MersV1, Main, Exploration, bibRecord, 003611

Expression profile of nine novel genes differentially expressed in hepatitis B virus-associated hepatocellular carcinomas

Identifieur interne : 003611 ( Main/Exploration ); précédent : 003610; suivant : 003612

Expression profile of nine novel genes differentially expressed in hepatitis B virus-associated hepatocellular carcinomas

Auteurs : Mi-Young Kim [Corée du Sud] ; Eun Park [Corée du Sud] ; Jung-Hyang Park [Corée du Sud] ; Dong-Hyun Park [Corée du Sud] ; Woo-Sung Moon [Corée du Sud] ; Back-Hwan Cho [Corée du Sud] ; Hee-Sup Shin [Corée du Sud] ; Dae-Ghon Kim [Corée du Sud]

Source :

Oncogene : (Basingstoke) [ 0950-9232 ] ; 2001.

RBID : Pascal:02-0194135

Descripteurs français

English descriptors

KwdEn :
- Associated virus, Base Sequence, Blotting, Northern, Carcinogenesis, Carcinoma, Hepatocellular (etiology), Carcinoma, Hepatocellular (genetics), Carcinoma, Hepatocellular (metabolism), Carcinoma, Hepatocellular (virology), Cell Transformation, Neoplastic, Cell Transformation, Viral, DNA, Neoplasm (genetics), DNA, Viral (genetics), Gene, Gene Expression Profiling, Gene Expression Regulation, Neoplastic, Gene Expression Regulation, Viral, Gene expression, Gene therapy, Genes, Hepatitis B virus (genetics), Hepatitis B virus (physiology), Hepatitis B, Chronic (complications), Hepatocellular carcinoma, Humans, Liver Neoplasms (etiology), Liver Neoplasms (genetics), Liver Neoplasms (metabolism), Liver Neoplasms (virology), Molecular Sequence Data, Neoplasm Proteins (biosynthesis), Neoplasm Proteins (genetics), Polymerase chain reaction, RNA, Messenger (biosynthesis), RNA, Neoplasm (biosynthesis), Sequence Analysis, DNA, Subtraction Technique, Viral Proteins (biosynthesis), Viral Proteins (genetics), Viral hepatitis C, Virus Integration.
MESH :
- chemical , biosynthesis : Neoplasm Proteins, RNA, Messenger, RNA, Neoplasm, Viral Proteins.
- chemical , genetics : DNA, Neoplasm, DNA, Viral, Neoplasm Proteins, Viral Proteins.
- complications : Hepatitis B, Chronic.
- etiology : Carcinoma, Hepatocellular, Liver Neoplasms.
- genetics : Carcinoma, Hepatocellular, Hepatitis B virus, Liver Neoplasms.
- metabolism : Carcinoma, Hepatocellular, Liver Neoplasms.
- physiology : Hepatitis B virus.
- virology : Carcinoma, Hepatocellular, Liver Neoplasms.
- Base Sequence, Blotting, Northern, Cell Transformation, Neoplastic, Cell Transformation, Viral, Gene Expression Profiling, Gene Expression Regulation, Neoplastic, Gene Expression Regulation, Viral, Genes, Humans, Molecular Sequence Data, Sequence Analysis, DNA, Subtraction Technique, Virus Integration.

Abstract

Chronic hepatitis B virus (HBV) infection is known to be one of the major causes in the development of hepatocellular carcinoma (HCC), although the biomolecular mechanism(s) involved remain unclear. To identify the cellular gene(s) involved in HBV-associated hepato-carcinogenesis, we used the mRNA differential display method and examined three paired tumor and nontumor tissues, all of which had chromosomally integrated HBV-DNA through chronic infection. Using 240 different combinations of three one-base anchored oligo-dT primers and 80 arbitrary 13-mers, genes decreased or increased in expression more than twofold between each tumor tissue and its paired nontumor tissue were identified. Twenty-nine known genes and four novel genes were differentially over-expressed in the HCC tumor tissues. In contrast, 27 known genes and five novel genes were under-expressed in those tumor tissues. The nucleotide sequences of the nine novel gene fragments were determined and their expression patterns were examined in 40 HCC samples. HA61T2, PT18, HG63T1, and HG57T1 were preferentially over-expressed in 32 cases (80%, P<0.001), 24 cases (60%), 23 cases (57.5%) and 22 cases (55%) of the 40 tumor tissues, respectively. There was an increased frequency of HG57T1 over-expression in HCC patients with HBV-positive serology and low serum alpha-feto protein (AFP) levels (P < 0.05). DNT10, PT8, PT19, ENT25 and HA6T4 were under-expressed in 26 cases (65%), 23 cases (57.5%), 21 cases (53%), 20 cases (50%) and 18 cases (45%) of the 40 tumor samples, respectively. There was a strong correlation of DNT10 under-expression with high serum AFP level in HCC patients, irrespective of HBV serology (P<0.01). HA6T4 was preferentially under-expressed in HCC tumors in patients with HBV-positive serology and high serum AFP levels (P < 0.05). Thus, the functional analyses of the known and novel genes identified in this study should prove valuable to further understand the mechanism(s) of hepatocarcino-genesis.

Affiliations:

Corée du Sud

Le document en format XML

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<term>Base Sequence</term>
<term>Blotting, Northern</term>
<term>Carcinogenesis</term>
<term>Carcinoma, Hepatocellular (etiology)</term>
<term>Carcinoma, Hepatocellular (genetics)</term>
<term>Carcinoma, Hepatocellular (metabolism)</term>
<term>Carcinoma, Hepatocellular (virology)</term>
<term>Cell Transformation, Neoplastic</term>
<term>Cell Transformation, Viral</term>
<term>DNA, Neoplasm (genetics)</term>
<term>DNA, Viral (genetics)</term>
<term>Gene</term>
<term>Gene Expression Profiling</term>
<term>Gene Expression Regulation, Neoplastic</term>
<term>Gene Expression Regulation, Viral</term>
<term>Gene expression</term>
<term>Gene therapy</term>
<term>Genes</term>
<term>Hepatitis B virus (genetics)</term>
<term>Hepatitis B virus (physiology)</term>
<term>Hepatitis B, Chronic (complications)</term>
<term>Hepatocellular carcinoma</term>
<term>Humans</term>
<term>Liver Neoplasms (etiology)</term>
<term>Liver Neoplasms (genetics)</term>
<term>Liver Neoplasms (metabolism)</term>
<term>Liver Neoplasms (virology)</term>
<term>Molecular Sequence Data</term>
<term>Neoplasm Proteins (biosynthesis)</term>
<term>Neoplasm Proteins (genetics)</term>
<term>Polymerase chain reaction</term>
<term>RNA, Messenger (biosynthesis)</term>
<term>RNA, Neoplasm (biosynthesis)</term>
<term>Sequence Analysis, DNA</term>
<term>Subtraction Technique</term>
<term>Viral Proteins (biosynthesis)</term>
<term>Viral Proteins (genetics)</term>
<term>Viral hepatitis C</term>
<term>Virus Integration</term>
</keywords>
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<term>ADN viral (génétique)</term>
<term>ARN messager (biosynthèse)</term>
<term>ARN tumoral (biosynthèse)</term>
<term>Analyse de profil d'expression de gènes</term>
<term>Analyse de séquence d'ADN</term>
<term>Carcinome hépatocellulaire (génétique)</term>
<term>Carcinome hépatocellulaire (métabolisme)</term>
<term>Carcinome hépatocellulaire (virologie)</term>
<term>Carcinome hépatocellulaire (étiologie)</term>
<term>Données de séquences moléculaires</term>
<term>Gènes</term>
<term>Humains</term>
<term>Hépatite B chronique ()</term>
<term>Intégration virale</term>
<term>Protéines tumorales (biosynthèse)</term>
<term>Protéines tumorales (génétique)</term>
<term>Protéines virales (biosynthèse)</term>
<term>Protéines virales (génétique)</term>
<term>Régulation de l'expression des gènes tumoraux</term>
<term>Régulation de l'expression des gènes viraux</term>
<term>Séquence nucléotidique</term>
<term>Technique de Northern</term>
<term>Technique de soustraction</term>
<term>Transformation cellulaire néoplasique</term>
<term>Transformation cellulaire virale</term>
<term>Tumeurs du foie (génétique)</term>
<term>Tumeurs du foie (métabolisme)</term>
<term>Tumeurs du foie (virologie)</term>
<term>Tumeurs du foie (étiologie)</term>
<term>Virus de l'hépatite B (génétique)</term>
<term>Virus de l'hépatite B (physiologie)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>Neoplasm Proteins</term>
<term>RNA, Messenger</term>
<term>RNA, Neoplasm</term>
<term>Viral Proteins</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>DNA, Neoplasm</term>
<term>DNA, Viral</term>
<term>Neoplasm Proteins</term>
<term>Viral Proteins</term>
</keywords>
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<term>ARN tumoral</term>
<term>Protéines tumorales</term>
<term>Protéines virales</term>
</keywords>
<keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Hepatitis B, Chronic</term>
</keywords>
<keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Carcinoma, Hepatocellular</term>
<term>Liver Neoplasms</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Carcinoma, Hepatocellular</term>
<term>Hepatitis B virus</term>
<term>Liver Neoplasms</term>
</keywords>
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<term>ADN viral</term>
<term>Carcinome hépatocellulaire</term>
<term>Protéines tumorales</term>
<term>Protéines virales</term>
<term>Tumeurs du foie</term>
<term>Virus de l'hépatite B</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Carcinoma, Hepatocellular</term>
<term>Liver Neoplasms</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Carcinome hépatocellulaire</term>
<term>Tumeurs du foie</term>
</keywords>
<keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Virus de l'hépatite B</term>
</keywords>
<keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Hepatitis B virus</term>
</keywords>
<keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Carcinome hépatocellulaire</term>
<term>Tumeurs du foie</term>
</keywords>
<keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Carcinoma, Hepatocellular</term>
<term>Liver Neoplasms</term>
</keywords>
<keywords scheme="MESH" qualifier="étiologie" xml:lang="fr"><term>Carcinome hépatocellulaire</term>
<term>Tumeurs du foie</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Base Sequence</term>
<term>Blotting, Northern</term>
<term>Cell Transformation, Neoplastic</term>
<term>Cell Transformation, Viral</term>
<term>Gene Expression Profiling</term>
<term>Gene Expression Regulation, Neoplastic</term>
<term>Gene Expression Regulation, Viral</term>
<term>Genes</term>
<term>Humans</term>
<term>Molecular Sequence Data</term>
<term>Sequence Analysis, DNA</term>
<term>Subtraction Technique</term>
<term>Virus Integration</term>
</keywords>
<keywords scheme="Pascal" xml:lang="fr"><term>Analyse de profil d'expression de gènes</term>
<term>Analyse de séquence d'ADN</term>
<term>Données de séquences moléculaires</term>
<term>Gène</term>
<term>Carcinogenèse</term>
<term>Gènes</term>
<term>Humains</term>
<term>Hépatite B chronique</term>
<term>Intégration virale</term>
<term>Réaction chaîne polymérase</term>
<term>Expression génique</term>
<term>Régulation de l'expression des gènes tumoraux</term>
<term>Régulation de l'expression des gènes viraux</term>
<term>Séquence nucléotidique</term>
<term>Technique de Northern</term>
<term>Technique de soustraction</term>
<term>Thérapie génique</term>
<term>Carcinome hépatocellulaire</term>
<term>Hépatite virale C</term>
<term>Transformation cellulaire néoplasique</term>
<term>Transformation cellulaire virale</term>
<term>Virus associé</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en">Chronic hepatitis B virus (HBV) infection is known to be one of the major causes in the development of hepatocellular carcinoma (HCC), although the biomolecular mechanism(s) involved remain unclear. To identify the cellular gene(s) involved in HBV-associated hepato-carcinogenesis, we used the mRNA differential display method and examined three paired tumor and nontumor tissues, all of which had chromosomally integrated HBV-DNA through chronic infection. Using 240 different combinations of three one-base anchored oligo-dT primers and 80 arbitrary 13-mers, genes decreased or increased in expression more than twofold between each tumor tissue and its paired nontumor tissue were identified. Twenty-nine known genes and four novel genes were differentially over-expressed in the HCC tumor tissues. In contrast, 27 known genes and five novel genes were under-expressed in those tumor tissues. The nucleotide sequences of the nine novel gene fragments were determined and their expression patterns were examined in 40 HCC samples. HA61T2, PT18, HG63T1, and HG57T1 were preferentially over-expressed in 32 cases (80%, P<0.001), 24 cases (60%), 23 cases (57.5%) and 22 cases (55%) of the 40 tumor tissues, respectively. There was an increased frequency of HG57T1 over-expression in HCC patients with HBV-positive serology and low serum alpha-feto protein (AFP) levels (P < 0.05). DNT10, PT8, PT19, ENT25 and HA6T4 were under-expressed in 26 cases (65%), 23 cases (57.5%), 21 cases (53%), 20 cases (50%) and 18 cases (45%) of the 40 tumor samples, respectively. There was a strong correlation of DNT10 under-expression with high serum AFP level in HCC patients, irrespective of HBV serology (P<0.01). HA6T4 was preferentially under-expressed in HCC tumors in patients with HBV-positive serology and high serum AFP levels (P < 0.05). Thus, the functional analyses of the known and novel genes identified in this study should prove valuable to further understand the mechanism(s) of hepatocarcino-genesis.</div>
</front>
</TEI>
<affiliations><list><country><li>Corée du Sud</li>
</country>
</list>
<tree><country name="Corée du Sud"><noRegion><name sortKey="Kim, Mi Young" sort="Kim, Mi Young" uniqKey="Kim M" first="Mi-Young" last="Kim">Mi-Young Kim</name>
</noRegion>
<name sortKey="Cho, Back Hwan" sort="Cho, Back Hwan" uniqKey="Cho B" first="Back-Hwan" last="Cho">Back-Hwan Cho</name>
<name sortKey="Kim, Dae Ghon" sort="Kim, Dae Ghon" uniqKey="Kim D" first="Dae-Ghon" last="Kim">Dae-Ghon Kim</name>
<name sortKey="Moon, Woo Sung" sort="Moon, Woo Sung" uniqKey="Moon W" first="Woo-Sung" last="Moon">Woo-Sung Moon</name>
<name sortKey="Park, Dong Hyun" sort="Park, Dong Hyun" uniqKey="Park D" first="Dong-Hyun" last="Park">Dong-Hyun Park</name>
<name sortKey="Park, Eun" sort="Park, Eun" uniqKey="Park E" first="Eun" last="Park">Eun Park</name>
<name sortKey="Park, Jung Hyang" sort="Park, Jung Hyang" uniqKey="Park J" first="Jung-Hyang" last="Park">Jung-Hyang Park</name>
<name sortKey="Shin, Hee Sup" sort="Shin, Hee Sup" uniqKey="Shin H" first="Hee-Sup" last="Shin">Hee-Sup Shin</name>
</country>
</tree>
</affiliations>
</record>

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Expression profile of nine novel genes differentially expressed in hepatitis B virus-associated hepatocellular carcinomas

Expression profile of nine novel genes differentially expressed in hepatitis B virus-associated hepatocellular carcinomas

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