JMD Association for Molecular Pathology 2008 Annual Meeting
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Purchase Article
Right arrow View Shopping Cart
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Sonobe, M.
Right arrow Articles by Tanaka, F.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Sonobe, M.
Right arrow Articles by Tanaka, F.
JMD 2006, Vol. 8, No. 3
Copyright © 2006 American Society for Investigative Pathology & Association for Molecular Pathology

Lung Adenocarcinoma Harboring Mutations in the ERBB2 Kinase Domain

Makoto Sonobe*, Toshiaki Manabe{dagger}, Hiromi Wada* and Fumihiro Tanaka*

From the Department of Thoracic Surgery * and the Laboratory of Anatomic Pathology, {dagger} Kyoto University Hospital, Kyoto, Japan

Mutations in the ERBB2kinase domain have been reported in non-small cell lung cancer (NSCLC). Here, we describe a detailed search for ERBB2 gene mutations in tumors derived from NSCLC patients. Tumor specimens from 223 patients who underwent resection for NSCLC were examined for the presence of mutations in exons 19 and 20 of the ERBB2gene. Correlations were then made between the expression of these mutations and the clinical characteristics of the patients from which they were derived as well as the tumor’s pathological features. ERBB2mutations were observed in four of the above tumors (1.8%), all of which were adenocarcinomas. All ERBB2mutations were in-frame insertions that occurred in exon 20. The patients from whom these tumors were derived were nonsmokers. Three of the tumors were of the papillary subtype, and one was a mixed subtype that consisted of acinar, papillary, and solid components. None of the tumors had a bronchio-alveolar component nor did they have epidermal growth factor receptoror K-rascodon 12 mutations. In conclusion, patients with these tumors tended to be nonsmokers who had clinical features similar to those of lung cancer patients whose tumors expressed epidermal growth factor receptormutations, although their tumors showed slightly different pathological features.






HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2006 by the American Society for Investigative Pathology and the Association for Molecular Pathology.