人类癌症中MYC基因的染色体介导改变。
Chromosome-mediated alterations of the MYC gene in human cancer.
作者信息
Popescu N C, Zimonjic D B
机构信息
Laboratory of Experimental Carcinogenesis, Center for Cancer Research, National Cancer Institute, 37 Convent Drive MSC 4258, Bethesda, Maryland 20892-4258, USA.
出版信息
J Cell Mol Med. 2002 Apr-Jun;6(2):151-9. doi: 10.1111/j.1582-4934.2002.tb00183.x.
The step-wise accumulation of genetic and epigenetic alterations in cancer development includes chromosome rearrangements and viral integration-mediated genetic alterations that frequently involve proto-oncogenes. Proto-oncogenes deregulation lead to unlimited, self-sufficient cell growth and ultimately generates invasive and destructive tumors. C-MYC gene, the cellular homologue of the avian myelocitic leukemia virus, is implicated in a large number of human solid tumors, leukemias and lymphomas as well as in a variety of animal neoplasias. Deregulated MYC expression is a common denominator in cancer. Chromosomal rearrangements and integration of oncogenic viruses frequently target MYC locus, causing structural or functional alterations of the gene. In this article, we illustrate how genomic rearrangements and viruses integration affect MYC locus in certain human lymphomas and solid tumors.
癌症发展过程中遗传和表观遗传改变的逐步积累包括染色体重排以及病毒整合介导的遗传改变，这些改变常常涉及原癌基因。原癌基因失调会导致细胞无限增殖、自给自足生长，最终形成侵袭性和破坏性肿瘤。C-MYC基因是禽骨髓细胞性白血病病毒的细胞同源物，与大量人类实体瘤、白血病和淋巴瘤以及多种动物肿瘤形成有关。MYC表达失调是癌症的一个共同特征。染色体重排和致癌病毒整合常常靶向MYC基因座，导致该基因发生结构或功能改变。在本文中，我们阐述了基因组重排和病毒整合如何影响某些人类淋巴瘤和实体瘤中的MYC基因座。
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