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Proliferative drive and liver carcinogenesis: Too much of a good thing?

Teoh, Narcissus

Description

There have been innumerable studies published in the attempt to identify gene expression signatures in hepatocellular carcinoma (HCC). When all the regulators and targets of the differentially expressed genes are analyzed from larger studies, the most striking theme is upregulation of mitosis-promoting and cell proliferation genes in HCC compared with 'liver-specific gene clusters' in non-tumorous tissue. A major limitation of expression profiling is that it only provides a 'snapshot' of what...[Show more]

dc.contributor.authorTeoh, Narcissus
dc.date.accessioned2015-12-10T21:53:34Z
dc.identifier.issn0815-9319
dc.identifier.urihttp://hdl.handle.net/1885/38562
dc.description.abstractThere have been innumerable studies published in the attempt to identify gene expression signatures in hepatocellular carcinoma (HCC). When all the regulators and targets of the differentially expressed genes are analyzed from larger studies, the most striking theme is upregulation of mitosis-promoting and cell proliferation genes in HCC compared with 'liver-specific gene clusters' in non-tumorous tissue. A major limitation of expression profiling is that it only provides a 'snapshot' of what is an evolving process and thus cannot distinguish the differences in gene expression that are primary effectors of dysregulated growth from those that represent downstream consequences. The development of HCC in a chronically diseased liver, often referred to as hepatocarcinogenesis, is a multistep process characterized by the progressive accumulation and interplay of genetic alterations causing aberrant growth, malignant transformation of liver parenchymal cells, followed by vascular invasion and metastasis. This review will discuss HCC precursor lesions, draw on the 'proliferation cluster' genes highlighted from HCC expression profiling studies, relate them to a selection of regulatory networks important in liver regeneration, cell cycle control and their potential significance in the pathogenesis of HCC or primary liver cancer.
dc.publisherBlackwell Publishing Ltd
dc.sourceJournal of Gastroenterology and Hepatology
dc.subjectKeywords: beta catenin; cyclin D1; interleukin 6; protein p53; sonic hedgehog protein; transcription factor E2F; transforming growth factor beta; tumor suppressor protein; Wnt protein; cell cycle G1 phase; cell cycle regulation; cell cycle S phase; cell proliferati Cyclins; Dysplastic foci; Hepatitis B; Hepatitis C; Hepatocellular carcinoma; Hepatocyte proliferation; Interleukin 6; Liver regeneration; P53
dc.titleProliferative drive and liver carcinogenesis: Too much of a good thing?
dc.typeJournal article
local.description.notesImported from ARIES
local.identifier.citationvolume24
dc.date.issued2009
local.identifier.absfor110307 - Gastroenterology and Hepatology
local.identifier.ariespublicationu4201517xPUB163
local.type.statusPublished Version
local.contributor.affiliationTeoh, Narcissus, College of Medicine, Biology and Environment, ANU
local.description.embargo2037-12-31
local.bibliographicCitation.startpage1817
local.bibliographicCitation.lastpage1825
local.identifier.doi10.1111/j.1440-1746.2009.06121.x
dc.date.updated2016-02-24T10:40:52Z
local.identifier.scopusID2-s2.0-72149084678
local.identifier.thomsonID000272188700006
CollectionsANU Research Publications

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