PMID- 19253367
OWN - NLM
STAT- MEDLINE
DCOM- 20090414
LR  - 20181201
IS  - 1097-0215 (Electronic)
IS  - 0020-7136 (Linking)
VI  - 124
IP  - 11
DP  - 2009 Jun 1
TI  - Epidermal growth factor receptor gene mutations in papillary thyroid carcinoma.
PG  - 2744-9
LID - 10.1002/ijc.24250 [doi]
AB  - Recent studies have indicated that somatic mutations in the epidermal growth 
      factor receptor (EGFR) gene have been identified in a subset of patients with 
      nonsmall-cell lung cancer (NSCLC) and are associated with sensitivity to the 
      EGFR-tyrosine-kinase inhibitors. These mutations have been reported to be almost 
      exclusively found in a pulmonary adenocarcinoma subgroup of NSCLC, with a low 
      frequency in other solid tumors. We describe a patient with advanced-stage 
      papillary thyroid carcinoma (PTC) whose disease had been diagnosed as pulmonary 
      adenocarcinoma at first, and who had a marked response to the 
      EGFR-tyrosine-kinase inhibitor, gefitinib. An in-frame deletion in exon 19 that 
      eliminated 4 amino acids at positions 746 through 750, which is one of the common 
      drug-sensitive mutations in pulmonary adenocarcinoma, and a serine-to-proline 
      substitution at codon 752, were found in a tumor specimen of the patient. We 
      subsequently searched for mutations in the EGFR tyrosine kinase domain in primary 
      tumors from 23 patients with PTC, and drug-sensitive mutations commonly observed 
      in pulmonary adenocarcinoma were found in 7 of these patients. Our observation of 
      a high frequency of the EGFR-activating mutations in PTC suggests that the EGFR 
      mutation may be an important event in the development of PTC. EGFR gene 
      amplification, also considered to be a predictor of response to 
      EGFR-tyrosine-kinase inhibitors, was evaluated by fluorescence in situ 
      hybridization (FISH); however, only 1 FISH-positive tumor was detected. Our data 
      suggest that EGFR-tyrosine-kinase inhibitors may deserve consideration in the 
      treatment of a subset of patients with PTC, just as with pulmonary 
      adenocarcinoma.
FAU - Masago, Katsuhiro
AU  - Masago K
AD  - Department of Respiratory Medicine, Graduate School of Medicine, Kyoto 
      University, Kyoto, Japan.
FAU - Asato, Ryo
AU  - Asato R
FAU - Fujita, Shiro
AU  - Fujita S
FAU - Hirano, Shigeru
AU  - Hirano S
FAU - Tamura, Yoshihiro
AU  - Tamura Y
FAU - Kanda, Tomoko
AU  - Kanda T
FAU - Mio, Tadashi
AU  - Mio T
FAU - Katakami, Nobuyuki
AU  - Katakami N
FAU - Mishima, Michiaki
AU  - Mishima M
FAU - Ito, Juichi
AU  - Ito J
LA  - eng
PT  - Case Reports
PT  - Journal Article
PL  - United States
TA  - Int J Cancer
JT  - International journal of cancer
JID - 0042124
RN  - EC 2.7.10.1 (ErbB Receptors)
RN  - EC 2.7.11.1 (BRAF protein, human)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins B-raf)
SB  - IM
CIN - Int J Cancer. 2012 May 1;130(9):2215-7; author reply 2217-8. PMID: 21717456
MH  - Adult
MH  - Aged
MH  - Carcinoma, Papillary/drug therapy/*genetics
MH  - ErbB Receptors/antagonists & inhibitors/*genetics
MH  - Female
MH  - Humans
MH  - Male
MH  - *Mutation
MH  - Proto-Oncogene Proteins B-raf/genetics
MH  - Thyroid Neoplasms/drug therapy/*genetics
EDAT- 2009/03/03 09:00
MHDA- 2009/04/15 09:00
CRDT- 2009/03/03 09:00
PHST- 2009/03/03 09:00 [entrez]
PHST- 2009/03/03 09:00 [pubmed]
PHST- 2009/04/15 09:00 [medline]
AID - 10.1002/ijc.24250 [doi]
PST - ppublish
SO  - Int J Cancer. 2009 Jun 1;124(11):2744-9. doi: 10.1002/ijc.24250.