A new tumor spectrum recently introduced at Sloan-Kettering Institute is composed of the mouse tumors adenocarcinoma EO771, sarcoma T241, melanoma B16, Ridgway osteogenic sarcoma, carcinoma C1025, Mecca lymphosarcoma, and Ehrlich ascites tumor, and the rat tumor Walker carcinosarcoma 256. These tumors were chosen because of their biologic characteristics, described previously, and their sensitivity to 14 antitumor chemicals. This report presents the effects of the compounds on the growth of the tumors. At the end of therapy cyclophosphamide (NSC-26271) retarded the growth of all 8 tumors. Mitomycin C (NSC-26980) and 2′-deoxy-5-fluorouridine (NSC-27640) delayed the growth of 5 tumors; methotrexate (NSC-740), actinomycin D (NSC-3053), and 5-fluorouracil (NSC-19893) delayed the growth of 3. Urethan (NSC-746) and diethylstilbestrol (NSC-3070) had no effect on the growth of any tumor at the end of therapy, and 6 chemicals impaired the growth of only 1 or 2 tumors. Persistent retardation of tumor growth was observed 1 week after the end of therapy in 19 drug-tumor systems. Antitumor effects became significant only 1 week after the end of therapy in 9 drug-tumor systems. Previously described sensitivity of individual tumors in the present spectrum to certain classes of chemically related drugs has been confirmed. In addition it was found that, among the solid tumors tested, only adenocarcinoma EO771 is sensitive to urethan and diethylstilbestrol, only melanoma B16 and Mecca lymphosarcoma are sensitive to N-deacetylthiocolchicine (NSC-9170) and only Ridgway osteogenic sarcoma is sensitive to vinblastine (NSC-49842).


Supported by contract SA-43-ph-2445 from the Cancer Chemotherapy National Service Center, National Cancer Institute, National Institutes of Health, Public Health Service.

This content is only available via PDF.