THE CHROMOSOMAL BASIS OF HUMAN NEOPLASIA
THE CHROMOSOMAL BASIS OF HUMAN NEOPLASIA
复制标题
DOI：
10.1126/science.6336310
复制
发表时间：
1983-01-01
期刊：
影响因子：
56.9
通讯作者：
YUNIS, JJ
中科院分区：
文献类型：
--
作者：
YUNIS, JJ
用于人类染色体研究的高分辨率显带技术显示，所分析的大多数肿瘤的恶性细胞具有特征性的染色体缺陷。在许多白血病和淋巴瘤中发生具有精确断裂点的相同染色体片段的易位，并且在几种癌中缺失特定的染色体带。三体性，或一个特定的染色体一式三份的出现，是在少数肿瘤中观察到的唯一异常。有人提出，染色体重排在人类肿瘤中起着核心作用，并可能通过相关的基因组机制发挥其作用。因此，易位可以将癌基因放置在激活DNA序列旁边，缺失可以消除癌基因阻遏物，三体可以携带额外的基因剂量。
High-resolution banding techniques for the study of human chromosomes have revealed that the malignant cells of most tumors analyzed have characteristic chromosomal defects. Translocations of the same chromosome segments with precise breakpoints occur in many leukemias and lymphomas, and a specific chromosome band is deleted in several carcinomas. Trisomy, or the occurrence of a particular chromosome in triplicate, is the only abnormality observed in a few neoplasias. It is proposed that chromosomal rearrangements play a central role in human neoplasia and may exert their effects through related genomic mechanisms. Thus, a translocation could serve to place an oncogene next to an activating DNA sequence, a deletion to eliminate an oncogene repressor, and trisomy to carry extra gene dosage.