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应用比较基因组杂交技术对食管癌进行分子细胞遗传学分析。

Molecular cytogenetic characterization of esophageal cancer detected by comparative genomic hybridization.

机构信息

Departments of Medical Research and Laboratory Medicine, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan.

出版信息

J Clin Lab Anal. 2010;24(3):167-74. doi: 10.1002/jcla.20385.

Abstract

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.

摘要

食管癌(EC)的细胞遗传学改变检测。收集了 40 例原发性 EC 及其配对的附近非肿瘤组织。比较基因组杂交(CGH)技术可显示染色体片段的增益和丢失,并应用于从组织 DNA 中确定畸变。在非癌组织中,增益位于 19p(5/40,13%)、20q(5/40,13%),丢失位于 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%)和 8p(9/40,23%)。2 例非肿瘤组织无 CGH 改变。在 40 例原发性 EC 中,增益位于 8q(10/40,25%)、3q(9/40,23%)、2q(7/40,18%)和 13q(7/40,18%),丢失位于 1q(8/40,20%)、4q(8/40,20%)、3p(7/40,18%)、5q(7/40,18%)和 18q(7/40,18%)与配对的附近非癌组织相比。我们发现,1q、2p、3p、5q、6q、9p、11p、15q、16q、18q、21q 的缺失畸变和肿瘤及非肿瘤组织中的 20p 增益;然而,-4p、-7q、-8p、-10q、-12q、-13q、-14q 和 +17p、+19q、+22q 仅存在于非肿瘤组织中,+1q、+2pq、+3q、-4q、+4q、+5q、7p、+8q、+10q、+12q、+13q、+14q-17p、-19pq、-22q 在 EC 中。从这些结果中,我们认为 EC 癌症部位附近的大部分组织可能被视为癌前区域。癌症组织和非癌组织之间的变化可能在 EC 的发展中起作用。

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