This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Suzuki, T. Articles by Terada, M. Search for Related Content PubMed PubMed Citation Articles by Suzuki, T. Articles by Terada, M.

Frequent Loss of Heterozygosity on Chromosome 14q in Neuroblastoma¹

National Cancer Center Research Institute, 1-1, Tsukiji 5-chome, Chuo-ku, Tokyo 104 [T. S., J. Y., T. S., M. T.]; and Department of Pediatrics [T. S., H. M., M. O.] and Pediatric Surgery [I. O.], Nihon University, School of Medicine, Itabashi-ku, Tokyo 173, Japan

Using 29 polymorphic DNA markers which detect allelic deletion of genes at specific loci on 19 different chromosomes, we analyzed 14 neuroblastomas for possible loss of chromosomal heterozygosity. The incidence of loss of heterozygosity was high at the D14S1 locus on chromosome 14q, being detected in six of 12 patients (50%). In spite of the cytogenetic finding suggesting high frequency of chromosome 1p deletion, loss of heterozygosity at the MYCL locus on 1p32 was detected only in two of nine patients (22%). It was also found in two of 11 patients (18%) on 13q, but not on chromosomes 2, 3, 5, 6, 7, 8, 9, 10, 11, 12, 15, 16, 17, 18, 19, and 20. The present results indicate that recessive genetic changes involving sequences on chromosome 14q may play an important role in the development of neuroblastoma.

¹ This work was supported in part by a Grant-in-Aid for a Comprehensive 10-Year Strategy for Cancer Control from the Ministry of Health and Welfare of Japan, a Grant-in-Aid from the Ministry of Health and Welfare of Japan and a Grant-in-Aid from the Ministry of Education, Science and Culture of Japan. Takashi Suzuki is an awardee of a Research Resident Fellowship from the Foundation for Promotion of Cancer Research.

² To whom requests for reprints should be addressed, at Genetics Division, National Cancer Center Research Institute, 1-1 Tsukiji 5-chome, Chuo-ku, Tokyo 104, Japan.

Received 8/15/88. Revised 11/17/88. Accepted 11/28/88.

This article has been cited by other articles:

				D Kamnasaran and D W Cox Current status of human chromosome 14 J. Med. Genet., February 1, 2002; 39(2): 81 - 90. [Abstract] [Full Text] [PDF]

				N Bown Neuroblastoma tumour genetics: clinical and biological aspects J. Clin. Pathol., December 1, 2001; 54(12): 897 - 910. [Abstract] [Full Text] [PDF]

				K. Ogawa, M. Osanai, M. Obata, K. Ishizaki, and K. Kamiya Gain of chromosomes 15 and 19 is frequent in both mouse hepatocellular carcinoma cell lines and primary tumors, but loss of chromosomes 4 and 12 is detected only in the cell lines Carcinogenesis, November 1, 1999; 20(11): 2083 - 2088. [Abstract] [Full Text] [PDF]

				J. M. Maris and K. K. Matthay Molecular Biology of Neuroblastoma J. Clin. Oncol., July 1, 1999; 17(7): 2264 - 2264. [Abstract] [Full Text] [PDF]

				H. Caron, P. van Sluis, J. de Kraker, J. Bokkerink, M. Egeler, G. Laureys, R. Slater, A. Westerveld, P.A. VoUte, and R. Versteeg Allelic Loss of Chromosome 1p as a Predictor of Unfavorable Outcome in Patients with Neuroblastoma N. Engl. J. Med., January 25, 1996; 334(4): 225 - 230. [Abstract] [Full Text] [PDF]