Increased sister-chromatid exchanges accompany serial transplantation of murine S49.1 lymphoma.
Although many neoplasms may have a unicellular origin and clonal growth pattern (Nowell, 1976), established tumors show a remarkable degree of phenotypic heterogeneity with respect to metastatic potential, chromosome markers, metabolic functions, and membrane receptors and antigens (Fidler et al., 1978), suggesting that numerous events may occur in the selection of variant tumor cells in neoplastic development. The generation of tumor heterogeneity may occur via genetic and/or epigenetic mechanisms, in response to tumor-cell interactions within the host milieu (Chow and Greenberg, 1980), but these phenomena are currently poorly understood. In the present study, the incidence of sister-chromatid exchanges (SCE) was examined in control cultures of murine S49.1 lymphoma cells maintained in vitro, and in S49.1 cells serially propagated as tumors in syngeneic BALB/c mice. These experiments were performed in order to study the acquired genetic lability accompanying tumor progression, as reflected in the incidence of SCE.
D000818:Animals; D001973:Bromodeoxyuridine / Q000494:pharmacology; D002460:Cell Line; D003434:Crossing Over, Genetic / Q000187:drug effects; D005260:Female; D008223:Lymphoma / Q000235:genetics*; D051379:Mice; D008807:Mice, Inbred BALB C; D009374:Neoplasms, Experimental / Q000235:genetics; D012854:Sister Chromatid Exchange / Q000187:drug effects
D001973:Bromodeoxyuridine