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Antibodies directed against the common acute lymphoid leukemia antigen (CALLA) were obtained from 2 hybridomas: J5 (Schlossman, mice sensitized with patient ALL cells), and Vil-A1 (Knapp, sensitization with the Reh cell line). The percentage of lymphoid cells reacting with these 2 monoclonal antibodies were compared. Antibody dilution curves indicated that the dilutions used yielded maximum percentages of positive cells. The percentage of CALLA-positive cells with the J5 antibody was significantly (p less than 0.001) higher than that found with the Vil-A1 antibody in 16 non-neoplastic inflammatory tonsils and in 13 non-Hodgkin lymphoma and chronic lymphatic leukemia lymph-nodes (p less than 0.05). In contrast, the difference between CALLA positive cells with J5 and Vil-A1 was not significant (p greater than 0.5) in 19 acute lymphoid leukemias. The difference between the ALL-cells, presumably pre-B, and the B-cells from the non-ALL subjects was also statistically significant (p less than 0.01). The results suggest that the two hybridomas form antibodies against different CALLA epitopes. Vil-A1 seems somewhat more specific for ALL than J5.

20 male patients were treated for various tumors, most of them by combination therapy program including Cis-diammino-dichloroplatinum, Methotrexate and Bleomycin, the mean total dose for this last drug being 225 mg in 3 months (75 mg-300 mg). Spirometric tests, carbon monoxide diffusing capacity (DLCO) and its components Dm (membrane diffusing capacity) and Vc (capillary blood volume) were performed before each course and at the end of the chemotherapy, to assess their value in detecting Bleomycin pulmonary toxicity. There was no statistically significant change in any ventilatory nor diffusional test among these 20 patients, carefully selected for the absence of cardiopulmonary history. There was a slight decrease of DLCO for 3 patients having received 300 mg of Bleomycin. The lack of cardiopulmonary history, the mean total dose under the toxic threshold, and perhaps the insufficient delay between the end of the treatment and the last control test, may explain this absence of variability of functional tests.