Abstract

CELL suspensions from leukaemic tissues of the AKR strain of mice were transplanted into new-born Wistar rats1. Two consecutive intraperitoneal or intravenous injections, spaced one week apart, resulted in deaths from leukaemia of 40–50 per cent of the recipients. Two morphological variants of lymphoid leukaemia, ‘early’ and ‘late’ forms, were observed in the inoculated rats. The early leukaemias caused deaths within 4–8 weeks post partum by a rapid intra-abdominal or systemic proliferation of the injected leukaemic cells. The onset of late leukaemias was delayed to 12–24 weeks following injections. Morphologically, late leukaemias manifested as thymic lymphosarcomata followed by the appearance of primitive blast or lymphoid cells in the peripheral blood, hepatosplenomegaly and leukaemic lymphadenopathy. Subsequent transplantation assays disclosed a most interesting difference between the early and late leukaemias. Cell suspensions from early leukaemias were readily back-transplantable from the rat to young adult AKR mice. In contrast, grafts from late leukaemias failed to grow in similar AKR recipients but were fatal to new-born or weanling rats within 2–3 weeks after one intraperitoneal injection. Thus, late leukaemias were antigenically of the recipient rather than donor type. These different biological properties of the leukaemic cells suggested a differing aetiology in the two forms. Late leukaemias were considered viral neoplasms possibly caused by the leukaemogenic agent present in leukaemic tissues of AKR mice2. To substantiate this hypothesis several criteria must be fulfilled, such as: (a) induction of lymphoid leukaemia in rats by filtrates from either AKR leukaemic tissues or induced leukaemias of the C3H-strain; (b) transmissibility of the induced leukaemias by cell-free extracts in rats; (c) a very low spontaneous incidence of lymphoid leukaemia in rats to exclude acceleration of an inherent leukaemic potential. This communication is concerned with attempts to transmit late leukaemias in rats by serial cell-free passages.

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