Association of epidermal growth factor receptor (EGFR) gene copy number amplification with neck lymph node metastasis in areca-associated oral carcinomas

Wei Fan Chiang, Shyun Yeu Liu, Ching Yu Yen, Chin Nan Lin, Yen Chia Chen, Shu Chun Lin, Kuo Wei Chang

研究成果: 雜誌貢獻文章

44 引文 (Scopus)

摘要

Epidermal growth factor receptor (EGFR) has an important role in cell proliferation, differentiation, and transformation. Several alterations and activation of EGFR have been identified in tumors. Inhibitors that impair EGFR activity have been identified and studied for cancer therapy, so the present study was conducted to comprehensively assess the amplification, mutation, and expression of EGFR in areca-associated oral squamous cell carcinoma (OSCC), which might be beneficial for targeting therapy. Gene copy number amplifications of EGFR were identified in 33% (14/42) cases of OSCC. Six cases of OSCC had a high copy number amplification. Direct sequencing of PCR products of 20 representative cases of OSCC revealed no somatic mutation in the kinase domains of EGFR. Sixty-seven percent (28/42) of the OSCC cases had nuclear and/or cytosolic EGFR immunoreactivity. Significant increases in EGFR copy number and EGFR immunoreactivity were found in OSCC subjects compared with long-term areca chewers, or compared with match adjacent oral mucosa (P <0.0001 and P = 0.029, respectively). Interestingly, OSCC with nodal involvement had significantly higher EGFR gene copy number than OSCC without nodal involvement (3.194 ± 0.740 versus 1.733 ± 0.246; P = 0.050). Our data suggest that genomic amplification could be a genetic basis underlying activation of the EGFR pathway in areca-associated OSCC.
原文英語
頁(從 - 到)270-276
頁數7
期刊Oral Oncology
44
發行號3
DOIs
出版狀態已發佈 - 三月 2008
對外發佈Yes

指紋

Areca
erbB-1 Genes
Gene Dosage
Epidermal Growth Factor Receptor
Neck
Squamous Cell Carcinoma
Lymph Nodes
Neoplasm Metastasis
Carcinoma
Mutation
Mouth Mucosa
Cell Differentiation
Neoplasms
Cell Proliferation

ASJC Scopus subject areas

  • Oncology

引用此文

Association of epidermal growth factor receptor (EGFR) gene copy number amplification with neck lymph node metastasis in areca-associated oral carcinomas. / Chiang, Wei Fan; Liu, Shyun Yeu; Yen, Ching Yu; Lin, Chin Nan; Chen, Yen Chia; Lin, Shu Chun; Chang, Kuo Wei.

於: Oral Oncology, 卷 44, 編號 3, 03.2008, p. 270-276.

研究成果: 雜誌貢獻文章

Chiang, Wei Fan ; Liu, Shyun Yeu ; Yen, Ching Yu ; Lin, Chin Nan ; Chen, Yen Chia ; Lin, Shu Chun ; Chang, Kuo Wei. / Association of epidermal growth factor receptor (EGFR) gene copy number amplification with neck lymph node metastasis in areca-associated oral carcinomas. 於: Oral Oncology. 2008 ; 卷 44, 編號 3. 頁 270-276.
@article{524e30ececd14eb2b0c4684faf532e5a,
title = "Association of epidermal growth factor receptor (EGFR) gene copy number amplification with neck lymph node metastasis in areca-associated oral carcinomas",
abstract = "Epidermal growth factor receptor (EGFR) has an important role in cell proliferation, differentiation, and transformation. Several alterations and activation of EGFR have been identified in tumors. Inhibitors that impair EGFR activity have been identified and studied for cancer therapy, so the present study was conducted to comprehensively assess the amplification, mutation, and expression of EGFR in areca-associated oral squamous cell carcinoma (OSCC), which might be beneficial for targeting therapy. Gene copy number amplifications of EGFR were identified in 33{\%} (14/42) cases of OSCC. Six cases of OSCC had a high copy number amplification. Direct sequencing of PCR products of 20 representative cases of OSCC revealed no somatic mutation in the kinase domains of EGFR. Sixty-seven percent (28/42) of the OSCC cases had nuclear and/or cytosolic EGFR immunoreactivity. Significant increases in EGFR copy number and EGFR immunoreactivity were found in OSCC subjects compared with long-term areca chewers, or compared with match adjacent oral mucosa (P <0.0001 and P = 0.029, respectively). Interestingly, OSCC with nodal involvement had significantly higher EGFR gene copy number than OSCC without nodal involvement (3.194 ± 0.740 versus 1.733 ± 0.246; P = 0.050). Our data suggest that genomic amplification could be a genetic basis underlying activation of the EGFR pathway in areca-associated OSCC.",
keywords = "Amplification, EGFR, Oral cancer",
author = "Chiang, {Wei Fan} and Liu, {Shyun Yeu} and Yen, {Ching Yu} and Lin, {Chin Nan} and Chen, {Yen Chia} and Lin, {Shu Chun} and Chang, {Kuo Wei}",
year = "2008",
month = "3",
doi = "10.1016/j.oraloncology.2007.02.008",
language = "English",
volume = "44",
pages = "270--276",
journal = "Oral Oncology",
issn = "1368-8375",
publisher = "Elsevier Limited",
number = "3",

}

TY - JOUR

T1 - Association of epidermal growth factor receptor (EGFR) gene copy number amplification with neck lymph node metastasis in areca-associated oral carcinomas

AU - Chiang, Wei Fan

AU - Liu, Shyun Yeu

AU - Yen, Ching Yu

AU - Lin, Chin Nan

AU - Chen, Yen Chia

AU - Lin, Shu Chun

AU - Chang, Kuo Wei

PY - 2008/3

Y1 - 2008/3

N2 - Epidermal growth factor receptor (EGFR) has an important role in cell proliferation, differentiation, and transformation. Several alterations and activation of EGFR have been identified in tumors. Inhibitors that impair EGFR activity have been identified and studied for cancer therapy, so the present study was conducted to comprehensively assess the amplification, mutation, and expression of EGFR in areca-associated oral squamous cell carcinoma (OSCC), which might be beneficial for targeting therapy. Gene copy number amplifications of EGFR were identified in 33% (14/42) cases of OSCC. Six cases of OSCC had a high copy number amplification. Direct sequencing of PCR products of 20 representative cases of OSCC revealed no somatic mutation in the kinase domains of EGFR. Sixty-seven percent (28/42) of the OSCC cases had nuclear and/or cytosolic EGFR immunoreactivity. Significant increases in EGFR copy number and EGFR immunoreactivity were found in OSCC subjects compared with long-term areca chewers, or compared with match adjacent oral mucosa (P <0.0001 and P = 0.029, respectively). Interestingly, OSCC with nodal involvement had significantly higher EGFR gene copy number than OSCC without nodal involvement (3.194 ± 0.740 versus 1.733 ± 0.246; P = 0.050). Our data suggest that genomic amplification could be a genetic basis underlying activation of the EGFR pathway in areca-associated OSCC.

AB - Epidermal growth factor receptor (EGFR) has an important role in cell proliferation, differentiation, and transformation. Several alterations and activation of EGFR have been identified in tumors. Inhibitors that impair EGFR activity have been identified and studied for cancer therapy, so the present study was conducted to comprehensively assess the amplification, mutation, and expression of EGFR in areca-associated oral squamous cell carcinoma (OSCC), which might be beneficial for targeting therapy. Gene copy number amplifications of EGFR were identified in 33% (14/42) cases of OSCC. Six cases of OSCC had a high copy number amplification. Direct sequencing of PCR products of 20 representative cases of OSCC revealed no somatic mutation in the kinase domains of EGFR. Sixty-seven percent (28/42) of the OSCC cases had nuclear and/or cytosolic EGFR immunoreactivity. Significant increases in EGFR copy number and EGFR immunoreactivity were found in OSCC subjects compared with long-term areca chewers, or compared with match adjacent oral mucosa (P <0.0001 and P = 0.029, respectively). Interestingly, OSCC with nodal involvement had significantly higher EGFR gene copy number than OSCC without nodal involvement (3.194 ± 0.740 versus 1.733 ± 0.246; P = 0.050). Our data suggest that genomic amplification could be a genetic basis underlying activation of the EGFR pathway in areca-associated OSCC.

KW - Amplification

KW - EGFR

KW - Oral cancer

UR - http://www.scopus.com/inward/record.url?scp=39149095593&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=39149095593&partnerID=8YFLogxK

U2 - 10.1016/j.oraloncology.2007.02.008

DO - 10.1016/j.oraloncology.2007.02.008

M3 - Article

C2 - 17468034

AN - SCOPUS:39149095593

VL - 44

SP - 270

EP - 276

JO - Oral Oncology

JF - Oral Oncology

SN - 1368-8375

IS - 3

ER -