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) Submit a response Alert me when this article is cited Alert me when eLetters are posted 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 Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Parrella, P. Articles by Merbs, S. L. Search for Related Content PubMed PubMed Citation Articles by Parrella, P. Articles by Merbs, S. L.

Detection of c-myc Amplification in Uveal Melanoma by Fluorescent In Situ Hybridization

¹ From the Dipartimento Ricerca BioMedica, Section for Molecular Medicine and Gene Therapy, University Campus Bio Medico, Rome, Italy; ² Department of Otolaryngology—Head and Neck Surgery, Division of Head and Neck Cancer Research, and ³ Wilmer Ophthalmological Institute, Department of Ophthalmology, Johns Hopkins University School of Medicine, Baltimore, Maryland.

PURPOSE. Genetic abnormalities of chromosomal arm 8q have been reported by many studies in uveal melanoma. To better understand the role of 8q abnormalities in uveal melanoma development, copy number anomalies of the c-myc oncogene (located on 8q24.1) have been investigated.

METHODS. Forty-three uveal melanomas were analyzed by fluorescent in situ hybridization (FISH) with probes for c-myc and the chromosome 8 centromere. Results of the FISH analysis were compared with genetic changes previously detected by microsatellite analysis on chromosomes 3 and 6p.

RESULTS. Thirty uveal melanomas (70%) had extra copies of c-myc, 2 tumors (5%) had loss of c-myc, and 11 tumors (25%) had no abnormalities in c-myc copy number. Of those with extra copies of c-myc, 13 tumors (43%) had amplification of the c-myc gene, 14 tumors (47%) had an intermediate relative increase in the c-myc copy number, and 3 tumors (10%) had a simple gain of chromosome 8. An association between larger tumor size and c-myc amplification was found (P < 0.01). Although extra copies of c-myc were seen in tumors with retention of chromosome 3, remarkably only tumors with monosomy 3 showed amplification of c-myc (P = 0.03).

CONCLUSIONS. The specific amplification of the c-myc oncogene detected in at least 30% of primary uveal melanomas cannot be explained by the simple 8q abnormalities observed in cytogenetic studies. The striking association between c-myc amplification and monosomy 3 suggests a unique pathway of genetic progression in a subset of uveal melanomas.

This article has been cited by other articles:

				J. P. Ehlers, L. Worley, M. D. Onken, and J. W. Harbour Integrative Genomic Analysis of Aneuploidy in Uveal Melanoma Clin. Cancer Res., January 1, 2008; 14(1): 115 - 122. [Abstract] [Full Text] [PDF]

				T. Meir, R. Dror, X. Yu, J. Qian, I. Simon, J. Pe'er, and I. Chowers Molecular Characteristics of Liver Metastases from Uveal Melanoma Invest. Ophthalmol. Vis. Sci., November 1, 2007; 48(11): 4890 - 4896. [Abstract] [Full Text] [PDF]

				J. P. Ehlers, L. Worley, M. D. Onken, and J. W. Harbour DDEF1 Is Located in an Amplified Region of Chromosome 8q and Is Overexpressed in Uveal Melanoma Clin. Cancer Res., May 15, 2005; 11(10): 3609 - 3613. [Abstract] [Full Text] [PDF]

				J. P. Ehlers and J. W. Harbour NBS1 Expression as a Prognostic Marker in Uveal Melanoma Clin. Cancer Res., March 1, 2005; 11(5): 1849 - 1853. [Abstract] [Full Text] [PDF]

				L. Madi, S. Bar-Yehuda, F. Barer, E. Ardon, A. Ochaion, and P. Fishman A3 Adenosine Receptor Activation in Melanoma Cells: ASSOCIATION BETWEEN RECEPTOR FATE AND TUMOR GROWTH INHIBITION J. Biol. Chem., October 24, 2003; 278(43): 42121 - 42130. [Abstract] [Full Text] [PDF]