HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Rusch, V. W. Articles by Dmitrovsky, E. Search for Related Content PubMed PubMed Citation Articles by Rusch, V. W. Articles by Dmitrovsky, E.

The Journal of Thoracic and Cardiovascular Surgery, Vol 104, 1465-1469, Copyright © 1992 by The American Association for Thoracic Surgery and The Western Thoracic Surgical Association

ARTICLES

Ras oncogene point mutation: an infrequent event in bronchioloalveolar cancer

VW Rusch, VE Reuter, MG Kris, J Kurie, WH Miller Jr, DM Nanus, AP Albino and E Dmitrovsky
Laboratory of Molecular Medicine, Memorial Sloan-Kettering Cancer Center, New York, N.Y.

Ras oncogene point mutation, primarily activating the K-ras gene, has been reported in approximately one third of lung adenocarcinomas. This identifies a subset of early stage tumors clinically associated with smoking and an aggressive clinical course. Because of these findings, this study was undertaken to determine the occurrence of ras point mutations in bronchioloalveolar carcinoma. This uncommon form of lung adenocarcinoma is usually indolent but can sometimes present as a rapidly growing, multifocal tumor. Twenty tumor samples obtained at thoracotomy were examined for H-ras, K-ras, and N-ras oncogene mutational activation involving codons 12, 13, or 61. This was performed by an oligonucleotide hybridization technique following polymerase chain reaction amplification of these specific sequences. K- ras point mutation involving codon 12 was observed in two tumors, but not in the adjacent histologically benign lung tissue. These mutations were confirmed by direct sequencing of these polymerase chain reaction products. Both patients were smokers, had stage I tumors, and remain disease-free at 27 and 40 months postoperatively. No H-ras or N-ras point mutations were found. These findings suggest that ras activation is an infrequent event in bronchioloalveolar carcinoma. We speculate that ras activation is not a common transformational event in this form of lung adenocarcinoma.

This article has been cited by other articles:

				I. S. Sarkaria, M. F. Zakowski, D. Pham, M. Hezel, M. I. Ebright, S. Chuai, E. S. Venkatraman, M. G. Kris, V. W. Rusch, and B. Singh Epidermal Growth Factor Receptor Signaling in Adenocarcinomas With Bronchioloalveolar Components Ann. Thorac. Surg., January 1, 2008; 85(1): 216 - 223. [Abstract] [Full Text] [PDF]

				I. S. Sarkaria, D. Pham, R. A. Ghossein, S. G. Talbot, M. Hezel, M. E. Dudas, M. I. Ebright, S. Chuai, N. Memoli, E. S. Venkatraman, et al. SCCRO Expression Correlates With Invasive Progression in Bronchioloalveolar Carcinoma Ann. Thorac. Surg., November 1, 2004; 78(5): 1734 - 1741. [Abstract] [Full Text] [PDF]

				P. J. Mazzone, T. Mekhail, and A. C. Arroliga Is Lung Cancer in the Nonsmoker a Different Disease? Chest, August 1, 2004; 126(2): 326 - 329. [Full Text] [PDF]

				V. A. Miller, M. G. Kris, N. Shah, J. Patel, C. Azzoli, J. Gomez, L. M. Krug, W. Pao, N. Rizvi, B. Pizzo, et al. Bronchioloalveolar Pathologic Subtype and Smoking History Predict Sensitivity to Gefitinib in Advanced Non-Small-Cell Lung Cancer J. Clin. Oncol., March 15, 2004; 22(6): 1103 - 1109. [Abstract] [Full Text] [PDF]