Bartram C R
Eur J Pediatr. 1984 Jan;141(3):134-42. doi: 10.1007/BF00443210.
Recent applications of recombinant DNA techniques in cancer research led to the detection of cellular genes with potential transforming activity, called oncogenes (c-onc). Regularly they seem to be involved in normal cell differentiation and proliferation: a number of oncogene-encoded proteins specifically phosphorylates tyrosine, a key reaction in growth control. Certain human tumors exhibit activated forms of these genes and DNA fragments isolated from these neoplasms transform nonneoplastic cells (transfection assay). Oncogenes were first discovered and defined in a number of retroviruses; these viral oncogenes (v-onc) are thought to have been derived from the cellular oncogenes (c-onc). By integration of the v-onc genes into the host genome acute neoplastic transformation of the cell may occur. Several modes of oncogene activation are discussed that lead either to an increased dosage of gene product or to the formation of an altered gene product. The localization of oncogenes in the human genome near the breakpoints of specific chromosome aberrations involved in various neoplasms like Burkitt lymphoma and several leukemias emphasizes the importance of these genes in carcinogenesis.
重组DNA技术最近在癌症研究中的应用，使得具有潜在转化活性的细胞基因被检测出来，这些基因被称为癌基因（c-onc）。它们似乎通常参与正常细胞的分化和增殖：许多癌基因编码的蛋白质能特异性地使酪氨酸磷酸化，这是生长控制中的一个关键反应。某些人类肿瘤表现出这些基因的激活形式，并且从这些肿瘤中分离出的DNA片段能使非肿瘤细胞发生转化（转染试验）。癌基因最初是在一些逆转录病毒中被发现和定义的；这些病毒癌基因（v-onc）被认为来源于细胞癌基因（c-onc）。通过将v-onc基因整合到宿主基因组中，可能会发生细胞的急性肿瘤转化。文中讨论了几种癌基因激活的模式，这些模式要么导致基因产物的剂量增加，要么导致形成改变的基因产物。癌基因在人类基因组中的定位靠近与各种肿瘤（如伯基特淋巴瘤和几种白血病）相关的特定染色体畸变的断点，这强调了这些基因在致癌过程中的重要性。
