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Amplification and Expression of the Human Cyclin D Gene in Esophageal Cancer¹

Comprehensive Cancer Center and Institute of Cancer Research, Columbia University, College of Physicians and Surgeons, New York, New York 10032 [W. J., S. M. K., N. T., Y-J. Z., I. B. W.], and Cancer Institute, Chinese Academy of Medical Sciences, Beijing, People's Republic of China [S-H. L.]

Amplification of the hst-1 and int-2 genes on chromosome 11q13 has previously been found in over 20% of human primary esophageal cancers. However, these two genes do not appear to be transcribed in appreciable amounts. Recently, the human cyclin D gene (also referred to as prad1) has been mapped to the 11q13 locus. Here, we report coamplification of the cyclin D and hst-1 genes in 5 of 20 (25%) human squamous esophageal tumors. We also detected significant levels of cyclin D transcription in two esophageal carcinoma cell lines, even though they did not express detectable amounts of hst-1 transcription. These findings provide the first evidence for the amplification of a cyclin gene in human esophageal cancer and suggest that an increase in cyclin D gene dosage could be an important factor in the pathogenesis of esophageal cancer. Additionally, because the 11q13 locus is found to be amplified in many types of human tumors, cyclin gene amplification could also play an important role in the development of other forms of human cancer.

¹ Supported by National Cancer Institute Grant CA021111 to I. B. W. and an award from the Markey Charitable Trust.

² To whom requests for reprints should be addressed, at Comprehensive Cancer Center and Institute of Cancer Research, Columbia University, College of Physicians and Surgeons, Room 1509, 701 W. 168th Street, New York, NY 10032.

Received 1/21/92. Accepted 3/31/92.

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