Lymphoma development in mice and humans: diversity of initiation is followed by convergent cytogenetic evolution.
Human B cell lymphoma and murine T cell leukemia can be initiated by several agents. The present paper formulates some thoughts on the role of cytogenetic changes in the subsequent neoplastic process. Initiation creates long-lived preneoplastic cells. In some respects, they are comparable to in vitro-transformed ("immortalized") cell lines that maintain a diploid karyotype and are not tumorigenic in vivo. The development of a tumorigenic ("autonomous") clone is dependent on additional changes at the genetic level. In human B and murine T cell lymphoma, there are characteristic nonrandom chromosomal changes. The 14q+ marker appears to play a key role in human B cell lymphomas. The reciprocal 8;14 translocation in Burkitt lymphoma is a specialized subclass within this category. In murine T cell leukemia, trisomy 15 is the predominant change. The clustering of these nonrandom changes to tumors derived from a certain cell type rather than to tumors induced by a given etiological agent has important implications for the understanding of the genetic control of cellular responsiveness to growth-regulating forces in vivo.
D000406:AKR murine leukemia virus; D000818:Animals; D002051:Burkitt Lymphoma / Q000209:etiology; D002471:Cell Transformation, Neoplastic; D002472:Cell Transformation, Viral; D005814:Genes, Viral; D004854:Herpesvirus 4, Human; D006801:Humans; D007942:Leukemia, Experimental / Q000209:etiology* / Q000235:genetics; D008223:Lymphoma / Q000209:etiology* / Q000235:genetics; D051379:Mice; D010641:Phenotype; D013601:T-Lymphocytes