Molecular cytogenetic characterization of esophageal cancer detected by comparative genomic hybridization

Authors

  • Yuli C. Chang,

    1. Departments of Medical Research and Laboratory Medicine, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan
    2. Graduate Institute of Medical Research, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan
    Search for more papers by this author
  • Kun-Tu Yeh,

    1. Department of Pathology, Changhua Christian Hospital, Changhua, Taiwan
    Search for more papers by this author
  • Ta-Chih Liu,

    1. Departments of Medical Research and Laboratory Medicine, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan
    2. Graduate Institute of Medical Research, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan
    Search for more papers by this author
  • Jan-Gowth Chang

    Corresponding author
    1. Departments of Medical Research and Laboratory Medicine, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan
    2. Graduate Institute of Medical Research, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan
    • Department of Laboratory Medicine, Kaohsiung Medical University Hospital, No.100, Tzyou 1st Road, Kaohsiung 807, Taiwan
    Search for more papers by this author

Abstract

Aim: Detection of cytogenetic alterations in esophageal cancer (EC). A total of 40 cases of primary EC and their paired nearby nontumor tissues were collected. The comparative genomic hybridization (CGH) is the technique that brings out the gains and losses of chromosome fragments and was applied to determine the aberrations from the tissue DNA. In noncancer tissues, the gains were at 19p (5/40, 13%), 20q (5/40, 13%), and losses at 9p (13/40, 33%), 2q (10/40, 25%), 12q (10/40, 25%), 13q (10/40, 25%), 5q (9/40, 23%), 6q (9/40, 23%), 7q (9/40, 23%), and 8p (9/40, 23%). Two cases in nontumor tissues showed no CGH change. In the 40 cases of primary EC, the gains were at 8q (10/40, 25%), 3q (9/40, 23%), 2q (7/40, 18%), and 13q (7/40, 18%), and the losses were at 1q (8/40, 20%), 4q (8/40, 20%), 3p (7/40, 18%), 5q (7/40, 18%), and 18q (7/40, 18%) in comparison with paired nearby noncancerous tissues. We found that the loss aberrations were on 1q, 2p, 3p, 5q, 6q, 9p, 11p, 15q, 16q, 18q, 21q and gains on 20p in both tumor and nontumor tissues; nevertheless, −4p, −7q, −8p, −10q, −12q, −13q, −14q and +17p, +19q, +22q were only found in nontumor tissues and +1q, +2pq, +3q, −4q, +4q, +5q, 7p, +8q, +10q, +12q, +13q, +14q −17p, −19pq, −22q in EC. From these results, we suggest that most of the tissues near the cancer parts of EC may be considered as a precancerous region. The alteration between cancer and noncancer tissues may play a role in the development of EC. J. Clin. Lab. Anal. 24:167–174, 2010.© 2010 Wiley-Liss, Inc.

Ancillary