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Comparative Chemotherapy of AKR Lymphoma and Human Hematological Neoplasia¹

Children's Cancer Research Foundation, Boston, Massachusetts 02215; Southern Research Institute, Birmingham, Alabama 35205; and Drug Research and Development, Division of Cancer Treatment, National Cancer Institute, Bethesda, Maryland 20014

This study represents the first quantitative large-scale evaluation of therapy in a spontaneous tumor system in experimental animals, in which the results of various therapeutic programs in that system and selected tumors in man are compared. There is possibly a better correspondence of spontaneous AKR with non-Hodgkin's lymphoma and myeloma than for other hematological cancers, and it would be of interest to examine the various subcategories of non-Hodgkin's lymphoma with respect to correlation with the spontaneous AKR system.

There would appear to be no advantage in using the spontaneous AKR system for primary screening as compared with the currently used early leukemia L1210 system. With almost no exception the clinically active drugs identified as active by the spontaneous AKR system were also active against early L1210. The first generation of AKR leukemia gave results that corresponded well with the spontaneous AKR system.

The advanced leukemia L1210 system in similarity to the spontaneous AKR system is somewhat less sensitive than the early L1210 system. This is of interest since in both of these systems the disease is systemic when treatment is initiated. This would suggest that both of these systems could be utilized for detailed studies of remission induction and maintenance.

The spontaneous AKR system may be useful for the study not only of remission induction and maintenance, including consolidation therapy, but also for the evaluation of prophylactic treatment and the study of reinduction in the event that total "cell cure" may have been established.

¹ Supported in part by Contract PH43-71-2098 (Southern Research Institute) with Drug Research and Development, Division of Cancer Treatment, NIH, Bethesda, Md. Additional data derived from Contracts PH43-68-1283 (M. Kende and associates, Microbiological Associates, Inc.) and PH43-68-1021 (A. M. Shefner and associates, Illinois Institute of Technology) with Drug Research and Development, Division of Cancer Treatment, National Cancer Institute, NIH.

Received 6/ 4/73. Accepted 10/12/73.

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