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Conference Paper: Loss of tyrosine aminotransferase may involved in the pathogenesis of hepatocellular carcinoma

TitleLoss of tyrosine aminotransferase may involved in the pathogenesis of hepatocellular carcinoma
Authors
Issue Date2009
PublisherAmerican Association for Cancer Research
Citation
The 100th Annual Meeting of the American Association for Cancer Research, Denver, CO, 18-22 April 2009. In Cancer Research, 2009, v. 69, Abstract no. 624 How to Cite?
AbstractTyrosine aminotransferase gene (TAT) locates at chromosome arm 16q22.1, which is one of the most frequent deletion regions in hepatocellular carcinomas (HCC). Our previous study showed that none or low expression of TAT was observed both in HCC cases and cell lines. Over expression of TAT in HCC cell line QGY-7703 could inhibit tumorigenicity and cause spontaneous apoptosis. Later, a mouse model wasobtained by targeted disruption of the murine TAT in embryonic stem cells. Homozygous knockout mice (TAT -/-) lack TATmRNA and have a virtually complete TAT activity deficiency and significant higher tyrosine concentration. Feeding with high tyrosine food could induce the homozygous knockout mice develop corresponding phenotypes as Tyrosinaemia II- Richner-Hanhart syndrome in human patients. Also, 2 homozygous (TAT -/-) (3.50% n=57) and 1 heterozygous (TAT +/-) (1.25% n=80) spontaneously developed HCC within 1.5 years, while none wildtype developed tumor during the same time span. Thus, our results supposed that the loss of TAT may contribute to the pathogenesis of HCC.
Persistent Identifierhttp://hdl.handle.net/10722/62714
ISSN
2015 Impact Factor: 8.556
2015 SCImago Journal Rankings: 5.372

 

DC FieldValueLanguage
dc.contributor.authorDong, Sen_HK
dc.contributor.authorFu, Len_HK
dc.contributor.authorLu, Len_HK
dc.contributor.authorLu, Sen_HK
dc.contributor.authorGuan, XY-
dc.date.accessioned2010-07-13T04:07:36Z-
dc.date.available2010-07-13T04:07:36Z-
dc.date.issued2009en_HK
dc.identifier.citationThe 100th Annual Meeting of the American Association for Cancer Research, Denver, CO, 18-22 April 2009. In Cancer Research, 2009, v. 69, Abstract no. 624-
dc.identifier.issn0008-5472-
dc.identifier.urihttp://hdl.handle.net/10722/62714-
dc.description.abstractTyrosine aminotransferase gene (TAT) locates at chromosome arm 16q22.1, which is one of the most frequent deletion regions in hepatocellular carcinomas (HCC). Our previous study showed that none or low expression of TAT was observed both in HCC cases and cell lines. Over expression of TAT in HCC cell line QGY-7703 could inhibit tumorigenicity and cause spontaneous apoptosis. Later, a mouse model wasobtained by targeted disruption of the murine TAT in embryonic stem cells. Homozygous knockout mice (TAT -/-) lack TATmRNA and have a virtually complete TAT activity deficiency and significant higher tyrosine concentration. Feeding with high tyrosine food could induce the homozygous knockout mice develop corresponding phenotypes as Tyrosinaemia II- Richner-Hanhart syndrome in human patients. Also, 2 homozygous (TAT -/-) (3.50% n=57) and 1 heterozygous (TAT +/-) (1.25% n=80) spontaneously developed HCC within 1.5 years, while none wildtype developed tumor during the same time span. Thus, our results supposed that the loss of TAT may contribute to the pathogenesis of HCC.-
dc.languageengen_HK
dc.publisherAmerican Association for Cancer Research-
dc.relation.ispartofCancer Research-
dc.titleLoss of tyrosine aminotransferase may involved in the pathogenesis of hepatocellular carcinomaen_HK
dc.typeConference_Paperen_HK
dc.identifier.emailDong, S: dongsuisui@gmail.comen_HK
dc.identifier.emailFu, L: gracefu@graduate.hku.hken_HK
dc.identifier.emailGuan, XY: xyguan@hkucc.hku.hken_HK
dc.identifier.authorityGuan, XY=rp00454en_HK
dc.identifier.hkuros156544en_HK

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