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[Cancer Research 55, 2394-2399, June 1, 1995]
© 1995 American Association for Cancer Research

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Consistent Chromosome Abnormalities in Adenocarcinoma of the Pancreas1

Constance A. Griffin2, Ralph H. Hruban, Laura A. Morsberger, Tara Ellingham, Patricia P. Long, Elizabeth M. Jaffee, Karen M. Hauda, Stefan K. Bohlander and Charles J. Yeo

The Johns Hopkins School of Medicine, Baltimore, Maryland 21287 [C. A. G., R. H. H., L. A. M., T. E., P. P. L., E. M. J., K. M. H., C. J. Y.], and The University of Chicago, Chicago, Illinois [S. K. B.]

Little is known about the somatic genetic changes which characterize pancreatic adenocarcinoma. The identification of acquired genomic alterations would further our understanding of the biology of this neoplasm. We have studied 62 primary pancreatic adenocarcinomas obtained from surgical resections using classical cytogenetics and fluorescent in situ hybridization methods. Clonally abnormal karyotypes were observed in 44 neoplasms. Karyotypes were generally complex (greater than three abnormalities) and included both numerical and structural chromosome abnormalities. Many tumors contained at least one marker chromosome. The most frequent whole chromosomal gains were chromosomes 20 (eight tumors) and 7 (seven tumors). Losses were much more frequent: chromosome 18 was lost in 22 tumors followed in frequency by chromosomes 13 (16 tumors), 12 (13 tumors), 17 (13 tumors), and 6 (12 tumors). Structural abnormalities were frequent. Two hundred nine chromosome breakpoints were identified. Excluding Robertsonian translocations, the chromosomal arms most frequently involved were 1p (12); 6q (11); 7q and 17p (9 each); and 1q, 3p, 11p, and 19q (8 each). Portions of the long arm of chromosome 6 appeared to be lost in nine tumors. To determine whether the apparent losses of portions of 6q are real, four tumors with 6q deletions were hybridized with a biotin-labeled microdissection probe from 6q24-ter. Loss of one copy of this region was verified in three of four tumors. In addition, double minute chromosomes were identified in eight cases. To our knowledge, these represent the first primary specimens of pancreatic adenocarcinoma with cytogenetic evidence of gene amplification.

1 This work was supported by Grants RO1-CA-56130, 2P30-CA06973, and 1P50CA62924 from the National Cancer Institute.

2 To whom requests for reprints should be addressed, at The Johns Hopkins Oncology Center 1-109, 600 North Wolfe Street, Baltimore, MD 21287-8934.

Received 12/15/94. Accepted 3/30/95.




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HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
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Copyright © 1995 by the American Association for Cancer Research.