刘杰
胃癌前病变癌变概率的判别模式
个性化签名
- 姓名:刘杰
- 目前身份:
- 担任导师情况:
- 学位:
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学术头衔:
博士生导师, 教育部“新世纪优秀人才支持计划”入选者
- 职称:-
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学科领域:
肿瘤学
- 研究兴趣:胃癌前病变癌变概率的判别模式
刘杰,男,39岁,医学博士,教授,“国家教育部新世纪优秀人才资助计划”获得者(2004);解放军总后勤部“科技新星”(2004);世界胃肠病学大会“青年优秀医师奖”获得者(2002)。87年毕业于第四军医大学并留校,现为第四军医大学西京医院消化病研究所及消化肿瘤生物学国家重点实验室教授、主任医师。两次赴美从事肝癌分子克隆共5年。首次建立了胃癌前病变癌变概率的判别模式,克隆出4个国际上未见报道的肿瘤相关新基因,发现了2条乙肝病毒X基因致癌信号转导新通路。先后共发表SCI收录的英文论文24篇,其中包括国际肝脏病权威杂志Hepatology 3篇,国际癌基因权威杂志Oncogene 3篇等。论文有96次被53种SCI收录的不同国际英文期刊引用,并受邀参与编写在美国出版的《Method in Molecular Medicine》(分子医学研究方法), 《Progress on Liver Cancer Research》(肝癌研究进展)和《Immunohistochemistry and In Situ Hybridization of Human Carcinomas》(人类肿瘤的免疫组化和原位分子杂交) 三部国际英文专著。 2005年7月,以刘杰教授为第一作者兼通讯作者的研究论文,在英国Nature系列的临床实用肿瘤学杂志上发表(Nature 姊妹刊),并被美国医师联合会推举为美国临床医师的临床教材,具有较好的国际影响。
先后承担国家自然科学基金课题,国家教育部“新世纪优秀人才支持计划”课题,国家科技部人类肝脏蛋白组计划分题等10余项,获军队及省科技进步二等奖各一项,现任国家科技部国际合作重点项目评议专家组成员,国家自然科学基金委同行评议专家组成员,世界胃肠病学会会员,中华消化学会肿瘤分会委员,《世界核心医学期刊文摘?胃肠病学》杂志编委等职。
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刘杰, N. Lale Satiroglu Tufan*, Zhaorui Llan*, MJie Liu*, Jingbo Pan*, Patrick Arbuthnot†, Michael Kew†, Marcy M Clayton*, Minghua Zhu† and Mark A Feitelson*
Neoplasia,-0001,():
-1年11月30日
Hepatitis B virus encoded X antigen (HBxAg) may contribute to the development of hepatocelIular carcin-oma (HCC) by up-or downregulating the expression of cellular genes that promote cell growth and urvival. To test this hypothesis, HBxAg-positive and-negative HepG2 cells were constructed. and the patterns of cellular gene expression compared by polymerase chain reaction select cDNA subtraction. The full-length clone of one of these upregulated genes (URG), URG4, encoded a rotein of about 104kDa. URG4 was strongly expressed jn hepatitis B-infected Iiver and in HCC cells. where it costained with HBxAg, and was weakly ex
hepatitis B virus, hepalilis Bx antigen, hepatocellular carcinoma, onccgene pathogenesin
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刘杰, Mark A. Feitelson , Helena M. G. P. V. Reis, Jie Liu, Zhaorui Lian and Jingbo Pan
[Frontiers in Bioscience 10, 1558-1572, May 1, 2005,-0001,():
-1年11月30日
Hepatitis B and related viruses that infect mammalian hosts encode the "X" protein that has been shown to contribute importantly to the pathogenesis of chronic liver disease (CLD) and to the evelopment of hepatocellular carcinoma (HCC). In a variety of tissue culture systems, hepatitis B virus (HBV) X antigen, or HBxAg, has been shown to trigger apoptosis, while other evidence suggests that HBxAg inhibits apoptosis and stimulates the cell cycle by constitutively activating a number of signaling pathways that are important for hepatocellular growth and survival. These apparently contrasting properties of HBxAg may be associated with differences in the X protein itself, since carboxy-terminaltruncated forms of HBxAg appear to be associated with HCC lesions. Alternatively, or in addition, these differences may be due to the cell type, state of cell differentiation, and whether expression occurs in resting or dividing cells. Further, the association between HBxAg expression and chromosomal instability, may also contribute to the apparently contrasting fates of HBxAg positive cells. It is proposed that in many of these systems, the different outcomes of HBxAg expression may be due to the nature of the cellular response to HBxAg, and not due to differences in the fundamental properties of HBxAg, the latter of which promote cell survival, cell cycle rogression, and the development of HCC.
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刘杰, BILL S. SUN, JINGBO PAN, MARCY M. CLAYTON, JIE LIU, XIAOPING YAN, ALEXEY A. MATSKEVICH, DAVID S. TRAYER, MICHAEL GERBER, AND MARK A. FEITELSON, *
JOURNAL OF CELLULAR PHYSIOLOGY 201: 447-458 (2004),-0001,():
-1年11月30日
HepG2 cells stably transfected with a full-length, infectious hepatitis C virus (HCV) cDNA demonstrated consistent replication of HCV for more than 3 years. Intracellular minus strand HCV RNA was present. Minus strand synthesis was NS5B dependent, and was sensitive to interferon alpha (IFNa) treatment. NS5B and HCV core protein were detectable. HCV stimulated HepG2 cell growth and survival in culture, in soft agar, and accelerated tumor growth in SCID mice. These mice becameHCVRNApositive in blood, where the virus was also sensitive to IFNa. The RNA banded at the density of HCV, and was resistant to RNase prior to extraction. Hence,HCVstably replicates inHepG2cells, stimulates epatocellular growth and tumorigenesis, and is susceptible to IFNa both in vitro and in vivo. J. Cell. Physiol. 201: 447-458, 2004.
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【期刊论文】Human S15a Expression Is Upregulated by Hepatitis B Virus X Protein
刘杰, Zhaorui Lian, Jie Liu, Li Li, Xianxing Li, N. Lale Satiroglu Tufan, Meng-Chao Wu, Hong-Yang Wang, Patrick Arbuthnot, Michael Kew, and Mark A. Feitelson, *
MOLECULAR CARCINOGENESIS 40: 34-46 (2004),-0001,():
-1年11月30日
The hepatitis B virus (HBV)-encoded X antigen (HBxAg) may contribute to the development of epatocellular carcinoma (HCC) through the upregulated expression of selected cellular genes. To identify these genes, RNAs isolated from HBxAg-positive and -negative HepG2 cells were compared by PCR select cDNA subtraction. One gene overexpressed in HBxAg-positive cells by Northern and Western blotting is the ribosomal protein S15a. The S15a mRNA is 535 base pairs, encoding a protein 130 amino acids long with a molecular weight of 14.3kDa. S15a expression was upregulated in HBV-infected livers, where it costained with HBxAg. Overexpression of S15a stimulated cell growth, colony formation in soft agar, and tumor formation in SCID mice. Hence, HBxAg upregulated the expression of S15a, the latter of which participates in the development of HCC, perhaps by altering the integrity of translation.
hepatocarcinogenesis, hepatitis B x antigen, ribosomal protein, translation
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刘杰, Zhaorui Lian, Jingbo Pan, Jie Liu, ShuMin Zhang, Minghua Zhu, Patrick Arbuthnot, Michael Kew and Mark A Feitelson*,
,-0001,():
-1年11月30日
The role of hepatitis B virus X antigen in the development of hepatocellular carcinoma was explored by stably transfecting HepG2 cells with an X antigen expression vector, and identifying the ierences in gene expression that distinguish X positive from X negative cells by subtractive PCR. One ierentially expressed gene, the human homolog of sui1 (hu-sui1), encodes a translation initiation factor whose expression was suppressed by X antigen in HepG2 cells. Hu-Sui1 was also expressed in nontumor liver but not in tumor cells from patients with hepatocellular carcinoma. ntroduc-tion of hu-sui1 into HepG2 cells inhibited cell growth in culture, in soft agar, and partially inhibited tumor formation in nude mice. Hence, the suppression of hu-sui1 by X antigen may result in the abrogation of negative growth regulation and contribute to the development of epatocellular carcinoma.
translation initiation, hepatitis B X antigen, Sui1, hepatocellular carcinoma
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【期刊论文】REVIEW Genetic mechanisms of epatocarcinogenesis
刘杰, Mark A Feitelson*, , Bill Sun, N Lale Satiroglu Tufan, Jie Liu, Jingbo Pan and Zhaorui Lian
Oncogene (2002) 21, 2593-2604,-0001,():
-1年11月30日
The development of hepatocellular carcinoma (HCC) is a multistep process associated with changes in host gene expression, some of which correlate with the appearance and progression of tumor. reneoplastic changes in gene expression result from altered DNA methylation, the actions of hepatitis B and C viruses, and point mutations or loss of heterozygosity (LOH) in selected cellular genes. Tumor progression is characterized by LOH involving tumor suppressor genes on many chromosomes and by gene ampli
hepatocellular carcinoma, hepatitis viruses, loss of heterozygosity, mutations
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刘杰, Xiao-Yan Cao, Jie Liu, Zhao-Rui Lian, Marcy Clayton, Jia-Lu Hu, Ming-Hua Zhu, Dai-Ming Fan and Mark Feitelson
World J Gastroenterol 2001; 7 (4): 575-578,-0001,():
-1年11月30日
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【期刊论文】Cloning of differentially expressed genes in human hepatocellular carcinoma and nontumor liver
刘杰, Xiao-Yan Cao, Jie Liu, Zhao-Rui Lian, Marcy Clayton, Jia-Lu Hu, Ming-Hua Zhu, Dai-Ming Fan and Mark Feitelson
World J Gastroenterol 2001; 7 (4): 579-582,-0001,():
-1年11月30日
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刘杰, JONATHAN LARKIN, MARCIA M. CLAYTON, JIE LIU, AND MARK A. FEITELSON,
HEPATOLOGY Vol. 34, No.4, 2001,-0001,():
-1年11月30日
Epidemiologic observations show a higher frequency of hepatitis B virus (HBV) serologic markers in chronic alcoholics compared with the general population. This may be the result of an increased susceptibility of alcoholics to infection and/or to an ethanol-mediated stimulation of HBV gene expression and replication. To test the latter hypothesis, HBV transgenic SCID mice, which support consistent levels of virus replication, were fed with a standard Lieber-DiCarli or isocaloric diet for 5 weeks. In ethanol-fed mice, the levels of hepatitis B surface antigen (HBsAg) and viral DNA in serum increased by up to 7-fold compared with mice fed the control diet. Ethanol-treated mice also had elevated HBV-RNA levels, and increased expression of surface, core, and X antigens in the liver, especially in the pericentral regions. None of these changes were observed in transgenic mice fed isocaloric diets. Thus, chronic alcohol consumption alters the patterns of HBV gene expression and replication in the serum and liver of HBV transgenic SCID mice, and may provide a partial explanation for the increased frequency of HBV markers among alcoholics. (HEPATOLOGY 2001; 34: 792-797.)
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【期刊论文】Activation of fibronectin gene expression by hepatitis B virus x antigen
刘杰, P. A. Norton, H. M. G. P. V. Reis, S. Prince, J. Larkin, J. Pan, J. Liu, Q. Gong, M. Zhu and M. A. Feitelson,
Journal of Viral Hepatitis, 2004, 11, 332-341,-0001,():
-1年11月30日
SUMMARY. The development of fibrosis and cirrhosis during chronic hepatitis B virus (HBV) infection correlates with the persistent expression of HBV x antigen (HBxAg), which acts in part, by stimulating selected signal transduction pathways, including nuclear factor jB (NF-jB). To identify NF-jB responsive genes that are differentially expressed in HBxAgpositive cells, HepG2 cells were stably transfected with HBxAg, and then with pZeoSV2 or pZeoSV2-IjBa. When RNAs from each culture were compared by PCR-select cDNA subtraction, fibronectin (FN) mRNA was shown to be strongly down-regulated by IjBa. Up-regulated expression of FN and co-expression between FN and HBxAg were observed in liver sections from HBV carriers that were stained for HBxAg and analysed for FN mRNA by in situ hybridization (ISH). In liver cell cultures, HBxAg increased the levels of FN mRNA and protein. This was because of the HBxAg-mediated trans-activation of the FN promoter, which was NF-jBdependent. HBxAg also antagonized the repression of the FN promoter by the tumour suppressor, p53. Hence, the FN gene may be a natural target for HBxAg trans-activation, perhaps through activation of NF-jB and inactivation of p53, thereby contributing to the accumulation of FN in the liver over the course of chronic HBV infection.
chronic HBV infection, extracellular matrix, hepatocellular carcinoma.,
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