LOSS OF HETEROZYGOSITY INVOLVING THE APC TUMOR SUPPRESSOR GENE IN HUMAN COLORECTAL CARCINOMA

ＬＯＳＳＯＦＨＥＴＥＲＯＺＹＧＯＳＩＴＹＩＮＶＯＬＶＩＮＧＴＨＥＡＰＣＴＵＭＯＲＳＵＰＰＲＥＳＳＯＲＧＥＮＥＩＮＨＵＭＡＮＣＯＬＯＲＥＣＴＡＬＣＡＲＣＩＮＯＭＡ￥ＸｕＷｅｎｈｕａｉ；徐文怀；ＹａｎｇＤｉｎｇｃｈｅｎｇ；杨定成（Ｄｅｐａｒｔｍｅｎｔｏｆ...     

The Paper Symposium on PLC VIRAL HEPATITIS（HBV AND HCV）BACKGROUND IN CHINESE PATIENTS WITH HEPATOCELLULAR CARCINOMA

ＴｈｅＰａｐｅｒＳｙｍｐｏｓｉｕｍｏｎＰＬＣＶＩＲＡＬＨＥＰＡＴＩＴＩＳ（ＨＢＶＡＮＤＨＣＶ）ＢＡＣＫＧＲＯＵＮＤＩＮＣＨＩＮＥＳＥＰＡＴＩＥＮＴＳＷＩＴＨＨＥＰＡＴＯＣＥＬＬＵＬＡＲＣＡＲＣＩＮＯＭＡＹｕＺｈｕｙｕａｎ；余竹元；ＴａｎｇＺｈａｏｙｏ...     

TWO－STAGE RESECTION FOR ADVANCED HEPATOCELLULAR CARCINOMA─PRELIMINARY RESULTS OF 16 CASES

ＴＷＯ－ＳＴＡＧＥＲＥＳＥＣＴＩＯＮＦＯＲＡＤＶＡＮＣＥＤＨＥＰＡＴＯＣＥＬＬＵＬＡＲＣＡＲＣＩＮＯＭＡ─ＰＲＥＬＩＭＩＮＡＲＹＲＥＳＵＬＴＳ　ＯＦ１６ＣＡＳＥＳＬｉａｎｇＬｉｊｉａｎ；Ｌｕｍｉｎｇｄｅ；ＨｕａｎｇＪｉｅｆｕ；ＰｅｎｇＢａｏｇａｎｇ梁...     

ANTI-METASTATIC EFFECT OF ONCOLYSATES FROM MURINE MELANOMA CELLS TRANSFECTED WITH RECOMBINANT VACCINIA VIRUS ENCODING HUMAN IL-2

ＡＮＴＩＭＥＴＡＳＴＡＴＩＣＥＦＦＥＣＴＯＦＯＮＣＯＬＹＳＡＴＥＳＦＲＯＭＭＵＲＩＮＥＭＥＬＡＮＯＭＡＣＥＬＬＳＴＲＡＮＳＦＥＣＴＥＤＷＩＴＨＲＥＣＯＭＢＩＮＡＮＴＶＡＣＣＩＮＩＡＶＩＲＵＳＥＮＣＯＤＩＮＧＨＵＭＡＮＩＬ２１ＷａｎＴａｏ万涛Ｃａｏ...     

SYNERGISM BETWEEN PHOTODYNAMIC THERAPY OF ALUMINUM SULFONATED PHTHALOCYANINE AND HYPERTHERMIA ON MOUSE HEPATOMA IN VIVO AND I

ＳＹＮＥＲＧＩＳＭＢＥＴＷＥＥＮＰＨＯＴＯＤＹＮＡＭＩＣＴＨＥＲＡＰＹＯＦＡＬＵＭＩＮＵＭＳＵＬＦＯＮＡＴＥＤＰＨＴＨＡＬＯＣＹＡＮＩＮＥＡＮＤＨＹＰＥＲＴＨＥＲＭＩＡＯＮＭＯＵＳＥＨＥＰＡＴＯＭＡＩＮＶＩＶＯＡＮＤＩＮＶＩＴＲＯＦｕＭａｉｗｕ;傅乃...     

HEPATITIS B AND C VIRUSES AND THEIR INTERACTION IN THE PTHOGENESIS OF HEPATOCELLULAR CARCINOMA

王树林，张耀铮ＨＥＰＡＴＩＴＩＳＢＡＮＤＣＶＩＲＵＳＥＳＡＮＤＴＨＥＩＲＩＮＴＥＲＡＣＴＩＯＮＩＮＴＨＥＰＴＨＯＧＥＮＥＳＩＳＯＦＨＥＰＡＴＯＣＥＬＬＵＬＡＲＣＡＲＣＩＮＯＭＡ￥ＷａｎｇＳｈｕｌｉｎ；ＺｈａｎｇＹａｏｚｈｅｎｇ；（Ｄｅｐａｒｔｍｅｎｔ...     

QUALITATIVE STUDY OF SIALOMUCINS CHANGES DURING N－METHYL－N－NITROSOUREA－INDUCED C OLONIC CARCINOGENESIS IN MICE

ＱＵＡＬＩＴＡＴＩＶＥＳＴＵＤＹＯＦＳＩＡＬＯＭＵＣＩＮＳＣＨＡＮＧＥＳＤＵＲＩＮＧＮ－ＭＥＴＨＹＬ－Ｎ－ＮＩＴＲＯＳＯＵＲＥＡ－ＩＮＤＵＣＥＤＣＯＬＯＮＩＣＣＡＲＣＩＮＯＧＥＮＥＳＩＳＩＮＭＩＣＥＷａｎｇＱｉａｎｇ王强；ＷａｎｇＹｕａｎｈｅ王元和；...     

IN VITRO AND IN VIVO CHEMOTACTIC EFFECT OF MIP-1a GENE TRANSFECTED TUMOR VACCINE ON IMMUNE EFFECTOR CELLS

ＩＮＶＩＴＲＯＡＮＤＩＮＶＩＶＯＣＨＥＭＯＴＡＣＴＩＣＥＦＦＥＣＴＯＦＭＩＰ－１ａＧＥＮＥＴＲＡＮＳＦＥＣＴＥＤＴＵＭＯＲＶＡＣＣＩＮＥＯＮＩＭＭＵＮＥＥＦＦＥＣＴＯＲＣＥＬＬＳ１ＣｈｅｎＧｕｏｙｏｕ陈国友ＣａｏＸｕｅｔａｏ２曹雪涛ＬｅｉＨｏｎｇ雷虹...     

EVALUATION OF REVERSE PASSIVE HEMAGGLUTINATION （RPHA） FECAL OCCULT BLOOD TEST IN SCREENING OF COLORECTAL NEOPLASIA

ＥＶＡＬＵＡＴＩＯＮＯＦＲＥＶＥＲＳＥＰＡＳＳＩＶＥＨＥＭＡＧＧＬＵＴＩＮＡＴＩＯＮ（ＲＰＨＡ）ＦＥＣＡＬＯＣＣＵＬＴＢＬＯＯＤＴＥＳＴＩＮＳＣＲＥＥＮＩＮＧＯＦＣＯＬＯＲＥＣＴＡＬＮＥＯＰＬＡＳＩＡＹｕＨａｉ；ＺｈｏｕＬｕｎ；ＺｈｅｎＢｅｉｙｉ；Ｑ...     

GRANISETRON COMPARED WITH ONDANSETRON PLUSDEXAMETHASONE IN THE PREVENTION OF NAUSEAAND VOMITING INDUCED BY A INTENSELYEMETOGE

ＧＲＡＮＩＳＥＴＲＯＮＣＯＭＰＡＲＥＤＷＩＴＨＯＮＤＡＮＳＥＴＲＯＮＰＬＵＳＤＥＸＡＭＥＴＨＡＳＯＮＥＩＮＴＨＥＰＲＥＶＥＮＴＩＯＮＯＦＮＡＵＳＥＡＡＮＤＶＯＭＩＴＩＮＧＩＮＤＵＣＥＤＢＹＡＩＮＴＥＮＳＥＬＹＥＭＥＴＯＧＥＮＩＣＣＨＥＭＯＴＨＥＲＡＰ...     

应用原位PCR法检测肝癌组织中的HBV DNA

目的 探讨乙型肝为病毒（ＨＢＶ）与肝细胞癌（ＨＣＣ）的关系。方法 采用直接原位聚合酶链反应（ｉｎｓｉｔｕＰＣＲ，ＩＳＰＣＲ）对６４例福尔马林固定石蜡包埋的ＨＣＣ组织（其中６１例附癌周组织）切片中的ＨＢＶＤＮＡ进行检测，与并传统的免疫组织化学原位杂交和组织抽提酸ＰＣＲ法进行了比较。结果 ＩＳＰＣＲ对石蜡包埋的ＨＣＣ组织中ＨＢＶＤＮＡ检测高度敏感，检出率为７１．９％（４６／６４），而相应组织应用免疫组     

启东肝癌高发区乙肝病毒流行株全基因分析

目的：通过对江苏启东地区乙型肝炎病毒（HBV）全基因序列的分析，探讨该地区肝癌高发的分子病毒学病因。方法：以蛋白酶K消化后，酚／氯仿抽提7例肝炎和7例肝癌患者血清中DNA。应用聚合酶链反应（PCR），扩增血清中HBV基因全长，克隆至T载体后行全自动测序。以PHYLIP软件构建的系统进化树判断HBV的基因型；以Clastal W软件对序列进行突变分析。结果：14例标本中有12例为C基因型，2例为B基因型。肝癌和肝炎组中HBV基因型类别分布无差异。有5例HBV发生了PreS2的缺失突变，其中肝癌标本4例（57．1％），肝炎标本仅1例（14．3％）。HBV基因组中常见的点突变为PreS1区的nt．3116及核心启动子区的nt．1762／1764，发生率高达78．6％（11／14）。与肝炎组相比，肝癌中点突变发生率显著增高的位点为前C区nt．1899G→A的突变（P=0．01）及核心启动子区nt．1653C→T的突变（P=0．05）。结论：启东地区HBV以C基因型为主；启东HBV基因组中可能存在着与肝癌相关的点突变和缺失突变。     

广西肝癌高发区原发性肝细胞癌 HBV X 基因的整合及影响因素分析

目的 了解广西肝癌高发区乙型肝炎病毒（hepatitis B virus,HBV）X区基因在肝细胞癌（hepatocellular carcinoma,HCC）染色体中的整合及影响因素。方法 以30例与HBV相关的原发性肝细胞癌患者为研究对象。提取HCC组织及癌旁组织标本DNA作为模板,以HBV X基因上游序列和人类基因组Alu重复序列为引物,应用重复序列-多聚酶链反应（Alu-PCR）扩增整合的HBV X片段及两侧的人类基因组DNA片段。扩增产物进行测序,计算目的片段整合率并分析相关的影响因素。结果 18例HCC组织检测到HBV X基因的整合片段,整合率为60.00%（18/30）;26例癌旁组织检测到HBV X基因的整合片段,整合率为86.67%（26/30）。癌旁组织HBV病毒整合率高于HCC组织,差异有统计学意义（χ²=5.445,P=0.020）。不同性别、年龄、HBeAg、HBV DNA、ALT、AST的HCC癌组织及其癌旁组织HBV X基因整合率比较差异均无统计学意义（P＞0.05）。结论 广西肝癌高发区癌旁组织比HCC组织HBV整合率高,说明HBV整合发生在感染早期。HBV X基因整合与HCC患者性别、年龄、HBeAg、HBV DNA、ALT、AST无明显关系。     

Hepatitis B virus reactivation after three-dimensional conformal radiotherapy in patients with hepatitis B virus-related hepatocellular carcinoma

PURPOSE: To investigate whether three-dimensional conformal radiotherapy (3D-CRT) influences hepatitis B virus (HBV) reactivation and chronic hepatitis B (CHB) exacerbation in patients with HBV-related hepatocellular carcinoma (HCC). METHODS AND MATERIALS: Of the 48 HCC patients with HBV who underwent 3D-CRT to the liver, 16 underwent lamivudine therapy before and during 3D-CRT (Group 1) and 32 did not receive antiviral therapy before 3D-CRT (Group 2). To analyze spontaneous HBV reactivation, we included a control group of 43 HCC patients who did not receive any specific treatment for HCC or CHB. RESULTS: The cumulative rate of radiation-induced liver disease for Groups 1 and 2 was 12.5% (2 of 16) and 21.8% (7 of 32), respectively (p > 0.05). The cumulative rate of HBV reactivation was significantly greater in Group 2 (21.8%, 7 of 32) than in Group 1 (0%, 0/16) or the control group (2.3%, 1 of 43; p < 0.05 each). The cumulative rate of CHB exacerbation, however, did not differ significantly between Groups 2 (12.5%, 4 of 32) and 1 (0%, 0 of 16) or the control group (2.3%, 1 of 43; p > 0.05 each). The CHB exacerbations in the 4 Group 2 patients had radiation-induced liver disease features but were differentiated by serum HBV DNA changes. Two of these patients required antiviral therapy and effectively recovered with lamivudine therapy. CONCLUSIONS: In patients with HBV-related HCC undergoing 3D-CRT, HBV reactivation and consequent CHB exacerbation should be considered in the differential diagnosis of radiation-induced liver disease, and antiviral therapy might be considered for the prevention of liver function deterioration after RT.     

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     

Hepatitis B virus-induced hepatocellular carcinoma

Many factors are considered to contribute to hepatitis B virus (HBV) associated hepatocellular carcinoma (HCC), including products of HBV, HBV integration and mutation, and host susceptibility. HBV X protein (HBx) can interfere with several signal pathways that associated with cell proliferation and apoptosis, and the impact of HBx C-terminal truncation in the development of HCC has been implicated. Recent studies by advanced sequencing technologies have revealed recurrent HBV DNA integration sites in hepatoma cells and susceptible genes/SNPs play an important role in the pathogenesis of liver cancer. Epigenetic changes, immune and inflammatory factors are also important contributing factors for liver cancer. This mini-review provides an overview on the recent development of HBV induced HCC.     

肝硬变和肝癌组织内HCV RNA及HBV X基因的存在及意义

采用原位分子杂交对７９例肝硬变及６４例肝细胞癌组织进行ＨＣＶ ＲＮＡ和ＨＢＶ Ｘ基因定位检测，ＨＣＶ ＲＮＡ，ＨＶＢ Ｘ基因在两种组织的阳性率分别是４８％及７２％；３９％，及８１％；二者同时阳性在两种组织分别为３８％及３３％。ＨＣＶ ＲＮＡ主要定位于肝细胞和癌细胞胞浆内，阳性细胞呈散在、灶状及弥漫分布三种形式。ＨＢＶ Ｘ基因在肝细胞及肝癌细胞中的分布呈胞浆型、核型及核浆型，阳性细胞也呈上述三种分布     

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