Abstract
There is increasing evidence that many of the nonrandom chromosomal alterations found in neoplastic cells represent mechanisms by which human proto-oncogenes are “activated” and play an important role in carcinogenesis. Most tumors have karyotypic abnormalities [1,2]. In any given tumor, all the cells frequently show the same, or related, alteration, indicating that the cytogenetic change is conferring a selective advantage on the cells carrying it. As various nonrandom karyotypic alterations have been recognized in malignant tumors, specific translocations have been among the most common. Recent studies of such rearrangements, particularly in human leukemia and lymphoma, have begun to indicate the specific oncogenes involved and certain of the mechanisms by which their function may be critically altered. In the following sections, current findings and hypotheses will be briefly reviewed, emphasizing our own investigations. The field is moving rapidly, and significant additional data will undoubtedly be available by the time this summary is published.
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Nowell, P.C., Croce, C.M. (1986). Oncogene Activation by Chromosome Translocation. In: Notkins, A.L., Oldstone, M.B.A. (eds) Concepts in Viral Pathogenesis II. Springer, New York, NY. https://doi.org/10.1007/978-1-4612-4958-0_11
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DOI: https://doi.org/10.1007/978-1-4612-4958-0_11
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