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Biomedical subjects

C C Stock

Publications and source records attributed to C C Stock.

At least 37 records · Page 2Linked to original sources
PubMed1978

Antitumor tests of amygdalin in transplantable animal tumor systems.

Except for oral administration, there was no grossly observed toxicity from carefully administered high doses of amygdalin in the experimental systems used. The compound in high doses was ineffective against the DMBA-induced rat mammary carcinoma and the following transplanted experimental tumors: Sarcoma 180, plasma cell tumor LPC-1, leukemia L1210, Mecca lymphosarcoma, Ridgway osteogenic sarcoma, sarcoma T241, mammary carcinoma E0771, Taper liver tumor, Ehrlich carcinoma (solid and ascites), and Walker carcinosarcoma 256. Amygdalin did not noticeably influence the toxicity or impair the efficacy of these chemotherapeutic agents in their respective systems: Cytosine arabinoside, methotrexate, cytoxan, or 5-fluorouracil in L1210; the latter two in LPC-1; 6-mercaptopurine in Ridgway osteogenic sarcoma; estradiol-17beta or 2alpha-methyldihydrotestosterone propionate in the DMBA-induced rat mammary carcinoma.

Amygdalin↗
PubMed1978

Antitumor tests of amygdalin in spontaneous animal tumor systems.

In a series of 6 experiments with CD8F1 mice with spontaneous mammary adenocarcinomas Sugiura noted by macrovisual observation with some histology an overall average of 21% of mice with lung metastases when treated with 1,000--2,000 mg/kg/day of amygdalin compared with 90% of the control mice. The significance attributed to those early observations is seriously challenged by the negative findings of 3 independent investigators, by 2 out of 3 negative cooperative experiments in which Sugiura participated, and particularly by the blind experiment in which he and others under blind readings found no anticancer activity. Treatment of Swiss albino mice showed no destructive effect upon their spontaneous mammary adenocarcinomas. Of the treated mice, 22% were found by macrovisual observation to have lung metastases while 91% were noted among the controls. The results are subject to questions raised in the discussion. Amygdalin at 2,000 mg/kg/day was ineffective both in treating and preventing the development of spontaneous leukemia in AKR mice. At 1,000 mg/kg/day it was not found effective in preventing or significantly delaying the development of spontaneous mammary tumors in CD8F1 mice. In summary, we do not have evidence to support taking amygdalin to clinical trial, although other considerations may require that one be conducted.

Adenocarcinoma↗
PubMed1977

Alterations in glycosphingolipids of plasma membranes from Morris hepatoma 5123TC.

Neutral glycosphingolipids and gangliosides were quantified in lipid extracts from normal rat liver and Morris hepatoma 5123TC and their isolated plasma membranes to determine differences in these components in the cell surface membranes of malignant cells. Glycosphingolipids present in rat liver and hepatoma were concentrated in plasma membranes, and glycosphingolipid patterns in plasma membranes reflected those of their respective whole cells. Neutral glycospingolipids of plasma membranes from normal liver and from hepatoma consisted of ceramide mono- and dihexosides, together accounting for 83 to 86% of the total neutral glycosphingolipids and some ceramide tri- and tetrahexosides. In plasma membranes from hepatoma, the concentration of neutral glycosphingolipids was generally greater than in plasma membranes from normal liver. Gangliosides of plasma membranes from hepatoma were altered more drastically, since trisialogangliosides, present in plasma membranes from normal liver, were absent, while hematosides, monosialogangliosides, and disialogangliosides were increased an average eight-fold. These data are compatible with a concept of incomplete synthesis of trisialogangliosides in hepatoma and an accumulation precursor gangliosides.

Animals↗
PubMed1977

Comparative effects of a series of prolactin inhibitors, 17beta-estradiol and 2alpha-methyldihydrotestosterone propionate, on growth of 7,12-dimethylbenz(a)anthracene-induced rat mammary carcinomas.

Eight ergot alkaloids and ergoline derivatives, effective prolactin inhibitors, were tested for activity against DMBA-induced rat mammary carcinomas. Compounds were administered daily, 5 times/week for 4 weeks, and rats were observed for an additional 4 weeks. Groups treated with androgen and estrogen were used as positive controls. Those ergot compounds and ergolines that proved to be highly effective in reducing tumor size or in inducing regression of tumors to nonpalpability were Deprenon (D-6-methyl-8-ergolin-I-ylacetic acid amide) and ergocryptine; effective to an intermediate degree were Dironyl [N-(D-6-methyl-8-isoergolin-I-yl)-N',N'-diethylurea], ergocornine, and Lysenyl [N-(D-6-methyl-8-isoergolenyl)-N',N'-diethyl-urea]; and effective to a minimal degree were Lergotrile (2-chloro-6-methylergoline-8beta-acetonitrile), CB-154, and 6605-VUFB (D-6-methyl-8-cyanomethylergolin-I). Remission of many individual carcinomas was brief, and duration of complete regression (all tumors in the rat were nonpalpable) was less than 10 weeks.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1976

Deveopment of resistance to combinations of six antimetabolites in mice with L1210 leukemia.

The development of resistance to combinations of 6-mercaptopurine, 6-thioguanine, 6-methylmercaptopurine riboside, methotrexate, 5-fluorouracil, and cytosine arabinoside was studied in L1210 leukemia through 60 transfer generations. The treatment schedules were either simultaneous or offset. In simultaneous administration, one sixth of the LD10 of each of the six drugs was administered within a few minutes, daily for 6 days. In offset administration, the drugs were given either in the above-listed order or in reversed order, with one drug given each day. In the simultaneous combination treatment protocol 31 transfer generations were necessary to reach partial resistance, but in the two offset combination schedules only five and three generations were needed. The relative rate of development of resistance to the individual drugs was slower in the three combination schedules than in single-drug schedules. Resistance to 6-mercaptopurine and 6-thioguanine was completed after four generations on the offset combination schedules, but only after 28 generations on the simultaneous schedule.

Animals↗