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

This Article Full Text Alert me when this article is cited Alert me if a correction is posted Citation Map 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 Mitsudomi, T. Articles by Takahashi, T. Search for Related Content PubMed PubMed Citation Articles by Mitsudomi, T. Articles by Takahashi, T.

J Thorac Cardiovasc Surg 1997;114:354-360
© 1997 Mosby, Inc.

GENERAL THORACIC SURGERY

MUTATIONS OF THE P53 TUMOR SUPPRESSOR GENE AS CLONAL MARKER FOR MULTIPLE PRIMARY LUNG CANCERS

Received for publication March 11, 1997; revisions requested April 22, 1997; revisions received May 12, 1997; accepted for publication May 14, 1997. Address for reprints: Tetsuya Mitsudomi, MD, Chief, Department of Thoracic Surgery, Aichi Cancer Center Hospital, 1-1 Kanokoden, Chikusa-ku, Nagoya 464, Japan.

Abstract

Objectives: Second primary lung cancers are prevalent after treatment for initial lung cancer, and the lung is also one of the most frequent sites for recurrence after removal of early-stage lung cancer. The objective of the present study is to clarify the clonal origin of the second tumor with the p53 gene mutation used as a clonal marker. Methods: Of 794 consecutive patients who underwent pulmonary resection for primary lung cancer from 1980 to 1993, 22 required second pulmonary resection during the follow-up period, with a median interval of 38 months. We examined 16 of these patients for mutations of the p53 gene occurring in exons 5 through 8 by the polymerase chain reaction/single strand conformation polymorphism method. Differential diagnosis was also made on a morphologic basis, considering the degree of cellular differentiation and cytologic subtypes. Results: Nine of the 16 patients analyzed had at least one p53 mutation in their tumors. We were thus able to make molecular diagnoses for these patients. The mutational status of the p53 gene was discordant in all nine patients, suggesting a different clonal origin despite the fact that six of them had almost identical histologic features. Conclusions: Analysis of p53 gene mutations was thus useful in distinguishing second primary lung cancers from recurrent tumors. The observed heterogeneity of p53 status was also in line with the "field cancerization" concept.

This article has been cited by other articles:

				N. Girard, I. Ostrovnaya, C. Lau, B. Park, M. Ladanyi, D. Finley, C. Deshpande, V. Rusch, I. Orlow, W. D. Travis, et al. Genomic and Mutational Profiling to Assess Clonal Relationships Between Multiple Non-Small Cell Lung Cancers Clin. Cancer Res., August 15, 2009; 15(16): 5184 - 5190. [Abstract] [Full Text] [PDF]

				K. Steiling, J. Ryan, J. S. Brody, and A. Spira The Field of Tissue Injury in the Lung and Airway Cancer Prevention Research, November 1, 2008; 1(6): 396 - 403. [Abstract] [Full Text] [PDF]

				Y.-L. Chang, C.-T. Wu, S.-C. Lin, C.-F. Hsiao, Y.-S. Jou, and Y.-C. Lee Clonality and Prognostic Implications of p53 and Epidermal Growth Factor Receptor Somatic Aberrations in Multiple Primary Lung Cancers Clin. Cancer Res., January 1, 2007; 13(1): 52 - 58. [Abstract] [Full Text] [PDF]

				M. Berwick, I. Orlow, A. J. Hummer, B. K. Armstrong, A. Kricker, L. D. Marrett, R. C. Millikan, S. B. Gruber, H. Anton-Culver, R. Zanetti, et al. The Prevalence of CDKN2A Germ-Line Mutations and Relative Risk for Cutaneous Malignant Melanoma: An International Population-Based Study. Cancer Epidemiol. Biomarkers Prev., August 1, 2006; 15(8): 1520 - 1525. [Abstract] [Full Text] [PDF]

				C. B Begg, A. J Hummer, U. Mujumdar, B. K Armstrong, A. Kricker, L. D Marrett, R. C Millikan, S. B Gruber, H. A. Culver, R. Zanetti, et al. A design for cancer case-control studies using only incident cases: experience with the GEM study of melanoma Int. J. Epidemiol., June 1, 2006; 35(3): 756 - 764. [Abstract] [Full Text] [PDF]

				T. Koga, Y. Horio, T. Mitsudomi, T. Takahashi, and Y. Yatabe Identification of MGB1 as a Marker in the Differential Diagnosis of Lung Tumors in Patients with a History of Breast Cancer by Analysis of Publicly Available SAGE Data J. Mol. Diagn., May 1, 2004; 6(2): 90 - 95. [Abstract] [Full Text] [PDF]

				C. Paris, J. Benichou, S. Bota, S. Sagnier, J. Metayer, S. Eloy, J-B. Auliac, G. Nouvet, and L. Thiberville Occupational and nonoccupational factors associated with high grade bronchial pre-invasive lesions Eur. Respir. J., February 1, 2003; 21(2): 332 - 341. [Abstract] [Full Text] [PDF]

				S. BOTA, J.-B. AULIAC, C. PARIS, J. METAYER, R. SESBOUE, G. NOUVET, and L. THIBERVILLE Follow-up of Bronchial Precancerous Lesions and Carcinoma in Situ Using Fluorescence Endoscopy Am. J. Respir. Crit. Care Med., November 1, 2001; 164(9): 1688 - 1693. [Abstract] [Full Text] [PDF]

				R. B. Ponn Lightning Can Strike Twice : Second Primary Lung Cancers Chest, December 1, 2000; 118(6): 1526 - 1529. [Full Text] [PDF]

				S. Shimizu, Y. Yatabe, T. Koshikawa, N. Haruki, S. Hatooka, M. Shinoda, M. Suyama, M. Ogawa, N. Hamajima, R. Ueda, et al. High Frequency of Clonally Related Tumors in Cases of Multiple Synchronous Lung Cancers as Revealed by Molecular Diagnosis Clin. Cancer Res., October 1, 2000; 6(10): 3994 - 3999. [Abstract] [Full Text]