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

This Article Full Text Full Text (PDF) 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 Author home page(s): Jae Yong Park Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Lee, E. B. Articles by Park, J. Y. Search for Related Content PubMed PubMed Citation Articles by Lee, E. B. Articles by Park, J. Y. Related Collections Lung - cancer

Ann Thorac Surg 2003;75:1597-1600
© 2003 The Society of Thoracic Surgeons

---

Original article: general thoracic

Loss of heterozygosity on the long arm of chromosome 21 in non–small cell lung cancer

^a Department of Thoracic and Cardiovascular Surgery, Kyungpook National University Hospital, Jung-gu, Daegu, South Korea
^b Department of Anatomical Pathology, Kyungpook National University Hospital, Jung-gu, Daegu, South Korea
^c Department of Internal Medicine, Kyungpook National University Hospital, Jung-gu, Daegu, South Korea
^d Department of Department of Biochemistry, School of Medicine, Kyungpook National University, Jung-gu, Daegu, South Korea

Accepted for publication November 25, 2002.

^* Address reprint requests to Dr Lee, Department of Thoracic and Cardiovascular Surgery, Kyungpook National University Hospital, 50 Samdeok 2-ga, Jung-gu, Daegu 700-721, South Korea.
e-mail: bay{at}knu.ac.kr

BACKGROUND: In Down syndrome, the incidence of solid tumors including lung cancer is considerably lower than that of the general population. The low risk of lung cancer in individuals with Down syndrome may be related to the gene-dosage effect of the extra chromosome 21. It may suggest that tumor suppressor genes playing a role in the pathogenesis of lung cancer may be present on chromosome 21.

METHODS: A total of 39 surgically resected non–small cell lung cancers were analyzed using nine microsatellite markers for 21q. Loss of heterozygosity was considered to be present when the signal intensity of the allele in tumor DNA was less than 50% of that in the corresponding normal DNA.

RESULTS: Loss of heterozygosity for at least one locus was detected in 22 of 39 tumors (56.4%). Allelic loss was frequently detected at three distinct regions: at the locus D21S1432 on 21q21.1, the region between D21S1435 and D21S1442 on 21q21.2 to 21.3, and the region between D21S1270 and D21S1445 on 21q22.1.

CONCLUSIONS: These results indicate that loss of heterozygosity on 21q may play an important role in the pathogenesis of non–small cell lung cancer.

This article has been cited by other articles:

				R. M. Brena and J. F. Costello Genome-epigenome interactions in cancer Hum. Mol. Genet., April 15, 2007; 16(R1): R96 - R105. [Abstract] [Full Text] [PDF]