Harper M E, Franchini G, Love J, Simon M I, Gallo R C, Wong-Staal F
Nature. 1983;304(5922):169-71. doi: 10.1038/304169a0.
The transforming genes of acutely transforming retroviruses are derived from conserved cellular genes (c-onc genes) which are believed to be important in normal cell growth and differentiation. Recent studies indicate that altered expression of c-onc genes, for example, by insertion of viral genomes, gene amplification or chromosomal translocation, can lead to development of malignant diseases in man and animals. c-myb and c-fes are homologues of the transforming genes of avian myeloblastosis virus and feline sarcoma virus (Gardner and Snyder-Theilen strains), respectively. c-myb is transcribed preferentially in immature haematopoietic cells and probably codes for a protein important in differentiation of these cells. The viral fes gene, like several other viral onc genes, encodes a tyrosine-specific protein kinase. However, c-fes transcripts have not been detected in the types of human cells examined so far. c-myb and c-fes have been assigned to human chromosomes 6 and 15, respectively. Specific aberrations involving these chromosomes have been observed at high frequency in several human neoplasms. We have now sublocalized c-myb to 6q22-24 and c-fes to 15q25-26 by in situ hybridization of the human c-onc probes to human mitotic chromosome preparations. These chromosomal segments are indeed involved in nonrandom translocations in several human tumours. The results encourage further investigation into the role of onc genes in the pathogenesis of specific neoplasms.
急性转化型逆转录病毒的转化基因源自保守的细胞基因（原癌基因），这些基因被认为在正常细胞生长和分化中起重要作用。最近的研究表明，原癌基因表达的改变，例如通过病毒基因组的插入、基因扩增或染色体易位，可导致人和动物发生恶性疾病。c-myb和c-fes分别是禽成髓细胞瘤病毒和猫肉瘤病毒（加德纳和斯奈德-泰伦毒株）转化基因的同源物。c-myb在未成熟造血细胞中优先转录，可能编码一种对这些细胞分化很重要的蛋白质。病毒fes基因与其他几种病毒癌基因一样，编码一种酪氨酸特异性蛋白激酶。然而，到目前为止，在所检测的人类细胞类型中尚未检测到c-fes转录本。c-myb和c-fes已分别定位于人类染色体6和15。在几种人类肿瘤中已高频观察到涉及这些染色体的特定畸变。我们现在通过将人类原癌基因探针与人类有丝分裂染色体标本进行原位杂交，将c-myb亚定位到6q22-24，将c-fes亚定位到15q25-26。这些染色体区段确实参与了几种人类肿瘤的非随机易位。这些结果鼓励进一步研究癌基因在特定肿瘤发病机制中的作用。
