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Article: Upregulated Akt signaling adjacent to gastric cancers: Implications for screening and chemoprevention

TitleUpregulated Akt signaling adjacent to gastric cancers: Implications for screening and chemoprevention
Authors
KeywordsCarcinogenesis
Chronic inflammation
Preneoplasia
Issue Date2005
PublisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/canlet
Citation
Cancer Letters, 2005, v. 225 n. 1, p. 53-59 How to Cite?
AbstractMost gastric adenocarcinomas arise as a longterm complication of Helicobacter pylori infection of the stomach, but the high prevalence of this infection limits the cost-effectiveness of antibiotic eradication as a cancer prevention strategy. Here we have used phosphorylation-specific antibodies against the Akt kinase consensus sequence to detect downstream substrates of this oncogenic signaling pathway in normal and malignant gastric tissues. In vitro studies confirm that phosphorylation of Akt and its substrates is inducible by epithelial mitogens such as epidermal growth factor (EGF), which is implicated in the pathogenesis of H. pylori gastritis. Control clinical studies confirm far stronger Akt substrate phosphorylation in primary human breast cancers than in matched adjacent normal breast tissues; unexpectedly, however, increased Akt signaling is apparent in both primary stomach cancers and adjacent normal gastric tissues. These findings raise the possibility of a preneoplastic field defect induced in morphologically normal tissues, and suggest that immunoassays of mucosal Akt activity could guide preventive surveillance and/or intervention in patients at risk of gastric cancer. Moreover, since recent reports confirm Akt inhibition by COX-2 inhibitors, these data support the chemopreventive efficacy of such drugs for at-risk individuals. © 2004 Elsevier Ireland Ltd. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/78574
ISSN
2015 Impact Factor: 5.992
2015 SCImago Journal Rankings: 2.331
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorKok, LAen_HK
dc.contributor.authorDiong, SLen_HK
dc.contributor.authorWong, WKen_HK
dc.contributor.authorEpstein, RJen_HK
dc.date.accessioned2010-09-06T07:44:23Z-
dc.date.available2010-09-06T07:44:23Z-
dc.date.issued2005en_HK
dc.identifier.citationCancer Letters, 2005, v. 225 n. 1, p. 53-59en_HK
dc.identifier.issn0304-3835en_HK
dc.identifier.urihttp://hdl.handle.net/10722/78574-
dc.description.abstractMost gastric adenocarcinomas arise as a longterm complication of Helicobacter pylori infection of the stomach, but the high prevalence of this infection limits the cost-effectiveness of antibiotic eradication as a cancer prevention strategy. Here we have used phosphorylation-specific antibodies against the Akt kinase consensus sequence to detect downstream substrates of this oncogenic signaling pathway in normal and malignant gastric tissues. In vitro studies confirm that phosphorylation of Akt and its substrates is inducible by epithelial mitogens such as epidermal growth factor (EGF), which is implicated in the pathogenesis of H. pylori gastritis. Control clinical studies confirm far stronger Akt substrate phosphorylation in primary human breast cancers than in matched adjacent normal breast tissues; unexpectedly, however, increased Akt signaling is apparent in both primary stomach cancers and adjacent normal gastric tissues. These findings raise the possibility of a preneoplastic field defect induced in morphologically normal tissues, and suggest that immunoassays of mucosal Akt activity could guide preventive surveillance and/or intervention in patients at risk of gastric cancer. Moreover, since recent reports confirm Akt inhibition by COX-2 inhibitors, these data support the chemopreventive efficacy of such drugs for at-risk individuals. © 2004 Elsevier Ireland Ltd. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/canleten_HK
dc.relation.ispartofCancer Lettersen_HK
dc.rightsCancer Letters. Copyright © Elsevier Ireland Ltd.en_HK
dc.subjectCarcinogenesisen_HK
dc.subjectChronic inflammationen_HK
dc.subjectPreneoplasiaen_HK
dc.titleUpregulated Akt signaling adjacent to gastric cancers: Implications for screening and chemopreventionen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0304-3835&volume=225&issue=1&spage=53&epage=9&date=2005&atitle=Upregulated+Akt+signaling+adjacent+to+gastric+cancers:+implications+for+screening+and+chemoprevention.en_HK
dc.identifier.emailEpstein, RJ: repstein@hku.hken_HK
dc.identifier.authorityEpstein, RJ=rp00501en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.canlet.2004.11.021en_HK
dc.identifier.pmid15922857-
dc.identifier.scopuseid_2-s2.0-19544385752en_HK
dc.identifier.hkuros122937en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-19544385752&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume225en_HK
dc.identifier.issue1en_HK
dc.identifier.spage53en_HK
dc.identifier.epage59en_HK
dc.identifier.isiWOS:000229850600005-
dc.publisher.placeIrelanden_HK
dc.identifier.scopusauthoridKok, LA=8509255600en_HK
dc.identifier.scopusauthoridDiong, SL=8509255200en_HK
dc.identifier.scopusauthoridWong, WK=7403972446en_HK
dc.identifier.scopusauthoridEpstein, RJ=34975074500en_HK

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