| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
Departments of Otolaryngology [A. M., D. S.], Oncology [D. S., M. M., S. B.], and Pathology [E. G.], Division of Head and Neck Cancer Research, Johns Hopkins University, School of Medicine, Baltimore, Maryland 21205; and Department of Pathology [R. V.], Duke University, Durham, North Carolina 27710
We analyzed the pattern of allelic loss in 33 primary human small cell lung cancers (SCLCs) using highly informative microsatellite markers on chromosomes 2p, 3p, 5q, 6, 9, 13q, and 17p. Nineteen of these tumors (58%) displayed loss of heterozygosity on chromosome 9. Fourteen SCLCs demonstrated loss of heterozygosity for all informative markers on both chromosomal arms; two tumors demonstrated partial loss on chromosome 9p. In one tumor, a multiplex polymerase chain reaction assay disclosed a homozygous deletion at 9p2122 including the markers IFN-
, D9S126, and D9S171. Two SCLCs retained all informative markers on 9p but showed allelic loss of the entire 9q arm, while one case had a partial loss of proximal 9q extending into all of 9p. Analysis of other chromosomal arms showed loss of heterozygosity on 3p (93%), 5q (75%), 6p (46%), 6q (47%), 13q (75%), and 17p (93%). It was necessary to test multiple markers at several loci because of the frequent expression of microsatellite instability that confounded our mapping efforts in SCLCs with replication errors. This study demonstrates the frequent loss of a suppressor gene locus on chromosome 9p2122 and identifies novel suppressor loci on 6p, 6q, and 9q in primary SCLC.
1 Supported by National Cancer Institute Lung Spore Grant CA-58184-01 and by Schweizerische Stiftung für medizinisch-biologische Stipendien (A. M.).
2 To whom requests for reprints should be adressed, at Department of Otolaryngology, Division of Head and Neck Cancer Research, Johns Hopkins School of Medicine, 720 Rutland Avenue, Baltimore, MD 21205.
Received 2/10/94. Accepted 3/21/94.
This article has been cited by other articles:
![]() |
H. Izumi, J. Inoue, S. Yokoi, H. Hosoda, T. Shibata, M. Sunamori, S. Hirohashi, J. Inazawa, and I. Imoto Frequent silencing of DBC1 is by genetic or epigenetic mechanisms in non-small cell lung cancers Hum. Mol. Genet., April 15, 2005; 14(8): 997 - 1007. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. M. Garcia-Castellano, A. Villanueva, J. H. Healey, R. Sowers, C. Cordon-Cardo, A. Huvos, J. R. Bertino, P. Meyers, and R. Gorlick Methylthioadenosine Phosphorylase Gene Deletions Are Common in Osteosarcoma Clin. Cancer Res., March 1, 2002; 8(3): 782 - 787. [Abstract] [Full Text] [PDF] |
||||
![]() |
Y. Hatta, Y. Yamada, M. Tomonaga, I. Miyoshi, J. W. Said, and H. P. Koeffler Detailed Deletion Mapping of the Long Arm of Chromosome 6 in Adult T-Cell Leukemia Blood, January 15, 1999; 93(2): 613 - 616. [Abstract] [Full Text] [PDF] |
||||
![]() |
V. G. Gorgoulis, P. Zacharatos, A. Kotsinas, T. Liloglou, A. Kyroudi, M. Veslemes, A. Rassidakis, T. D. Halazonetis, J. K. Field, and C. Kittas Alterations of the p16-pRb Pathway and the Chromosome Locus 9p21–22 in Non-Small-Cell Lung Carcinomas : Relationship with p53 and MDM2 Protein Expression Am. J. Pathol., December 1, 1998; 153(6): 1749 - 1765. [Abstract] [Full Text] [PDF] |
||||
![]() |
P Cairns, L Mao, A Merlo, D. Lee, D Schwab, Y Eby, K Tokino, P van der Riet, J. Blaugrund, and D Sidransky Rates of p16 (MTS1) mutations in primary tumors with 9p loss Science, July 15, 1994; 265(5170): 415 - 417. [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Cancer Research | Clinical Cancer Research |
| Cancer Epidemiology Biomarkers & Prevention | Molecular Cancer Therapeutics |
| Molecular Cancer Research | Cancer Prevention Research |
| Cancer Prevention Journals Portal | Cancer Reviews Online |
| Annual Meeting Education Book | Meeting Abstracts Online |