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Article: Mutations of PIK3CA in gastric adenocarcinoma

TitleMutations of PIK3CA in gastric adenocarcinoma
Authors
Issue Date2005
PublisherBioMed Central Ltd. The Journal's web site is located at http://www.biomedcentral.com/bmccancer/
Citation
Bmc Cancer, 2005, v. 5 How to Cite?
AbstractBackground: Activation of the phosphatidylinositol 3-kinase (PI3K) through mutational inactivation of PTEN tumour suppressor gene is common in diverse cancer types, but rarely reported in gastric cancer. Recently, mutations in PIK3CA, which encodes the p110α catalytic subunit of PI3K, have been identified in various human cancers, including 3 of 12 gastric cancers. Eighty percent of these reported mutations clustered within 2 regions involving the helical and kinase domains. In vitro study on one of the "hot-spot" mutants has demonstrated it as an activating mutation. Methods: Based on these data, we initiated PIK3CA mutation screening in 94 human gastric cancers by direct sequencing of the gene regions in which 80% of all the known PIK3CA mutations were found. We also examined PIK3CA expression level by extracting data from the previous large-scale gene expression profiling study. Using Significance Analysis of Microarrays (SAM), we further searched for genes that show correlating expression with PIK3CA. Results: We have identified PIK3CA mutations in 4 cases (4.3%), all involving the previously reported hotspots. Among these 4 cases, 3 tumours demonstrated microsatellite instability and 2 tumours harboured concurrent KRAS mutation. Data extracted from microarray studies showed an increased expression of PIK3CA in gastric cancers when compared with the non-neoplastic gastric mucosae (p < 0.001). SAM further identified 2910 genes whose expression levels were positively associated with that of PIK3CA. Conclusion: Our data suggested that activation of the PI3K signalling pathway in gastric cancer may be achieved through up-regulation or mutation of PIK3CA, in which the latter may be a consequence of mismatch repair deficiency. © 2005 Li et al; BioMed Central Ltd.
Persistent Identifierhttp://hdl.handle.net/10722/54188
ISSN
2015 Impact Factor: 3.265
2015 SCImago Journal Rankings: 1.627
PubMed Central ID
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLi, VSWen_HK
dc.contributor.authorWong, CWen_HK
dc.contributor.authorChan, TLen_HK
dc.contributor.authorChan, ASWen_HK
dc.contributor.authorZhao, Wen_HK
dc.contributor.authorChu, KMen_HK
dc.contributor.authorSo, Sen_HK
dc.contributor.authorChen, Xen_HK
dc.contributor.authorYuen, STen_HK
dc.contributor.authorLeung, SYen_HK
dc.date.accessioned2009-04-03T07:39:06Z-
dc.date.available2009-04-03T07:39:06Z-
dc.date.issued2005en_HK
dc.identifier.citationBmc Cancer, 2005, v. 5en_HK
dc.identifier.issn1471-2407en_HK
dc.identifier.urihttp://hdl.handle.net/10722/54188-
dc.description.abstractBackground: Activation of the phosphatidylinositol 3-kinase (PI3K) through mutational inactivation of PTEN tumour suppressor gene is common in diverse cancer types, but rarely reported in gastric cancer. Recently, mutations in PIK3CA, which encodes the p110α catalytic subunit of PI3K, have been identified in various human cancers, including 3 of 12 gastric cancers. Eighty percent of these reported mutations clustered within 2 regions involving the helical and kinase domains. In vitro study on one of the "hot-spot" mutants has demonstrated it as an activating mutation. Methods: Based on these data, we initiated PIK3CA mutation screening in 94 human gastric cancers by direct sequencing of the gene regions in which 80% of all the known PIK3CA mutations were found. We also examined PIK3CA expression level by extracting data from the previous large-scale gene expression profiling study. Using Significance Analysis of Microarrays (SAM), we further searched for genes that show correlating expression with PIK3CA. Results: We have identified PIK3CA mutations in 4 cases (4.3%), all involving the previously reported hotspots. Among these 4 cases, 3 tumours demonstrated microsatellite instability and 2 tumours harboured concurrent KRAS mutation. Data extracted from microarray studies showed an increased expression of PIK3CA in gastric cancers when compared with the non-neoplastic gastric mucosae (p < 0.001). SAM further identified 2910 genes whose expression levels were positively associated with that of PIK3CA. Conclusion: Our data suggested that activation of the PI3K signalling pathway in gastric cancer may be achieved through up-regulation or mutation of PIK3CA, in which the latter may be a consequence of mismatch repair deficiency. © 2005 Li et al; BioMed Central Ltd.en_HK
dc.languageengen_HK
dc.publisherBioMed Central Ltd. The Journal's web site is located at http://www.biomedcentral.com/bmccancer/en_HK
dc.relation.ispartofBMC Canceren_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.rightsB M C Cancer. Copyright © BioMed Central Ltd.en_HK
dc.subject.mesh1-Phosphatidylinositol 3-Kinase - geneticsen_HK
dc.subject.meshAdenocarcinoma - geneticsen_HK
dc.subject.meshMutationen_HK
dc.subject.meshStomach Neoplasms - geneticsen_HK
dc.subject.meshMicrosatellite Repeatsen_HK
dc.titleMutations of PIK3CA in gastric adenocarcinomaen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1471-2407&volume=5&spage=29&epage=&date=2005&atitle=Mutations+of+PIK3CA+in+gastric+adenocarcinomaen_HK
dc.identifier.emailChan, TL: tlchan@hku.hken_HK
dc.identifier.emailChan, ASW: agnes@genome.hku.hken_HK
dc.identifier.emailChu, KM: chukm@hkucc.hku.hken_HK
dc.identifier.emailLeung, SY: suetyi@hkucc.hku.hken_HK
dc.identifier.authorityChan, TL=rp00418en_HK
dc.identifier.authorityChan, ASW=rp00288en_HK
dc.identifier.authorityChu, KM=rp00435en_HK
dc.identifier.authorityLeung, SY=rp00359en_HK
dc.description.naturepublished_or_final_versionen_HK
dc.identifier.doi10.1186/1471-2407-5-29en_HK
dc.identifier.pmid15784156en_HK
dc.identifier.pmcidPMC1079799-
dc.identifier.scopuseid_2-s2.0-22144491262en_HK
dc.identifier.hkuros98945-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-22144491262&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume5en_HK
dc.identifier.isiWOS:000228165300001-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridLi, VSW=55055323800en_HK
dc.identifier.scopusauthoridWong, CW=35148671700en_HK
dc.identifier.scopusauthoridChan, TL=7402687537en_HK
dc.identifier.scopusauthoridChan, ASW=37019607500en_HK
dc.identifier.scopusauthoridZhao, W=55248923400en_HK
dc.identifier.scopusauthoridChu, KM=7402453538en_HK
dc.identifier.scopusauthoridSo, S=35238727400en_HK
dc.identifier.scopusauthoridChen, X=8978110800en_HK
dc.identifier.scopusauthoridYuen, ST=8323342200en_HK
dc.identifier.scopusauthoridLeung, SY=7202044886en_HK

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