Chromosomal abnormalities of adenocarcinoma of the pancreas: identifying early and late changes
Chromosomal abnormalities of adenocarcinoma of the pancreas: identifying early and late changes
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DOI：
10.1016/j.cancergencyto.2007.06.004
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发表时间：
2007-10-01
影响因子：
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通讯作者：
Griffin, Constance A.
中科院分区：
文献类型：
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作者：
Kowalski, Jeanne;Morsberger, Laura A.;Griffin, Constance A.
在上皮性肿瘤中发现的高水平的核型复杂性阻碍了其细胞遗传学进化的表征。这种途径在胰腺腺癌中的推导尤其有限，因为只有少数胰腺癌在疾病的早期阶段被切除，因此报道的对异常核型进行分析的原发性癌的数量很少。在这里，我们报告克隆核型异常鉴定的g带分析36原发性胰腺癌获得的患者接受惠普尔切除治疗的目的。36例癌中多数为二倍体或三倍体（33 / 36;91%）。在确定了完整核型的所有癌中都发现了数值改变。在至少8到28例癌症中，所有的染色体都参与了整个染色体的获得、失去或同时获得和失去。最常见的丢失是18号染色体（占36例癌症的78%）、17号（56%）、6号（44%）、21号（42%）、22号（42%）、Y号（36%）和4号（33%）。在36例肿瘤中，有10例观察到20号染色体增加。结构异常很常见，导致部分染色体的增加和减少，每个癌中位数为7个部分不平衡（范围1-15）。16个癌包含双分钟染色体，均匀染色区域，或两者兼而有之，表明基因扩增。将这36例癌与Mitelman数据库（http://cgap.nei.nih.gov/Chromosomes/Mitelman）中发表的核型原发性癌的数据进行汇总，我们定义了核型进化的途径。最常见的染色体不平衡是-18(67.6%)、-10年(34.3%)、4(31.4%)+ 20(31.4%)、-15 p(23.8%)、-14 p(22.9%) + 2(21.9%), 5例(21.9%),-13 p(20%) + 16(20%)、-21 p(19%)、-17 (19%),p + lq(19.0%)。早期发现的复发性失衡为-1p、-15p、-18、-7q、-8p、-17p和-5；后期经常性失衡为+Ilq、+7q、+6p、-19p和+2。与其他上皮癌的类似分析报告相反，我们没有发现多核型进化途径的证据。(C) 2007爱思唯尔公司版权所有。
The high level of karyotypic complexity found in epithelial neoplasms hinders the characterization of their cytogenetic evolution. Derivation of such pathways in adenocarcinoma of the pancreas has been particularly limited, because only a few pancreatic carcinomas are resected at an early stage of disease and so the number of primary carcinomas for which analysis of abnormal karyotypes has been reported is small. Here we report the clonal karyotypic abnormalities identified by G-banding analysis of 36 primary pancreatic carcinomas obtained from patients undergoing a Whipple resection with curative intent. The majority of the 36 carcinomas were diploid or triploid (33 of 36; 91%). Numerical alterations were found in all carcinomas for which a complete karyotype was determined. All the chromosomes were involved in gain, loss, or both gain and loss of the entire chromosome, in at least 8 and up to 28 of the carcinomas. Most commonly lost were chromosomes 18 (in 78% of the 36 carcinomas), 17 (56%), 6 (44%), 21 (42%), 22 (42%), Y (36%), and 4 (33%). Gain of chromosome 20 was observed in 10 of the 36 carcinomas. Structural abnormalities were common, resulting in partial chromosomal gains and losses, with a median number of 7 partial imbalances per carcinoma (range, 1-15). Sixteen carcinomas contained double-minute chromosomes, homogeneously staining regions, or both, indicating gene amplification. Pooling data for these 36 carcinomas with the primary carcinomas with karyotypes published in the Mitelman database (http://cgap.nei.nih.gov/Chromosomes/Mitelman), we defined pathways of karyotypic evolution. The most frequent chromosomal imbalances were -18 (67.6%), -10 (34.3%), -4 (31.4%), +20 (31.4%), -15p (23.8%), -14p (22.9%), +2 (21.9%), -5 (21.9%), -13p (20%), +16 (20%), -21p (19%), -17p (19%), +lq (19.0%). Recurrent imbalances identified as occurring early were -1p, -15p, -18, -7q, -8p, -17p, and -5; late recurrent imbalances were +Ilq, +7q, +6p, -19p, and +2. In contrast to reports from similar analyses in other epithelial carcinomas, we did not find evidence for multiple karyotypic evolutionary pathways. (C) 2007 Elsevier Inc. All rights reserved.