tumorigenicity greatly, and the B7 molecule can augment the activation of the CTLs against colorectal cancer, and it plays an important role in CTL effector function as well.

A preliminary study on ras protein expression in human esophageal cancer and precancerous lesions

INTRODUCTIONThe esophageal carcinoma is a common malignanttumor in Linzhou City (Linxian) of Henan Provincein northern China.Although the etiology andnatural history of csophageal carcinoma are notclear,a substantial amount of evidence has beenprovided to suggest that the development of humanesophageal squamous cell carcinomas (SCC) is amultistage progressive process.An

Current status of gene therapy in gastroenterology

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LOCALIZATION OF TYPE I AND TYPE Ⅲ PROCOLLAGEN mRNAs IN BREAST SCIRRHOUS CARCINOMA BYIN SITU HYBRIDIZATION

Scirrhous carcinoma is charactertzed by reinarkable amount of collagen fibrils, mainly type I and type III collagens. The origin of collagens is still under debate.cDNA fragments of type I and type III procollagens were subcloned into Gemini pGEM vectors to synthesize the 35Slabeled cRNA probes. By in situ hybridization, we have found the fibroblasts surrounding the tumor cells and cords contained abundent type I and type III procollagen mRNAs which decreased with the distance of fibroblasts from the tumor cells. In all freshly prepared tissues, the tumor cells also contained significant pro α1 (I) and pro α1 (III) mRNAs, but no or little pro α2 (I) mRNA. The results indicated that type I and type III collagens in human scirrhous carcinoma of breast are mainly produced by fibroblasts. Tumor cells also perticipate in the disposition of collagen fibrils, probably type I trimer and type III collagens in accordance with what was observed in biochemical

乳腺隆突性皮肤纤维肉瘤21例临床病理及分子学特征

目的探讨乳腺隆突性皮肤纤维肉瘤(dermatofibrosarcoma protuberans of the breast,DFSP-B)的临床病理学及分子学特征。方法回顾性分析21例DFSP-B的临床病理学、免疫表型及分子学特征,行HE、免疫组化及分子检测,并复习相关文献。结果21例DFSP-B患者男性6例,女性15例,年龄22~75岁(平均39.76岁,中位年龄36岁)。肿瘤最大径1~15 cm(平均4.7 cm,中位3 cm)。镜下瘤细胞呈席纹状、漩涡状及束状排列,核分裂象2~15个/10 HPF,侵犯脂肪及乳腺组织,符合DFSP-B;其中经典型DFSP-B 15例,经典型伴巨细胞纤维母细胞瘤(giant cell fibroblastoma,GCF)1例,黏液型2例,纤维肉瘤型隆突性皮肤纤维肉瘤(fibrosarcomatous-dermatofibrosarcoma protuberans,FS-DFSP)2例,FS-DFSP伴黏液型1例。免疫表型:CD34(21/21)、H3K27Me3(21/21)、β-catenin(21/21,胞膜)和WT-1(4/8,胞质)均阳性,Ki-67增殖指数为5%~50%。FISH检测DFSP-B中PDGFB基因分离阳性(7/8);3例FS-DFSP中PDGFB基因分离阳性(1/1),COL1A1-PDGFB融合阳性(1/1)。2例行NGS检测,其中1例FS-DFSP检测到CDKN2A基因(p.L16fs)突变及MSH6基因(p.F1088fs)突变;1例经典型伴GCF型检测到MLH1基因(p.R487)突变及TP53基因p.R273H体系突变。结论DFSP-B诊断需结合临床病理、免疫表型及PDGFB基因检测,治疗以手术切除为主,必要时可行放疗及靶向治疗,预后较好。

RRS1对乳腺癌细胞增殖和迁移的影响及其作用机制

目的探讨核糖体合成调控因子1(RRS1)基因对乳腺癌BT549细胞增殖和迁移的影响及其作用机制。方法通过Western Blot实验检测人乳腺癌细胞系(MDA-MB-231、MDA-MB-468、BT549、MCF-7细胞)和人正常乳腺上皮MCF-10A细胞RRS1蛋白的表达量。通过免疫荧光检测RRS1在BT549细胞中的定位。慢病毒感染法建立RRS1敲低的BT549细胞系,采用实时荧光定量PCR(RT-qPCR)和Western Blot实验检测感染阴性对照慢病毒细胞(Con组)和感染shRNA-RRS1慢病毒细胞(sh-RRS1组)中RRS1 mRNA和蛋白相对表达量。采用CCK8实验和集落形成实验检测RRS1对BT549细胞增殖能力的影响,通过细胞划痕实验、Transwell实验检测RRS1对BT549细胞迁移能力的影响。采用Western Blot实验检测两组细胞AKT-mTOR相关信号通路蛋白及其下游缺氧诱导因子-1α(HIF-1α)蛋白、血管内皮生长因子(VEGF)蛋白相对表达量。结果MDA-MB-231、MDA-MB-468、BT549、MCF-7乳腺癌细胞系中RRS1相对表达量与人正常乳腺上皮MCF-10A细胞相比均显著增高(F=48.92,P<0.05)。免疫荧光染色显示,RRS1主要在BT549细胞的细胞核和核仁表达,细胞质也有少量表达。与Con组进行比较,sh-RRS1组RRS1 mRNA和蛋白表达量显著降低,增殖和迁移能力均明显减弱,p-AKT、p-mTOR、HIF-1α、VEGF蛋白表达量均显著降低(t=6.29~32.04,F=1368.00、2699.00,P<0.05)。结论RRS1可能通过AKT-mTOR通路促进乳腺癌细胞的增殖和迁移。

Integrated transcriptome interactome study of oncogenes and tumor suppressor genes in breast cancer

Breast cancer is the leading cause for mortality among women worldwide.Dysregulation of oncogenes and tumor suppressor genes is the major reason for the cause of cancer.Understanding these genes will provide clues and insights about their regulatory mechanism and their interplay in cancer.In the present study,an attempt is made to compare the functional characteristics and interactions of oncogenes and tumor suppressor genes to understand their biological role.431 breast cancer samples from seven publicly available microarray datasets were collected and analysed using GEO2R tool.The identified 416 differentially expressed genes were classified into five gene sets as oncogenes(OG),tumor suppressor genes(TSG),druggable genes,essential genes and other genes.The gene sets were subjected to various analysis such as enrichment analysis(viz.,GO,Pathways,Diseases and Drugs),network analysis,calculation of mutation frequencies and Guanine-Cytosine(GC)content.From the results,it was observed that the OG were having high GC content as well as high interactions than TSG.Moreover,the OG are found to have frequent mutations than TSG.The enrichment analysis results suggest that the oncogenes are involved in positive regulation of cellular protein metabolic process,macromolecule biosynthetic process and majorly in cell cycle and focal adhesion pathway in cancer.It was also found that these oncogenes are involved in other diseases such as skin diseases and viral infections.Collagenase,paclitaxel and docetaxel are some of the drugs found to be enriched for oncogenes.

circRASSF2靶向miR-1343-3p对乳腺癌MDA-MB-231细胞增殖和凋亡的影响

目的探讨circRASSF2对乳腺癌MDA-MB-231细胞增殖和凋亡的影响及分子机制。方法逆转录荧光定量聚合酶链反应(RT-qPCR)检测37例乳腺癌及癌旁组织中circRASSF2和miR-1343-3p表达水平;将乳腺癌MDA-MB-231细胞分为si-circRASSF2组、si-NC组、miR-NC组、miR-1343-3p组、si-circRASSF2+anti-miR-1343-3p组、si-circRASSF2+anti-miR-NC组;四甲基偶氮唑盐比色法(MTT)检测细胞活性;克隆形成实验检测细胞克隆形成数;Annexin V-FITC/PI双染法检测细胞凋亡情况;Western blot检测Cleaved-caspase 3、Cleaved-caspase 9蛋白相对表达水平;双荧光素酶报告实验检测circRASSF2和miR-1343-3p的靶向关系。结果与癌旁组织比较,乳腺癌组织中circRASSF2表达水平升高,miR-1343-3p表达水平降低(P<0.01)。与si-NC组比较,si-circRASSF2组MDA-MB-231细胞OD值降低,细胞克隆形成数减少,而凋亡率升高(P<0.05)。与miR-NC组比较,miR-1343-3p组MDA-MB-231细胞OD值降低,细胞克隆形成数减少,而凋亡率升高(P<0.05)。与miR-NC组比较,miR-1343-3p组WTcircRASSF2荧光素酶活性降低(P<0.05)。与si-circRASSF2+anti-miR-NC组比较,si-circRASSF2+anti-miR-1343-3p组MDA-MB-231细胞OD值、克隆形成数升高,凋亡率降低(P<0.05)。结论抑制circRASSF2表达可上调miR-1343-3p,进而抑制乳腺癌MDA-MB-231细胞增殖,促进其凋亡。

c-erbB-2、p53和Bcl-2蛋白表达在乳腺癌中的意义及其相关性的探讨

目的 探讨乳腺癌中ｃｅｒｂ Ｂ２、ｐ５３ 和Ｂｃｌ２ 蛋白表达与临床病理参数、预后和增殖细胞核抗原（ＰＣＮＡ） 、雌激素受体（ＥＲ）、孕激素受体（ＰＲ）的关系。 方法 应用亲和素生物素复合物（ＡＢＣ） 法免疫组织化学技术对８７例福尔马林固定石蜡包埋的乳腺癌组织进行回顾性研究。 结果 （１）ｃｅｒｂ Ｂ２ 和ｐ５３ 这两种蛋白的超表达与淋巴结转移、病理分级、核分裂、生存期短、ＰＣＮＡ强阳性表达、ＥＲ、ＰＲ阴性表达等不良因素呈正相关趋势（ Ｐ＞ ０－０５） 。（２）Ｂｃｌ２ 的阳性表达与瘤细胞的分化、淋巴结无转移、生存期长，ＥＲ、ＰＲ 的阳性表达等良好因素相关联，而且Ｂｃｌ２的阳性表达常会“减弱”或“抵抗”原癌基因的不良因素。 结论 多种癌基因（ 包括ｃｅｒｂ Ｂ２、ｐ５３ 和Ｂｃｌ２）