A randomized comparison of the relative efficacy and toxicity of daunorubicin (DNR) at 30 or 45 mg/sq m or adriamycin (ADM) at 30 mg/sq m, given on the first 3 days of a 7-day continuous infusion of cytosine arabinoside (ara-C) at 100 mg/sq m/day, shows the outcome to be dependent on anthracycline, dose, and patient age. DNR 45 is significantly better than DNR 30 or ADM 30 for inducing complete remissions (CR) in patients younger than 60 yr, (72%, 59%, 58% CRs, respectively). DNR 30 is better than DNR 45 or ADM 30 for inducing CR in patients older than 60 yr (47%, 31%, 35%, respectively). There was a corresponding shift in the induction mortality for the age, dose, and anthracycline groups. Adriamycin was significantly more toxic to the gastrointestinal tract than daunorubicin. The duration of complete remission, with cyclic courses of maintenance therapy, was independent of the patient's age, the dose, or choice of anthracycline used in induction, and of whether the maintenance courses were given every 4 wk or every 8 wk.

Because intensifying and increasing cyclophosphamide two or four times that given in standard clinical practice did not substantively improve outcome, such therapy should be reserved for the clinical trial setting.

Abstract.-A new nondefective hybrid virus has been plaque-isolated from the Ad.2-SV40 hybrid population. This virus replicates efficiently with one-hit kinetics in both human embryonic kidney and African green monkey kidney cells, induces an SV40 specific antigen which is detectable by immunofluorescence and complement-fixation using sera from SV40 tumor-bearing hamsters, and produces SV40-specific RNA detectable by DNA-RNA hybridization. The SV40-specific antigen induced by this virus is heat-stable, sensitive to inhibitors of DNA synthesis, serologically different from SV40 T and viral antigens, and is an unrecognized SV40 antigen.Since the initial reports describing the hybridization of human adenoviruses (Ad.) and SV40, two types of hybrid populations have been described: those free of detectable SV40 virions represented by the Ad.3 and Ad.7 populations; and those which release detectable SV40 virions represented by the Ad.1, 2, 4, 5, and 12 populations.'-3 Characterization of the infectivity and the SV40 T antigen-inducing capacity of the progeny of plaques isolated from human embryonic kidney (HEK) and African green monkey kidney (AGMK) cells have established that these hybrid populations consist of a mixture of nonhybrid Ad. virions and hybrid particles containing SV40 genome in Ad. capsids.4-7Studies on adenovirus plaque formation by the two types of Ad.-SV40 hybrid populations have shown that the nonhybrid component induces adenovirus plaques by one-hit kinetics in human embryonic kidney cells, indicating that one virion initiates plaque formation. In green monkey kidney cells, however, the induction of adenovirus plaques by these populations proceeds by two-hit kinetics, indicating that both a nonhybrid adenovirion and a defective hybrid particle (i.e., a particle requiring nonhybrid adenovirus to replicate in either human embryonic or green monkey kidney cells) are required to initiate adenovirus plaque formation.2' [4][5][6][7] Biological and biophysical studies on the Ad.7-SV40 hybrid population, E46 +, have shown that the adenovirus and SV40 DNA in these hybrid particles is covalently linked; thus, these particles are true molecular hybrids.8-'0 All efforts to obtain a pure clone of E46+ hybrid particles free of nonhybrid adenovirions have failed.4Biological studies on the Ad.2-SV40 (Ad.2++) t population have demonstrated that, in addition to nonhybrid Ad.2 virions, there are adenovirus encapsidated particles which are capable of producing SV40 plaques on AGMK monolayers by one-hit kinetics.2 These particles contain the infectious SV40 genome.The purpose of this paper is to describe the isolation from the Ad.2++ popula-1128

Four new nondefective adenovirus 2 (Ad2)-simian virus 40 (SV40) hybrid viruses have been isolated. Although these viruses (designated Ad2+ND2, Ad2+ND3, Ad2+ND4, and Ad2+ND,) were clonal derivatives of the same Ad2-SV40 hybrid population, they differ significantly from each other and from the previously isolated nondefective hybrid, Ad2+ND,, in their biological properties or in the amount of SV40-specific RNA,induced during lytic infection. Like Ad2+ND,, Ad2+ND2, and Ad2+ND4 pass serially in both human embryonic kidney (HEK) and primary African green monkey kidney cells. In contrast, Ad2+ND, and Ad2+ND5 pass serially only in HEK cells. Ad2+ND2 is like Ad2+ND1 in that it induces the SV40 U antigen, but not SV40 T antigen; however, in contrast to the perinuclear SV40 antigen induced by Ad2+ND,, the SV40 antigen induced by Ad2+ND2 is located peripherally in the cytoplasm as well as in the perinuclear region of infected cells. Ad2+ND4 induces both the SV40 T and U antigens. Ad2+ND3 and Ad2+ND5 do not induce serologically detectable SV40 antigens and are distinguished from each other on the basis of the relative quantities of SV40-specific RNA which they induce. The induction of different SV40-specific functions suggests the incorporation of different segments of SV40 DNA within the genomes of the respective hybrid viruses.