Expression of p53 and C-myc genes and its clinical relevance in the hepatocellular carcinomatous and pericarcinomatous tissues

AIM: To investigate the possible roles of p53 and C-mycgenes in the primary hepatocellular carcinogenesis and therelationship between the liver hyperplastic nodule(LHN) andhepatocellular carcinoma(HCC).METHODS: The expression of p53 and C-myc genes wasdetected immunohist-ochemically in 73 and 60 cases of HCCand pericarcinomatous tissues, respectively .RESULTS: The positive expression of p53 in HCC wassignificantly higher than that in pericarcinomatous tissues(P＜0.05). In pericarcinomatous tissues, the p53 expressionwas observed only in LHN, but not in liver cirrhosis (LC) andnormal liver tissues. The positive expression rate of C-mycin HCC or LHN was significantly higher than that in LC ornormal liver tissues (P＜0.05 and P＜0.01), however, nosignificant difference was found between HCC and LHN(P＞0.05). The positive expression rate of p53 and C-myc inHCC was correlated with the histological differentiation, thatin the poorly differentiated was significantly higher than thatin well differentiated samples (P＜0.05).CONCLUSION: The overexpression of p53 and C-myc genesmight play a role in the carcinogenesis of HCC; And LHNseems a preneoplastic lesion related to hepatocarcinogenesis;No evidence supports that LC contribute directly to thehepatocarcinogenesis.

Detecting the polymorphism sites of p53 and Fas genes of Han population in Zhejiang province

BACKGROUND： It is of significance for single nucleotide polymorphisms （SNPs）, a difference of rank, which exists widely in biology, genetics and other fields. OBJECTIVE： To detect polymorphism sites in exon-4 of p53 gene, promotor of Fas gene and intron-7 of Fas gene of healthy people in Han nationality in Zhejiang province. DESIGN： Simple random sampling. SETTING： Department of Surgery of the 118 Hospital of Chinese PLA.PARTICIPANTS： A total of 80 healthy people in Han nationality were selected from hospitals in Zhejiang province from August 2005 to January 2006. There were 43 males and 37 females aged from 3 to 78 years with the mean age of 39.5 years, and all subjects were consent. DNA which was used in genetic analysis was selected from peripheral venous blood of all subjects and maintained at -20℃.METHODS： Polymorphism sites in exon-4 of p53 gene, promotor of Fas gene and intron-7 of Fas gene were detected with directly DNA sequencing technique. MAIN OUTCOME MEASURES ： Polymorphism sites in exon-4 of p53 gene, promotor of Fas gene and intron-7 of Fas gene of healthy people in Han nationality in Zhejiang province. RESULTS： A total of 80 samples were involved in the final analysis. SNPs sites were found at the 119^th base of exon-4 of p53 gene （the 72^nd codon of p53 gene）, the 670^th base of upper start codon in promotor of Fas gene （Fas-670）, and the 995^th base of intron-7 of Fas gene, especially SNPs in the 995^th base of intron-7 pf Fas gene, i.e. C→A transversion, was a new site.CONCLUSION ： One unknown SNPs site is discovered in intron-7 of Fas gene of people in Han nationality in Zhejiang province. This study also proves that the 72^nd codon exists in p53 gene and the -670 polymorphism site exists in promotor of Fas gene.

H pylori (CagA) and Epstein-Barr virus infection in gastric carcinomas:Correlation with p53 mutation and c-Myc,Bcl-2 and Bax expression

AIM: To investigate the interrelationship between H pylori and Epstein-Barr virus (EBV) infection in the gastric carcinogenesis having in focus the p53 mutation and the c-Myc, Bcl-2 and Bax expression. METHODS: seventy-one gastric carcinoma tissues were assessed by polymerase chain reaction (PCR) for H pylori and in situ hybridization for EBV. c-Myc, Bcl-2 and Bax expression were detected by immunohistochemistry and single-stranded conformational polymorphism (SSCP) for p53 mutation. RESULTS: The positivity rates for H pylori and EBV were 94.4% and 8.45%, respectively. The majority of the cases displayed only the H pylori presence. All EBV positive cases were also H pylori positive. None infectious agent was observed in 5.55% of the cases. The intestinal type tumor was more frequent in the co-infected and non-infected groups. The female predominated in the non-infected group showing statistical significance (70.4% vs 29.6%, P=0.039). The Bcl-2 was only detected in the group exclusively infected by H pylori. However, c-Myc and Bax were detected in the three groups but with a low frequency in the co-infected group. Mutation of p53 was present in all groups, with the highest frequencies in the H pylori positive groups. CONCLUSION: The frequency of H pylori infection in gastric carcinomas was high. The presented data indicated that gastric carcinogenesis has different pathways depending of the presence of the two investigated infectious agents, suggesting a possible involvement of H pylori with apoptotic process. The low expression of c-Myc and Bax in the EBV-positive groups suggests that EBV may inhibit the expression of these proteins. Nevertheless, p53 mutation shows to be a relevant alteration, independent of both infectious agents.

Study of mutations of p53, APC and K-ras genes in 47 cases of intestinalmetaplasia of gastric mucosa

Objective:To study the role of the mutations of p53, APC and K-ras genes in 47 cases of 3 types of intestinal metaplasia (IM) of gastric mucosa. Methods:In 47 cases of IM, exons 5- 8 of p53 and exons 15 of APC were examined with PCR-SSCP and codon 12 of K-ras with PCR-RFLP to detect the existence of any mutations of these structures. Results:Muta- tions of p53, APC and K-ras were found in 29.8% (14/47),6.4% (3/47) and 6.4% (3/47) respectively in our series of patients who consisted of 33 with types I and II and 14 with type III of IM. The mutation rate of p53 was far higher in patients with type III IM (57.1%,8/14) than in those with types I and II IM(18.2%,6/33)(P <0.05). Though the mutation rate of APC and K-ras was also higher in the patients with type III IM than in those with types I and II IM, it was of no statistical significance (P >0.05). In one case of type III IM, mutation of both p53 and K-ras was found. Conclusion: The molecular changes of 3 types of IM are different. The mutation of p53 may be closely related to carcinogenesis in cases of type III IM and it serve as a sign for the early diagnosis of gastric carcinoma.

Effect of hydroxyapatite nanoparticles on the growth and p53/c-Myc protein expression of implanted hepatic VX_2 tumor in rabbits by intravenous injection

AIM： To evaluate the effect of hydroxyapatite nano- particles （Nano HAP） by intravenous injection on the inhibition of implanted hepatic VX2 tumor growth in rabbits and cell p53/c-Myc protein expression. METHODS： 60 hepatic VX2 tumor-bearing rabbits was randomly divided into five groups. Nano HAP collosol 20 mglkg, 40 mg/kg, 5-FU solutions 20 mg/mL, mixed liquor of 5-FU solution 20 mg/mL and Nano HAP collosol 20 mg/kg were infused by vein, normal saline conducted as the control. The general state, weight, liver function and gross tumor volume were detected dynamically. The expression of p53 and c-Myc gene protein in tumor tissue was detected by immunohistochemistry methods. RESULTS： The growth of implanted hepatic VX2 tumors was significantly inhibited in all therapy groups, 3 wk after the injection, the tumor control rates in Nano HAP collosol groups were 25.5% and 32.5% respectively, and the gross tumor volumes were obviously less than that of control group. （24.81 ± 5.17 and 22.73 ± 4.23 vs 33.32 ± 5.26, P 〈 0.05）. The tumor control rate of 5-FU group was 43.7% （18.74 4± 4.40 vs 33.32 ± 5.26, P 〈 0.05）, but the general state of the animals after injection aggravated; and the adverse reaction in the drug combination group obviously decreased. Due to the effect of Nano HAP, the positive expression of tumor associated the mutated p53 and c-Myc in tumor tissue was decreased obviously compared with the control group. CONCLUSION： Nano HAP has evident inhibitory action on rabbit implanted hepatic VX2 tumor in vivo, which may be the result of decreasing the expression of the mutated p53 and c-myc, and drug combination can obviously decrease the adverse reaction of 5-FU.

Effects of Cadmium on Telomerase Activity,Expressions of TERT,C-myc and P53,and Apoptosis of Rat Hepatocytes

This study investigated the effect of cadmium on the telomerase activity,the expression of TERT,c-myc and p53 and the apoptosis of rat hepatocytes.The rats were administrated 5,10 and 20 μmol/kg cadmium chloride intraperitoneally and sacrificed 48 h after the initial treatment.The telomerase activity of the rat hepatocytes was measured by the telomeric repeat amplification protocol (TRAP),and apoptosis was detected by flow cytometry.The mRNA expressions of TERT,c-myc and p53 were measured by reverse transcription-polymerase chain reaction (RT-PCR).C-myc and P53 proteins were determined by immunochemistry.The results showed that cadmium chloride increased the hepatocellular telomerase activity in a dose-dependant manner and induced the apoptosis of hepatocytes significantly.The value of relative coefficient between the telomerase activity and the apoptosis rate was 0.9398.RT-PCR revealed that specific bands corresponding to the TERT mRNA,c-myc mRNA,and p53 mRNA were displayed at 185,342 and 538 bp respectively.Cadmium chloride could substantially increase the mRNA expressions of TERT,c-myc and p53 in rat hepatocytes,as compared with control.Moreover,cadmium chloride at the doses of 5,10 and 20 μmol/kg could increase the content of P53 protein in rat hepatocytes obviously,but only that at the doses of 10 and 20 μmol/kg substantially promoted the c-myc protein level in rat hepatocytes.Our study herein suggested that cadmium may contribute to the carcinogenesis by activating telomerase,and overexpressing the mRNAs of TERT,c-myc and p53,and causing apoptosis of normal cells.

The Relationship between Mouth Squamous Cell Carcinoma (MSCC) with HPV Infection and the Presence of p53 &c-myc Mutation

Introduction: Now the molecular epidemiology is a new experience. It’s was noted that ninety percent of mouth cancers are squamous cell carcinomas and recorded 0.96% year of all cancers in Indonesia. Human papilloma virus (HPV) was implicated in pathogenesis of cancer. As a remark, that mutations of p53 and c-myc are found 50% in cancer. Objective: Aims of this research were to know the relationship between the mouth squamous cell carcinoma (MSCC) with HPV infection, the presence of p53, and c-myc genes mutation. Methods and Material: Tissue biopsy frozen sections from Benign Mouth Squamous Cell (BMSC) and MSCC patients were collected from Mouth and Dental Department of Muwardi District Hospital in Solo—Indonesia. To amplify L1-HPV gene for fixed the HPV etiology, amplified p53 and c-myc genes continued with SSCP analysis and followed with measurement using densitometer to see mutation existence. The collected data were analyzed with Chi Square Test. Results: None of the sample of patients with BMSC with positive HPV showed p53 gene mutation or c-myc gene. From eleven samples obtained from patients with MSCC who were positive HPV showed 18.2% had mutations in the p53 gene and 9.1% had mutations in c-myc gene. The chisquare test was shown to have significant differences between the MSCC with HPV infection and the presence of p53 and c-myc genes mutation. Conclusion: HPV is a risk ingredient for MSCC.

EXPRESSION OF P53 AND C-MYC IN MOUSE LUNG CANCER INDUCED BY COAL BURNING

Previous epidemiological studies have shown association between coal burning and human lung cancer.To confirm relationship between coal burning and lung cancer formation and progression the expression of p53 and c-myc in 13 mouse lung cancer induced by coal burning smoke and 5 mouse lung tissue control was studied by DNA-RNA in situ hybridization (ISH). Nine of 13 specimens showed c-myc overexpression but it occurred only 1 of adjacent tissue. There was over pression of p53 mRNA in all 13 lung cancer and 5 adjacent tissue. None in the controls was expression of P53 and c-myc detected. When compared to controls,there was significant higher expression of c-myc gene (P=0.002) and p53 gene (P=0.0001 ).The results confirm that overexpression of p53 and c-myc are common molecular events of lung cancer by coal burning smoke and provide further evidence that smoke from coal burning is a causative agent of lung cancer.

大黄素对肝癌细胞SMMC-7721抑制作用及P_(53)、C-myc蛋白的表达

目的 研究大黄素对肝癌细胞 SMMC-7721 的生长抑制作用和 P53、C-myc 蛋白的表达。方法 应用 MTT法观察大黄素、5-FU 对 SMMC-7721 的生长抑制作用,免疫组化法染色(SP 法)测定细胞凋亡时 P53、C-myc 蛋白的表达情况。结果 大黄素对肝癌细胞 SMMC-7721 有明显的生长抑制作用,其 IC50为 21.6 mol/L。大黄素对 SMMC-7721的抑制作用优于 5-FU(P<0.05);大黄素作用于细胞后,P53、C-myc 蛋白均有一定程度下调,而 C-myc 下调较 P53明显。结论 大黄素对 SMMC-7721 有明显的生长抑制作用,作用于 SMMC-7721 后 P53、C-myc 蛋白的表达均有下调。

CyclinD1 c-myc和p53的表达与肝细胞癌生物学行为关系

目的:探讨肝细胞癌(Hepatocellularcarcinoma,HCC)及癌旁肝组织CyclinD1、c-myc及p53蛋白表达的意义及其与肝癌生物学行为关系。方法:采用EnVisionTMplus免疫组织化学方法检测CyclinD1、c-myc及p53蛋白在52例HCC及癌旁肝组织中的表达。结果:CyclinD1及c-myc在HCC组织中的阳性率明显高于在癌旁肝组织中的阳性率(P<0.05),在HCC中p53的阳性表达与CyclinD1、c-myc的阳性表达呈正相关(r=0.4637,P=0.0022、r=0.3445,P=0.0273,);CyclinD1、c-myc及p53在人肝癌组织中的检出率与肝外转移、术后复发及肿瘤分化程度明显有关(P<0.05),CyclinD1的检出率与门静脉癌栓明显有关(P<0.05),p53的检出率与血清AFP和TSGF水平有显著性差异(P<0.05);CyclinD1、c-myc及p53的检出率与临床分期、肿瘤大小、肿瘤个数、HBsAg状况无明显关系。结论:CyclinD1、c-myc及p53蛋白的过表达可促使肝癌细胞增殖,使肝癌细胞具有更强的侵袭力,与肝癌的发生、发展密切相关。

Hp感染与胃癌及癌前病变中p53、bcl-2、c-myc基因表达关系的研究

目的:研究幽门螺杆菌(Hp)感染的胃癌及癌前病变患者胃粘膜p53、bcl-2、c-myc基因的表达,以探讨Hp在胃癌发生、发展过程中的作用机制。方法:应用免疫组化方法测定60例胃癌组织、18例异型增生、29例肠上皮化生、35例萎缩性胃炎、29例浅表性胃炎组织中bcl-2、c-myc基因蛋白表达情况,PCR/SSCP测定p53基因第5～8外显子突变,Hp阳性由快速尿素酶法和HE染色确定。结果:胃癌组Hp阳性41例,阴性19例。在胃癌组织中p53、bcl-2、c-myc基因阳性表达分别为38例(63.3%)、38例(63.3%)、18例(30.0%)。p53、c-myc基因在胃癌中阳性表达率显著高于异型增生(P<0.05)。bcl-2在异型增生组织中的阳性表达率与胃癌、肠上皮化生相比无显著性差异(P>0.05)。p53、bcl-2、c-myc基因表达与胃癌分期、淋巴结转移均无显著性关系(P>0.05),但bcl-2与胃癌类型、分化程度显著相关(P<0.05)。每一种病变类型Hp阳性组p53、bcl-2、c-myc基因蛋白的阳性表达率均高于Hp阴性组,两者之间有显著性差异(P<0.05)。结论:Hp感染者具有更多肿瘤生物学行为,可以引起抑癌基因p53第5～8外显子突变,癌基因c-myc、凋亡调节基因bcl-2表达增加,Hp可能为促癌剂,在胃癌的发生发展中起一定作用。

幽门螺杆菌感染与C-myc基因和P53基因表达与胃癌的相关性研究

目的探讨幽门螺杆菌(Hp)感染情况与C-myc基因及P53基因的表达与胃癌的相关性。方法用W-S染色法观察不同胃病黏膜组织中Hp感染情况,采用免疫组化检测技术检测不同胃病组织的C-myc基因和P53基因表达产物。结果胃癌及癌前病变组Hp感染率明显高于慢性浅表性胃炎组(P<0.01),C-myc基因和P53基因的表达也显著高于慢性浅表性胃炎组(P<0.01)。Hp感染阳性组的C-myc基因和P53基因表达明显高于Hp感染阴性组(P<0.01)。结论Hp感染可能通过激活C-myc基因,同时使P53基因失活从而诱发胃黏膜的癌变。

伴神经内分泌分化非小细胞肺癌中p53、bcl-2及c-myc的表达

目的 研究伴神经内分泌 (neuroendocrine,NE)分化的非小细胞肺癌 (NSCLC)中p53、bcl 2和c myc的特异性表达。方法 随机搜集 60例手术切除的NSCLC石蜡标本 ,采用免疫组化S P法检测神经元特异性烯醇化酶 (NSE)、嗜铬颗粒蛋白A(CgA)、突触素 (Syn)及p53、bcl 2、c myc基因蛋白的表达。结果 NSCLC中NSE、CgA、Syn的阳性表达率分别为 45 .0 0 % (2 7/ 60 )、1 3 .33% (8/ 60 )、31 .67% (1 9/ 60 )。结合三者的表达确定伴有NE分化的占 41 .67% (2 5/ 60 ) ;NE分化与肺癌的分化程度有密切关系 (P <0 .0 5) ;伴神经内分泌分化非小细胞肺癌 (NSCLC NE)的转移率较高 ,临床分期较高。NSCLC NE中bcl 2、p53和c myc的阳性表达率分别为68.0 0 % (1 7/ 2 5)、80 .0 0 % (2 0 / 2 5)和 68.0 0 % (1 7/ 2 5) ,其中bcl 2、p53的表达与NE分化有密切关系 (P <0 .0 5)。结论 NSCLC中有相当一部分伴有NE分化 ,NSCLC NE具有与其它NSCLC不同的生物学特性。NSCLC NE中可以检测到高表达的bcl 2蛋白、突变型p53蛋白 ,p53突变导致的bcl 2 /Bax的失衡在NSCLC

EB病毒、p53、bcl-2、c-myc和Rb蛋白在非霍奇金淋巴瘤发病及病情演化中的价值

目的:探讨EB病毒(EBV)与bcl-2、突变型p53、c-myc和Rb蛋白在非霍奇金淋巴瘤(NHL)发病及病情演化中的价值。方法:用免疫组化S-P法对140例NHL进行EBV、bcl-2、突变型p53、c-myc和Rb蛋白检测,并选择同期增生性淋巴结炎51例作为对照组。结果:EBV、p53、bcl-2和c-myc蛋白在NHL表达的阳性率和Rb蛋白表达的阴性率均高于对照组,两组比较差异有显著性(P<0.05);EBV与突变型p53、bcl-2、Rb、c-myc蛋白在NHL中表达无相关性(P>0.05);突变型p53、bcl-2在不同恶性程度NHL中的表达有显著性差异(P<0.05);EBV、突变型p53、bcl-2、Rb、c-myc蛋白在不同临床分期NHL中的表达有显著性差异(P<0.05)。结论:EBV、突变型p53、bcl-2、和c-myc蛋白与NHL的发病存在正相关关系,Rb蛋白则为负相关关系;EBV和突变型p53、bcl-2、c-myc、Rb蛋白在NHL的发病中系相对独立的因素;突变型p53、bcl-2蛋白表达与NHL恶性程度成正相关关系;EBV、突变型p53、bcl-2、和c-myc蛋白与NHL病情恶化成正相关关系,Rb蛋白则为负相关关系。

急性白血病细胞bcl-2、c-myc和p53基因表达的研究

目的 :研究bcl 2、c myc、p53基因在急性白血病 (AL)细胞中的表达及其与AL的分型、临床特征、疗效及预后因素的关系。方法 :采用免疫组化方法检测 54例初治AL骨髓细胞bcl 2、c myc、p53蛋白表达情况 ,分析其与FAB分型、临床特征、疗效及预后因素的关系。结果 :AL骨髓细胞中bcl 2、c myc及 p53基因的表达显著高于正常对照组 (P <0 .0 5)。bcl 2、c myc、p53基因表达在急性髓系白血病 (AML)与急性淋巴细胞白血病(ALL)差异不显著 ;在AML亚型中 ,bcl 2在M4 及M5中的表达高于M1 、M2 和M3(P <0 .0 5) ;而c myc及p53的表达在各亚型中差异无显著性意义 (P >0 .0 5)。bcl 2的表达与初诊时的白细胞数呈正相关 (r =0 .44,P <0 .0 5) ,与疗效呈负相关 (r =- 0 .40 ,P <0 .0 5) ,与c myc的表达呈正相关 (r =0 .51 ,P <0 .0 5) ;c myc的表达与初诊时的白细胞数呈正相关 (r =0 .50 ,P <0 .0 5)。结论 :bcl 2、c myc、p53基因的紊乱可能在AL的发病中起着重要作用 ,还与白血病的某些临床特征。

慢性缺氧大鼠肺内(肺血管壁)细胞增殖、凋亡及c-myc、p53基因表达研究

目的和方法：应用免疫组织化学、原位末端标记技术及Ｎｏｒｔｈｅｒｎ杂交等方法检测慢性缺氧大鼠肺内特别是肺血管壁细胞增殖、凋亡及相关基因ｃｍｙｃ、ｐ５３表达。结果：正常及慢性缺氧大鼠肺内检出一定比率的增殖、凋亡阳性细胞，两类细胞在肺内呈不均匀散在分布。在缺氧大鼠肺内，增殖阳性细胞绝大部分是肺小血管壁细胞，凋亡性染色细胞在肺小血管壁上较对照组少见。缺氧１、２周组大鼠肺内细胞增殖指数显著增高而凋亡指数显著减少，细胞增殖凋亡比值分别约为对照组３与３５倍。ｃｍｙｃ及ｐ５３是细胞增殖、凋亡密切相关的两种癌（抑癌）基因，前者在缺氧大鼠肺内表达显著增加，而后者（野生型）表达显著减少。结论：可能由于ｃｍｙｃ及ｐ５３基因异常表达所致的细胞增殖、凋亡失衡参与了慢性缺氧性肺血管结构改建的调节。

脂肪肉瘤c-myc和p53基因蛋白的表达及意义

背景与目的:原癌基因c-myc和抑癌基因p53与脂肪肉瘤的关系的研究较少,脂肪肉瘤中是否存在p53基因突变文献报道不一,本文拟探讨脂肪肉瘤中c-myc、p53基因蛋白表达的水平及意义,以期为本组肿瘤发生发展及病理诊断、鉴别诊断提供一定的分子生物学资料。方法:采用链菌素抗生物素-生物素(labelledstreptavidin-biotin,LSAB)免疫组化法、聚合酶链反应-单链构象多态性分析(Singlestrandconformationpolymorphismanalysisofpolymerasechainreactionproducts,PCR-SSCP)及DNA序列分析方法。结果:c-myc和p53蛋白在脂肪肉瘤表达阳性率分别为38.09%(16/42)和48.08%(25/52)。不同类型脂肪肉瘤,分化良好者阳性率均明显低于分化较差者。脂肪肉瘤中c-myc和p53蛋白表达呈正相关。c-myc和p53蛋白表达在原发者和复发者之间的差异均无统计学意义。p53第6、7、8外显子PCR-SSCP分析,2例多形性脂肪肉瘤出现异常泳动带。DNA序列分析证实1例第8外显子第268位编码区出现错义突变(AAC→ATC),另1例第6外显子第221位编码区出现可疑杂合性同义突变(GAG→GAA)。结论:c-myc和p53蛋白与脂肪肉瘤的形成及分化和恶性程度有关,它们可作为判断脂肪肉瘤分化程度及恶性程度参考指标之一,但与肿瘤复发无关。在脂肪肉瘤发生发展中两者可能起协同作?

视黄酸对胃癌细胞生长和p53及c-myc基因表达的影响

目的：探讨视黄酸对胃癌细胞生长和基因表达的影响。方法：以ＭＴＴ法测定细胞生长，软琼脂集落形成实验测定癌细胞恶性程度，Ｎｏｒｔｈｅｒｎｂｌｏｔ测定ｐ５３及ｃｍｙｃ基因表达水平。结果：１０－６ｍｏｌ／Ｌ全反式视黄酸（ＡＴＲＡ）能够有效地抑制ＭＧｃ８０３和ＢＧＣ８２３细胞生长，但不能抑制ＭＫＮ４５细胞生长；ＡＴＲＡ还能够降低３株胃癌细胞形成集落的能力。ＭＧｃ８０３和ＢＧＣ８２３细胞经ＡＴＲＡ诱导后，ｐ５３基因的表达水平提高，ｃｍｙｃ基因的表达水平下降，但ＭＫＮ４５细胞中ｐ５３基因和ｃｍｙｃ基因表达与ＡＴＲＡ诱导无关。视黄酸受体ＲＡＲα基因在３株细胞中呈低水平表达，经ＡＴＲＡ诱导后，在ＭＧｃ８０３和ＢＧＣ８２３细胞中表达水平提高，但在ＭＫＮ４５细胞中表达水平不变。

喉癌切缘中eIF4E、p53、ras和c-myc表达与预后的研究

【目的】探讨eIF4E、p53、ras和c-myc在喉癌切缘中的表达及其与预后的关系。【方法】42例临床分期为Ⅱ、Ⅲ期的喉癌患者被分别行手术治疗,共得喉癌切缘标本112个,采用免疫组化的方法检测肿瘤原发灶和切缘中eIF4E、p53、ras和c-myc的表达。【结果】喉癌原发灶eIF4E、p53、ras和c-myc阳性率分别是100%(42/42),57.1%(24/42),40.5%(17/42)和33.3%(14/42);手术切缘eIF4E、p53、ras、c-myc和两个以上基因阳性率分别是42.8%(18/42)、14.3%(6/42)、9.5%(4/42),9.5%(4/42)和21.4%(9/42),生存分析提示切缘eIF4E、p53或两个以上基因阳性组复发率高,5年生存率低;COX回归分析提示切缘eIF4E表达阳性与预后相关。【结论】喉癌切缘eIF4E阳性的患者复发率高,预后不良。eIF4E在喉癌手术切缘的表达可考虑作为预测喉癌预后的独立风险指标。