Expression of ras gene in experimental hepatocarcinogenesis in tree shrews

Objective: In order to investigate the relationship between the expression of ras gene and the development of hepatocellular carcinoma (HCC). Materials and Methods: The experimental tree shrews were divided into four groups: group A, infected human hepatitis B virus (HBV) and exposed to aflatoxin B1 (AFB1); group B, infected human HBV alone; group C, only exposed to AFB1; group D, use as controls. The serial bioptic liver tissues were detected for ras p²¹ protein using immunohistochemical method. Results: The total p²¹ protein positive rates in group A, B, C and D were 35.3%, 5.3%, 13.3%, 0, respectively, thus the significant difference were showed between group A and group B (P<0.05); The HCC incidences in group A, B, C and D were 47.1%, 0, 13.3%, 0, respectively, and there was a significant difference between group A and C (P<0.05). The incidences of HCC in the animals with and without p²¹ protein positive in group A were 100% and 18.2%, respectively, and there was a significant difference among them (P<0.01). Conclusion: HBV and AFB1 play a remarkable synergistic role in the development of HCC; they can enhance the expression of ras gene. The over-expression of ras gene is closely related to pathogenesis of HCC in tree shrews. This study was supported by National Natural Science Foundation of China (No. 39260033).     

茶多酚在树肝癌形成中的化学预防作用

目的　探讨茶多酚对黄曲霉素B1(AFB1)和乙型肝炎病毒(HBV)诱发树肝细胞癌作用的影响。方法　成年树分成三组:A组(AFB1+HBV+茶多酚组)、B组(AFB1+HBV组)和C组(空白对照组),实验期间定期抽血检查HBV感染标志和进行剖腹手术取肝组织活检,观察各组肝癌发生率、肝癌出现时间、HBV感染持续时间,并采用免疫组化方法检测肝癌形成过程中p53、bcl- 2、bax、survivin、GSTA1、SOD1、IL -2和SCF等蛋白在各组各时段的表达情况。结果　在实验第90、105、120、135、150、165周各个时段中,A组的肝癌发生率均低于B组;A组首例肝癌出现时间及肝癌平均出现时间均晚于B组;A组HBV感染标志(HBsAg,HBeAg和HBcAb)的平均持续时间短于B组;在诱癌中期(实验第60 周)及肝癌组织内突变型p53、凋亡抑制基因bcl -2和survivin蛋白的表达率均为A组低于B组。但上述差异在统计学上大部分无显著性。结论　茶多酚对黄曲霉毒素B1和HBV诱发树肝癌有一定程度的保护作用;可以促进树体内的HBV感染标志的消除。茶多酚可能是通过促进终致癌物的解毒、抗氧化作用、提高免疫功能、诱导肿瘤细胞凋亡等途径起到预防树肝癌的作用。     

乙肝病毒/黄曲霉毒素双暴露因素下肝癌13号染色体畸变以及RB1基因表达的初步研究

目的探讨乙肝病毒/黄曲霉毒素双暴露下肝细胞性肝癌(hepatocellular carcinoma,HCC)13号染色体遗传学改变的特点,以及对定位于13q14.2基因座位点抑癌基因RB1的影响。方法 32例手术切除且经病理证实为HCC的癌组织,按照乙肝病毒与黄曲霉毒素的暴露情况,分为4个亚组:A组HBV(+)/AFB1(+)10例;B组HBV(+)/AFB1(-)10例;C组HBV(-)/AFB1(+)6例;D组HBV(-)/AFB1(-)6例。应用微阵列比较基因组杂交技术(ArrayCGH)检测包括13号染色体在内的23对染色体区段的变化情况,并通过RT-PCR检测RB1mRNA的表达情况。结果 32例中有15例染色体13q14.2发生缺失,缺失率为46.9%(15/32)。13q14.2缺失的发生频率在A组、B组、C组、D组中分别为80.0%(8/10)、50.0%(5/10)、33.3%(2/6)和0%(0/6)。其中A组分别与C组、D组比较,差异具有统计学意义(P<0.05);B组与D组比较,差异亦有统计学意义(P<0.05)。RT-PCR检测显示RB1mRNA的表达半定量灰度值在13q14.2缺失组中显著低于13q14.2无缺失组(P=0.003)。结论染色体13q畸变在HCC中是一个常见的分子生物学事件,其中13q14.2的缺失可能与HBV和AFB1双暴露的协同作用有关,HCC中13q14.2的缺失是导致RB1基因失活的因素之一。     

用原位杂交对树鼩肝组织乙型肝炎病毒DNA定位及其与黄曲霉毒素B_1在肝癌发生中的作用

用生物素标记的HBV DNA探针对经83～158周实验的55只树鼩肝组织的福尔马林固定、石蜡包埋的切片进行原位分子杂交研究。在45只接种过人HBV的树鼩中,有30只在肝细胞检出HBV DNA。这55只树鼩,有41只摄入了AFB_1,其中肝细胞HBV DNA阳性的A组22只,有10只发生了HCC;19只HBVDNA阴性的B组,只发生2例HCC,两组差别显著(P<0.05)。未接触过AFB_1的14只树鼩中,肝细胞HBVDNA阳性的8只(C组),发生1例HCC;而HBV DNA阴性的6只(D组)无HCC发生。提示HBV和AFB_1在诱发树鼩HCC中起协同作用;并支持HBV感染与HCC存在病因学关系的观点。该实验HBV DNA阳性物质主要分布于癌外肝细胞胞浆内,少数位于肝细胞核。癌组织内HBV DNA阳性率低于癌外肝组织。与在人肝癌研究的结果一致。表明树鼩是研究HBV致癌分子机理的较好的模型。     

广西乙肝病毒／黄曲霉毒素B1双暴露人肝细胞癌中PTENmRNA表达及突变的初步研究

目的探讨乙肝病毒／黄曲霉毒素B1双暴露相关肝细胞性肝癌（HCC）中PTEN基因的突变特点及其mRNA的表达水平。方法108例HCC来自广西不同地区样本,按照乙肝病毒与黄曲霉毒素的暴露情况,分为4个亚组：A组：HBV（＋）／AFB1-DNA（＋）,共48例;B组：HBV（＋）／AFB1-DNA（-）,共27例;C组：HBV（-）／AFB1-DNA（＋）,共19例;D组：HBV（-）／AFB1-DNA（-）,共14例。采用PCR联合基因直接测序法,检测108例肝癌组织中PTEN基因第4、5、8外显子的突变情况。同时采用RT—PCR法检测其基因mRNA的表达状况。结果（1）PTEN基因第4、5、8外显子测序结果未发现发生在外显子上的突变。但在第4外显子与第4内含子交界处有61例发生大片段的缺失,缺失率为56.4％。②PTEN缺失率在A、B、C、D组中分别为60．4％、62．9％、47．3％和46．6％,其差异在4个亚组间均无统计学意义（P〉0．05）。@PTENmRNA在4个亚组中的表达半定量灰度值分别为：A组：0．54±0．13;B组：0．59±0．16;C组：0．97±0．16;D组：0．92±0．13。其中,A、B组分别与C、D组相比,其差异均具有统计学意义（PAC=0．002,PAD=0．032,PBC=0．000,PBC=0．011）。结论在广西乙型肝炎病毒／黄曲霉毒素B1的双暴露肝细胞癌中,PTENmRNA的表达下调是一个常见的分子生物学事件,PTENmRNA表达下调可能主要与HBV感染有关。AFB1对PTENmRNA的表达下调可能有协同作用。     

A study on sequence variations in pre‐S/surface,X and enhancer II/core promoter/precore regions of occult hepatitis B virus in non‐B,non‐C hepatocellular carcinoma patients in Taiwan

This study was to investigate the clinical significance and virologic factors of occult hepatitis B virus (HBV) infection in hepatocellular carcinoma (HCC) patients without hepatitis B surface antigen (HBsAg) or anti‐hepatitis C virus (non‐B, non‐C) in Taiwan. Serum HBV DNA (occult HBV) was detected in 90 of 222 non‐B, non‐C HCC patients and 24 of 300 non‐B, non‐C controls without HCC. Of 90 occult HBV‐infected HCC patients, the sequences of HBV pre‐S/surface, X and enhancer II/core promoter/precore genes were analyzed from 40 patients. Direct sequencing of such genes was also performed in 24 non‐B, non‐C controls without HCC and 40 HBsAg‐positive HCC controls. Compared with non‐B, non‐C controls without HCC, non‐B, non‐C subjects with HCC had significantly higher prevalence of occult HBV (p < 0.0001). Moreover, M1I and Q2K in pre‐S2 gene and G1721A were more common in occult HBV‐infected patients with HCC than in those without HCC. Compared with the HBsAg‐positive HCC controls, occult HBV‐infected HCC patients had higher frequencies of M1I and Q2K in pre‐S2 gene, G185R and S210N in surface gene, A36T and A44L in X gene, and G1721A in enhancer II gene, and had lower rates of pre‐S deletions and A1762T/G1764A, A1846T, G1896A and G1899A in core promoter/precore genes. Multivariate analysis showed Q2K in pre‐S2 gene, G1721A and A1846T were independent factors for occult HBV‐infected HCC. Our study suggested that the virological factors of HBV related to HCC were different between occult HBV‐infected and HBsAg‐positive patients. The G1721A, M1I and Q2K in pre‐S2 gene may be useful viral markers for HCC in occult HBV carriers. © 2009 UICC     

树鼩肝癌形成过程中p53和Bax的蛋白表达及其二者间的关系

目的：动态研究在树鼩肝癌形成过程中p53和Bax的蛋白表达以及它们之间的关系。方法：利用免疫组织化学S—P法，对实验组35例树鼩肝癌形成过程第30周、60周的肝癌组织及13例同期的空白对照组树鼩肝活检组织，进行p53、Bax蛋白的检测。结果：053、Bax基因在树鼩HCC形成过程中，它们的表达均呈递增趋势。结论：p53、Bax基因的表达无明显依存关系。动态观察Bax的表达对预测肝癌有一定作用。     

通过新生树鼩乙型肝炎病毒感染模型动态观察宿主体内TLR-4和IL-6的表达

目的 通过观察接种乙型肝炎病毒（hepatitis B virus,HBV）后新生树鼩体内细胞因子TLR-4和IL-6的变化,初步探讨HBV感染过程中宿主体内的免疫反应。方法 将31只树鼩幼崽分为实验组（n=25）和对照组（n=6）。实验组接种人HBV,接种后第8周至第24周定期检测树鼩外周血中乙肝表面抗原（HBsAg）和HBV- DNA,根据检测结果将实验组分为慢性感染组7只（血清HBsAg或HBV-DNA持续阳性时间达到24周）和疑似慢性感染组5只（血清HBsAg或HBV-DNA不连续出现2次或2次以上阳性）,其余13只HbsAg和HBV-DNA均阴性,不纳入研究;对照组不做任何处理。采用双抗体夹心法检测树鼩外周血TLR-4、IL-6蛋白表达水平,RT-PCR法检测树鼩肝组织中TLR-4、IL-6 mRNA的表达水平。 结果 观察期间内,慢性感染组和疑似慢性感染组外周血TLR-4与IL-6蛋白的表达均高于对照组（P＜0.05）;肝组织中IL-6的mRNA表达水平高于对照组（P＜0.05）;慢性感染组TLR-4 mRNA表达水平高于对照组（P＜0.05）。结论 TLR-4、IL-6在树鼩HBV感染模型中表达升高,可能在HBV感染过程中起重要作用。     

乙肝病毒/黄曲霉毒素B1双暴露相关性肝细胞癌的p53基因249位点突变与p53蛋白表达的关系

目的研究乙肝病毒/黄曲霉毒素B1双暴露相关性肝细胞癌的p53基因249位点突变与p53蛋白表达关系。方法通过IHG特殊免疫组织化学法检测55例手术切除经病理证实为原发性肝癌的HCC组织及10例正常肝组织中AFB1-DNA加合物的暴露情况,并根据是否同时存在HBV暴露加以分组,通过免疫组化S-P法检测并比较各组间p53蛋白的表达情况。同时,通过PCR结合直接测序的方法检测其p53基因第7外显子249密码子的突变情况。结果 p53基因第7外显子249位点的突变在实验组A与对照组C中均具有较高阳性突变率,其突变率分别为68.75%（22/32）、63.64%（7/11）,在对照组B中的突变率较低,为16.67%（2/12）,在正常对照组中无1例出现有突变。其中实验组A与对照组B及正常对照组D的比较差异具有统计学意义（P〈0.05）,而与对照组C比较差异无统计学意义（P〉0.05）;p53蛋白在其基因249位点突变阳性组与阴性组中的表达阳性率分别为92.86%（26/28）、60.87%（16/27）,差异具有统计学意义（P〈0.05）。结论 HCC的发生过程中,AFB1暴露与p53第7外显子249位点的突变密切关系相关,当同时存在乙肝病毒暴露的协同作用的情况下突变率更高;p53基因的突变可能是造成HCC中p53蛋白高表达的重要因素之一。     

原发性肝癌与乙型肝炎病毒X区基因变异的关系初探

目的 探讨乙型肝炎病毒X区基因变异与原发性肝癌的关系。方法 39例乙型肝炎病毒（HBV）感染患者的组织标本中,慢性肝病（CHB）14例、肝细胞癌（HCC）25例。采用聚合酶链反应（PCR）方法扩增组织中HBV X区基因,并对PCR产物进行DNA测序,分析常见变异位点的变异情况。结果 与CHB组相比,HCC组在X区发生插入或缺失变异及联合变异的位点及例数增多,并且A1762T与G1764A常发生双突变。HBV X 区变异频率较高位点依次为：C1655T／G、A1605C／G、A1762T、G1764A、A1772B、A1645C、C1687A、G1776T。结论 HBV X区存在点突变、插入或缺失变异及联合变异,可能在HCC的发生发展过程中起重要作用。     

Hepatitis B Virus Genetic Variation and TP53 R249S Mutation in Patients with Hepatocellular Carcinoma in Thailand

Chronic hepatitis B virus (HBV) infection and dietary exposure to aflatoxin B1 (AFB1) are major risk factorsfor hepatocellular carcinoma (HCC). The aim of this study was to evaluate the role of HBV genetic variationand the R249S mutation of the p53 gene, a marker of AFB1-induced HCC, in Thai patients chronically infectedwith HBV. Sixty-five patients with and 89 patients without HCC were included. Viral mutations and R249Smutation were characterized by direct sequencing and restriction fragment length polymorphism (RFLP)in serum samples, respectively. The prevalences of T1753C/A/G and A1762T/G1764A mutations in the basalcore promotor (BCP) region were significantly higher in the HCC group compared to the non-HCC group.R249S mutation was detected in 6.2% and 3.4% of the HCC and non-HCC groups, respectively, which was notsignificantly different. By multiple logistic regression analysis, the presence of A1762T/G1764A mutations wasindependently associated with the risk of HCC in Thai patients.     

肝细胞癌患者B和C基因型乙型肝炎病毒X蛋白的变异特点

背景与目的：X蛋白是乙型肝炎病毒(hepatitis B virus,HBV)最重要的致病因子之一,它在HBV相关性肝细胞癌(hepatocellular carcinoma,HCC)的发生发展中起着重要作用。目前已知B、C基因型HBV相关性HCC的临床及病理表现不尽相同,但目前尚不清楚这种差别是否与B、C基因型HBV X基因之间的差别有关。因此本实验拟研究B、C基因型间HBV X蛋白氨基酸差异及其在HCC患者中的变异及特点,初步探讨其与HCC发生、发展的关系。方法：PCR扩增22份乙型肝炎病毒表面抗原(HBsAg)阳性HCC患者血清HBV X基因,克隆、测序并以Vector NTI6．0软件分析其基因型。以DNAMAN软件对标准HBV及HCC来源的HBV X蛋白进行氨基酸同源分析。结果：检测的22个HBV X基因片段均属于B或C基因型。B、C基因型HBV X蛋白之间存在14个氨基酸的差异,HCC患者来源的B、C型HBV X蛋白存在4个氨基酸的共有变异,C型HBV X蛋白尚有6个型特异性变异。这些差异或变异氨基酸均位于X蛋白B、T细胞表位或反式激活区及调节区内。结论：B、C基因型HBV X蛋白之间存在氨基酸差异,且在HCC中发生基因型特异性变异,这些差异或变异氨基酸可能导致X蛋白免疫学功能及反式激活功能的不同。     

广西乙肝病毒/黄曲霉毒素B1双暴露人肝细胞癌中PTEN mRNA表达及突变的初步研究

目的探讨乙肝病毒/黄曲霉毒素B1双暴露相关肝细胞性肝癌(HCC)中PTEN基因的突变特点及其mRNA的表达水平。方法 108例HCC来自广西不同地区样本,按照乙肝病毒与黄曲霉毒素的暴露情况,分为4个亚组:A组:HBV(+)/AFB1-DNA(+),共48例;B组:HBV(+)/AFB1-DNA(-),共27例;C组:HBV(-)/AFB1-DNA(+),共19例;D组:HBV(-)/AFB1-DNA(-),共14例。采用PCR联合基因直接测序法,检测108例肝癌组织中PTEN基因第4、5、8外显子的突变情况。同时采用RT-PCR法检测其基因mRNA的表达状况。结果①PTEN基因第4、5、8外显子测序结果未发现发生在外显子上的突变。但在第4外显子与第4内含子交界处有61例发生大片段的缺失,缺失率为56.4%。②PTEN缺失率在A、B、C、D组中分别为60.4%、62.9%、47.3%和46.6%,其差异在4个亚组间均无统计学意义(P>0.05)。③PTEN mRNA在4个亚组中的表达半定量灰度值分别为:A组:0.54±0.13;B组:0.59±0.16;C组:0.97±0.16;D组:0.92±0.13。其中,A、B组分别与C、D组相比,其差异均具有统计学意义(PAC=0.002,PAD=0.032,PBC=0.000,PBD=0.011)。结论在广西乙型肝炎病毒/黄曲霉毒素B1的双暴露肝细胞癌中,PTEN mRNA的表达下调是一个常见的分子生物学事件,PTEN mRNA表达下调可能主要与HBV感染有关。AFB1对PTEN mRNA的表达下调可能有协同作用。     

The KIF1B (rs17401966) Single Nucleotide Polymorphism is not Associated with the Development of HBV-related Hepatocellular Carcinoma in Thai Patients

Hepatitis B virus (HBV) infection can become chronic and if left untreated can progress to hepatocellularcarcinoma (HCC).Thailand is endemic for HBV and HCC is one of the top five cancers, causing deaths amongThai HBV-infected males. A single nucleotide polymorphism (SNP) at the KIF1B gene locus, rs17401966,has been shown to be strongly associated with the development of HBV-related HCC. However, there are noThai data on genotypic distribution and allele frequencies of rs17401966. Thai HBV patients seropositivefor HBsAg (n=398) were therefore divided into two groups: a case group (chronic HBV with HCC; n=202)and a control group (HBV carriers without HCC; n=196). rs17401966 was amplified by polymerase chainreaction (PCR) and analyzed by direct nucleotide sequencing. The genotypic distribution of rs174019660for homozygous major genotype (AA), heterozygous minor genotype (AG) and homozygous minor genotype(GG) in the case group was 49.5% (n=100), 40.1% (n=81) and 10.4% (n=21), respectively, and in controlswas 49.5% (n=97), 42.3% (n=83) and 8.2% (n=16). Binary logistic regression showed that rs17401966 wasnot statistically associated with the risk of HCC development in Thai chronic HBV patients (p-value=0.998,OR=1.00 and 95% CI=0.68-1.48). In conclusion, the KIF1B gene SNP (rs174019660) investigated in thisstudy showed no significant association with HBV-related HCC in Thai patients infected with HBV,indicating that there must be other mechanisms or pathways involved in the development of HCC.     

HBV感染与hTERT基因表达在肝细胞癌组织中的相关性研究

目的 :研究hTERT基因在HBsAg阳性与阴性肝细胞癌 (hepatocellularcarcinoma ,HCC)患者组织中表达的差异 ,探讨HBV病毒感染与hTERT基因表达在HCC中的相关性。方法 :应用免疫组化 (SP法 )和半定量逆转录聚合酶链反应 (RT PCR)分别检测 73例HCC患者组织中hTERT蛋白及其mRNA的表达情况 ,其中HBsAg阳性 5 3例 ,HBsAg阴性 2 0例 ,比较二者表达的差异。结果 :hTERT蛋白在HBsAg阳性HCC组织中的阳性表达为 48/5 3 ,在HBsAg阴性HCC组织中阳性表达为 12 /2 0 ,两组病例hTERT蛋白表达阳性率差异有统计学意义 ,P <0 0 1;hTERTmRNA在HB sAg阳性HCC组织中阳性表达为 46/5 3 ,hTERTmR NA在HBsAg阴性HCC组织中阳性表达为 11/2 0 ,两组病例hTERTmRNA表达阳性率差异有统计学意义 ,P <0 0 5 ;统计学分析显示 ,HCC中HBsAg与hTERTmRNA的表达有显著关联性 ,与hTERT蛋白的表达强度成系统性的线性趋势 ,P <0 0 1。结论 :HBsAg阳性HCC组织中hTERT基因表达的阳性率和阳性强度均明显高于HBsAg阴性HCC组织 ,差异有统计学意义 ,P <0 0 5 ;HCC中HBV病毒感染与hTERT基因表达之间具有相关性 ,提示在HCC发生发展中可能存在二者的相互作用     

肝癌患者乙型肝炎病毒全基因组结构分析

目的 研究肝细胞癌患者乙型肝炎病毒(hepatitis B virus,HBV)全基因组的结构及特点。方法 PCR扩增并克隆乙型肝炎病毒表面抗原(HBsAg)阳性肝癌患者血清中HBV全基因组DNA,测序并进行基因结构分析。结果 获得不同肝癌患者来源的22株HBV全基因组DNA,均属于C或B基因型和adr或adw2血清型。与标准株相比,肝癌患者来源的HBV在表面抗原、核心抗原的B／T细胞表位、X蛋白的反式激活区及增强子Ⅱ、核心启动子区发生了一些有意义的共有变异。结论 HBV的基因型与基因变异可能与HBV相关性肝癌的发生发展有关。     

血小板衍生生长因子-D在肝细胞肝癌中的表达及其临床意义

目的研究血小板衍生生长因子(PDGF) D在肝细胞肝癌(HCC)中的表达及其与临床病理指标的关系。方法用RT-PCR方法检测PDGF-A、B、C、D及其受体PDGFRα和PDGFRβ基因在40例肝癌组织及对应的30例癌旁组织和10例正常肝组织标本中mRNA的表达。结果HCC组织中PDGF-A、B、C、D及其受体PDGFRα和PDGFRβ阳性表达分别为37.5%(15/40)、70%(28/40)、52.5%(21/40)、92.5％(37/40)、22.5％(9/40)、42.5%(17/40);与其相对应的癌旁组织的阳性表达率分别为23.3％(7/30)、16.7%(5/30)、16.7%(5/30)、26.7%(8/30)、13.3%(4/30)、16.7%(5/30);而正常肝组织中未见表达。在HCC组织中PDGF家族的表达均显著高于癌旁组织和正常组织,三组比较差异有统计学意义(P＜0.01),且PDGF-D的阳性表达显著高于PDGFs其他亚型(P＜0.05)。在HCC、癌旁、正常肝脏组织中PDGF-D平均光密度值为0.5900±0.0364、0.3954±0.0654、0,三者比较差异有统计学意义(P＜0.01)。HCC组织中PDGF-D的阳性表达与肿瘤的分化程度、淋巴及转移有关（P＜0.05）;与年龄、性别、肿瘤大小、血清AFP的值及门静脉癌栓无关(P＞0.05)。结论PDGF家族中以PDGF-D表达率最高且与肿瘤的分化程度和转移相关,提示PDGF家族,尤其是PDGF-D在HCC的发生、发展和转移中可能发挥着重要的作用,可作为肝癌辅助诊断指标和治疗靶点。     

XRCC1 Gene Polymorphism Increases the Risk of Hepatocellular Carcinoma in Egyptian Population

Several major risk factors for hepatocellular carcinoma (HCC) have been identified, including chronic infection of hepatitis B virus (HBV) and hepatitis C virus (HCV). Nevertheless, only a fraction of infected patients develops HCC during their lifetime suggesting that genetic factors might modulate HCC development. X-ray repair cross complementing group1 (XRCC1) participates in the repair pathways of DNA. Aim: to investigate the association between XRCC1 gene polymorphism and HCC in Egyptian chronic hepatitis C patients. Methods: This study was assessed on 40 patients with HCC secondary to chronic HCV infection who were compared to 20 cirrhotic HCV patients and 40- age and gender- matched healthy control group. After collection of relevant clinical data and basic laboratory tests, c.1517G>C SNP of XRCC1 gene polymorphism was performed by (PCR-RFLP) technique. Results: A statistically higher frequency of XRCC1 (CC, GC) genotypes and increased (C) allele frequency in patients with HCC was found in comparison to cirrhotic HCV patients as well as control group. In addition, patients with the XRCC1 (CC, GC) genotypes had significantly higher number and larger size of tumor foci and significantly higher Child Pugh grades. Multivariate analysis showed that the presence of c.1517G>C SNP of XRCC1 gene is an independent risk for the development of HCC in chronic HCV patients with 3.7 fold increased risk of HCC development. In conclusion: XRCC1 gene polymorphism could be associated with increased risk of HCC development in chronic HCV Egyptian patients.     

Role of hepatitis B virus genotype mixture, subgenotypes C2 and B2 on hepatocellular carcinoma: compared with chronic hepatitis B and asymptomatic carrier state in the same area

The role of genotype mixture and subgenotypes remains controversial in determining the clinical outcome of chronic hepatitis B virus (HBV) infection. We aimed to determine their role on the development and the recurrence of hepatocellular carcinoma (HCC). HBV genotypes, serum viral load and hepatitis B e antigen (HBeAg) seroconversion were determined in 462 HCC patients, 234 chronic hepatitis patients and 425 asymptomatic carriers born in Eastern China. In the 462 HCC patients, 62 (13.4%), 337 (72.9%) and 49 (10.6%) had HBV subgenotype B2, C2 and genotype mixture, respectively. Genotype mixture in HCC patients and hepatitis patients was associated with higher viral load than HBV C2 (P = 0.012, P = 0.000) and more frequent than asymptomatic carriers (P = 0.005, P = 0.000). HBV C2 was more prevalent in HCC patients compared with controls. Proportion of HBV B2 in HCC patients decreased consecutively from <30 to 50-59 years group (P = 0.024). Age-related changes of HBeAg seroconversion were not consistent with serum viral load in HCC patients with HBV B2 and genotype mixture, quite in contrast to hepatitis patients. By multivariate regression analysis, age >or=40 years and serum viral load (>or=10 000 copies/ml) were independently associated with hepatocarcinogenesis, whereas age 相似文献   

微波固化治疗肝癌抗肿瘤再生长的实验研究

探讨微波固化治疗肝癌对肿瘤再生长的抑制作用。方法：制作 Ｈ２２鼠肝癌皮下移植模型,对肿瘤分别进行微波固化（Ａ组）、手术切除（Ｂ组）及不治疗（Ｃ组）３种处理,然后对３组动物分别再次皮下接种不 量的Ｈ２２癌细胞。观察再接种癌灶的发癌情况。结果：再接种癌细胞后两个月内发癌率依再接种癌细胞数量而不同。接种１０＾７细胞的Ａ、Ｂ、Ｃ组发