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Epidermal growth factor receptor status in anaplastic thyroid carcinoma

Cited 35 time in Web of Science Cited 37 time in Scopus
Authors
Lee, Dae Ho; Lee, Geon Kook; Kong, Sun-Young; Kook, Myoung Chul; Yang, Sun Kyung; Park, So Yeon; Park, Seong Hoe; Keam, Bhumsuk; Park, Do Joon; Cho, Bo Youn; Kim, Seok Won; Chung, Ki-Wook; Lee, Eun Sook; Kim, Sun Wook
Issue Date
2006-11-03
Publisher
British Medical Association
Citation
J Clin Pathol. 2007 Aug;60(8):881-4. Epub 2006 Nov 1.
Keywords
AgedAged, 80 and overDNA Mutational Analysis/methodsDNA, Neoplasm/geneticsFemaleGene Amplification/geneticsGene Expression Regulation, Neoplastic/geneticsGenes, erbB-1/geneticsHumansImmunohistochemistry/methodsIn Situ Hybridization, Fluorescence/methodsMaleMiddle AgedMutation/geneticsProtein-Tyrosine Kinases/antagonists & inhibitors/geneticsReceptor, Epidermal Growth Factor/analysis/*geneticsThyroid Neoplasms/*genetics/pathology
Abstract
BACKGROUND: 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.
ISSN
0021-9746 (Print)
Language
English
URI
http://jcp.bmj.com/cgi/content/abstract/60/8/881

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=17079354

http://hdl.handle.net/10371/29784
DOI
https://doi.org/10.1136/jcp.2006.041251
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College of Medicine/School of Medicine (의과대학/대학원)Internal Medicine (내과학전공)Journal Papers (저널논문_내과학전공)
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