Publications by authors named "Z P Sofina"

Cortiphen, a newly developed hormonal cytostatic ester of 11-desoxy-17 alpha-hydroxycorticosterone and chlorophenacyl, is described. It was studied in transplantable, spontaneous and induced tumors of 7 sites: hemoblastosis (5), hepatoma (3), mammary gland (5), lung (2), gastrointestinal tract (3), sarcoma (2) and melanoma. Practically all the tumors were shown to respond to cortiphen action.

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The paper describes the antitumor activity of a newly-developed hormonocytostatic drug testiphenon--a complex ether of 5 alpha-dihydrotestosterone and chlorphenacyl (17 beta-[n-di/2-chloroethyl/aminophenylacetate]-5 alpha-androstan-17 beta-ol-3-on). Its antitumor properties were studied in 15 models of transplantable solid tumors and systemic neoplasms of mice and rats such as sarcoma 298, sarcoma 37, sarcoma-180, Lewis lung epidermoid carcinoma, carcinoma of the forestomach-5, large bowel adenocarcinoma, Harding-Passey's melanoma, cervical cancer-5, mammary adenocarcinoma Ca-755, hemoblastosis La, plasmacytoma MOPC-406, Rauscher's erythroblastosis, Walker's carcinosarcoma 256, sarcoma 45, alveolar carcinoma of the mammary gland and DMBA-induced mammary tumors of mice. The spectrum of antitumor activity of testiphenon proved wider than those of its components or other estrogeno-cytostatic drugs--phenestrol and estracyt.

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A hypothalamic hormone--melanostatin H-L-Pro-L-Leu-NH2- and its 9 analogs were synthesized and their antitumor properties studied. Melanostatin caused a 52-72% inhibition of tumor growth (p less than 0.05) in mice bearing adenocarcinoma of the mammary gland Ca-755, cervical carcinoma CC-5 and melanoma B-16.

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The effect of methylcobalamin on 3H-methotrexate uptake by tumor and normal tissues of mice with mammary adenocarcinoma (Ca-755) was studied. Methylcobalamin stimulated the rate of 3H-methotrexate influx into the tumor and small intestine but did not change its influx into the spleen. The effect was dependent on the dose of methylcobalamin.

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Leukemia L1210 cells with acquired resistance to 1-methyl-1-nitrosourea (MNU) (L1210/MNU) and 1.3-bis(2-chloroethyl)-1-nitrosourea (BCNU) (L1210/BCNU) were developed from leukemia L1210 cells sensitive to these drugs (L1210/0). The modal chromosome number of leukemia L1210/MNU and L1210/BCNU cells increases from 40 (L1210/0) to 41.

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