[Common proviral integration sites in C57BL mouse lymphoma induced by mouse radiation leukemia virus and absence of novel proviral sequences in DNA from radiation-induced lymphoma].

Radiation leukemia virus (RadLV)-induced lymphomas of C57BL mice display the appearance of novel proviral sequences at common sites of their DNAs. These results are compatible with the hypothesis of viral oncogenesis by promotor insertion. Radiation-induced tumors do not acquire detectable novel provirus, suggesting that activation of a transforming gene proceeds by a mechanism distinct from the former.