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Epidermal growth factor receptor status in anaplastic thyroid carcinoma

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dc.contributor.authorLee, Dae Ho-
dc.contributor.authorLee, Geon Kook-
dc.contributor.authorKong, Sun-Young-
dc.contributor.authorKook, Myoung Chul-
dc.contributor.authorYang, Sun Kyung-
dc.contributor.authorPark, So Yeon-
dc.contributor.authorPark, Seong Hoe-
dc.contributor.authorKeam, Bhumsuk-
dc.contributor.authorPark, Do Joon-
dc.contributor.authorCho, Bo Youn-
dc.contributor.authorKim, Seok Won-
dc.contributor.authorChung, Ki-Wook-
dc.contributor.authorLee, Eun Sook-
dc.contributor.authorKim, Sun Wook-
dc.date.accessioned2010-01-12T08:14:51Z-
dc.date.available2010-01-12T08:14:51Z-
dc.date.issued2006-11-03-
dc.identifier.citationJ Clin Pathol. 2007 Aug;60(8):881-4. Epub 2006 Nov 1.en
dc.identifier.issn0021-9746 (Print)-
dc.identifier.urihttp://jcp.bmj.com/cgi/content/abstract/60/8/881-
dc.identifier.urihttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=17079354-
dc.identifier.urihttps://hdl.handle.net/10371/29784-
dc.description.abstractBACKGROUND: The epidermal growth factor receptor (EGFR) has been reported to be overexpressed in anaplastic thyroid carcinoma (ATC). In vitro studies have shown that EGFR tyrosine kinase inhibitors (TKIs) greatly inhibit cellular growth and induced apoptosis in the ATC cell lines, while somatic mutations in the tyrosine kinase domain or an increased gene copy number are associated with increased sensitivity to TKIs in non-small cell lung cancer. AIM: To investigate the prevalence of EGFR overexpression, gene amplification and activating mutation in the tyrosine kinase domain in patients with ATC. METHODS: The EGFR gene status and protein expression were investigated by direct DNA sequencing of the hot-spot regions in exons 18, 19 and 21, fluorescence in situ hybridisation (FISH), and immunohistochemistry in tumour tissues from 23 patients with ATC. RESULTS: On mutational analysis and FISH, neither mutations in the hot-spots nor gene amplification was observed. However, high polysomy was identified in 14/23 (60.9%) patients with ATC. All cases with immunohistochemistry (IHC) positivity (n = 6) had high polysomy, whereas 8/17 (47.1%) cases with IHC negativity had high polysomy (p = 0.048). High polysomy was observed in all 10 cases with giant cell subtype, but in only 4/11 (36.3%) with squamoid and 0/2 with spindle cell sarcomatoid subtype. There was no statistically significant correlation between FISH positivity of ATC tumour and presence of well-differentiated component. CONCLUSION: Despite the low incidence of somatic EGFR gene mutation and amplification in the study samples, in view of the fact that high polysomy was often identified by FISH, as well as the current lack of therapeutic options, EGFR TKIs are worth investigating for treating the patients with ATC who have at least giant cell subtype.en
dc.language.isoenen
dc.publisherBritish Medical Associationen
dc.subjectAgeden
dc.subjectAged, 80 and overen
dc.subjectDNA Mutational Analysis/methodsen
dc.subjectDNA, Neoplasm/geneticsen
dc.subjectFemaleen
dc.subjectGene Amplification/geneticsen
dc.subjectGene Expression Regulation, Neoplastic/geneticsen
dc.subjectGenes, erbB-1/geneticsen
dc.subjectHumansen
dc.subjectImmunohistochemistry/methodsen
dc.subjectIn Situ Hybridization, Fluorescence/methodsen
dc.subjectMaleen
dc.subjectMiddle Ageden
dc.subjectMutation/geneticsen
dc.subjectProtein-Tyrosine Kinases/antagonists & inhibitors/geneticsen
dc.subjectReceptor, Epidermal Growth Factor/analysis/*geneticsen
dc.subjectThyroid Neoplasms/*genetics/pathologyen
dc.titleEpidermal growth factor receptor status in anaplastic thyroid carcinomaen
dc.typeArticleen
dc.contributor.AlternativeAuthor이대호-
dc.contributor.AlternativeAuthor이건국-
dc.contributor.AlternativeAuthor공선영-
dc.contributor.AlternativeAuthor국명철-
dc.contributor.AlternativeAuthor양선경-
dc.contributor.AlternativeAuthor박소연-
dc.contributor.AlternativeAuthor박성회-
dc.contributor.AlternativeAuthor김범석-
dc.contributor.AlternativeAuthor박도준-
dc.contributor.AlternativeAuthor조보연-
dc.contributor.AlternativeAuthor김석원-
dc.contributor.AlternativeAuthor정기욱-
dc.contributor.AlternativeAuthor이은숙-
dc.contributor.AlternativeAuthor김선욱-
dc.identifier.doi10.1136/jcp.2006.041251-
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