Abstract
Publisher Summary The mechanisms of oncogene activation involve the transposition of DNA. The question therefore arises as to whether the genetic transpositions found in many types of cancer, including those that are expressed in the form of specific chromosomal translocations or deletions, may act by similar mechanisms. Recent findings concerning nonrandom chromosomal changes-mainly reciprocal translocations in two tumor types of B-cell origin, murine plasmacytoma (MPC) and human Burkitt-type lymphoma (BL) suggest that this is probably the case. In MPC, the distal region of chromosome 15 is translocated to chromosome 12 in the majority of all examined tumors. In BL, the majority of the reported cases were found to carry a reciprocal t(8;14) translocation. It is noteworthy that the translocations represent a characteristic feature of the BL cell and are independent of geographical origin, clinical presentation, and Epstein–Barr virus (EBV) association. Thus it is clear that the recipient chromosome of the tumor-associated translocation carries immunoglobulin genes in both MPC and BL.
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