Volume 24, Issue 4 pp. 351-355
Research Article

High-resolution deletion mapping of chromosome arm 1p in pancreatic cancer identifies a major consensus region at 1p35

Werner Hilgers

Werner Hilgers

Department of Pathology, The Johns Hopkins Medical Institutions, Baltimore, Maryland

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David J. Tang

David J. Tang

Department of Pathology, The Johns Hopkins Medical Institutions, Baltimore, Maryland

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Avrahom Y. Sugar

Avrahom Y. Sugar

Department of Pathology, The Johns Hopkins Medical Institutions, Baltimore, Maryland

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Manu C. Shekher

Manu C. Shekher

Department of Pathology, The Johns Hopkins Medical Institutions, Baltimore, Maryland

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Ralph H. Hruban

Ralph H. Hruban

Department of Pathology, The Johns Hopkins Medical Institutions, Baltimore, Maryland

Department of Oncology, The Johns Hopkins Medical Institutions, Baltimore, Maryland

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Scott E. Kern

Corresponding Author

Scott E. Kern

Department of Pathology, The Johns Hopkins Medical Institutions, Baltimore, Maryland

Department of Oncology, The Johns Hopkins Medical Institutions, Baltimore, Maryland

632 Ross Bldg., The Oncology Center, The Johns Hopkins University School of Medicine, Baltimore, MD 21205.Search for more papers by this author

Abstract

Chromosomal arm 1p has long been suspected, on the basis of loss of heterozygosity (LOH) and other data, to harbor a tumor suppressor gene important in pancreatic carcinomas and other tumors. We constructed a high-resolution map of LOH at 1p in a panel of pancreatic adenocarcinomas. Using 44 markers, we identified LOH on 1p in 49% of 43 cancers. Breakpoints in 1p were identified in 15 of the carcinomas and could be used to ascertain consensus patterns. We found a major consensus region of LOH at 1p35 between loci D1S233 and D1S247. This region participates in the majority of LOH events on 1p in pancreatic cancer. These data provide a roadmap for further regional mapping, homozygous deletion searches, comparison to LOH patterns seen in other tumor types, and prioritization of studies using candidate genes. Genes Chromosomes Cancer 24:351–355, 1999. © 1999 Wiley-Liss, Inc.

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