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folic acid/sarcoma

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Methotrexate and folic acid effect in normal and sarcoma 180 bearing mice.

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Four- to six-fold surplus of folic acid in oral application reduced the toxicity of methotrexate administered repeatedly in high therapeutic doses. The therapeutic effect of methotrexate applied intraperitoneally to mice with the ascitic S 180 sarcoma, as measured by their survival, can be reliably
Normal and Rous sarcoma virus-infected chicken fibroblasts proliferate maximally in a culture medium containing a physiological (10 ng/ml) concentration of 5-methyltetrahydrofolic acid or folinic acid (5-formyltetrahydrofolic acid), while their maximal proliferation requires a hyperphysiological
In a culture medium of pH 7.4 and a folic acid concentration of 100 mug/liter that contains 5% heat-inactivated chicken plasma rather than serum, the rate of proliferation of normal chicken fibroblasts is determined by the concentration of calcium. Proliferation, rapid when the calcium concentration

Studies on inhibiting effect of aminopterin and other folic acid antagonist, and folic acid upon the Yoshida sarcoma.

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The effect of folic-acid derivatives on sarcoma 180.

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Rous sarcoma in folic acid-deficient chicks; morphology and bioassay.

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The growth of Rous sarcoma in folic acid deficient chicks.

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Reversal of aminopterin-induced inhibition of sarcoma 180 by folic acid.

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Investigations into the effect of thymonucleic acid fed to folic acid deficient chicks bearing Rous sarcomas.

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Effects of folic acid on cell division: studies in normal and regenerating organs and in Yoshida sarcoma in rats.

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The effect of combination of folic acid and anticancer drugs on the growth of sarcoma 180 in mice.

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Folic acid and other absorption tests in lymphosarcoma, chronic lymphocytic leukaemia, and some related conditions.

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An improved folic acid absorption test is described in detail. Using the folic acid and other absorption tests, a study of intestinal function has been made in eight patients with lymphosarcoma, eight with chronic lymphocytic leukaemia, two with Hodgkin's disease, and one each with reticulum cell

Effects of overexpression of gamma-Glutamyl hydrolase on methotrexate metabolism and resistance.

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Intracellular metabolism of methotrexate (MTX) to MTX-polyglutamates (MTXPG) is one determinant of cytotoxicity. Steady-state accumulation of MTXPG seems to depend on the activity of two enzymes: folylpolyglutamate synthetase (FPGS), which adds glutamate residues, and gamma-glutamyl hydrolase (GGH),

Retargeting of viral vectors to the folate receptor endocytic pathway.

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Viral vectors with high transfection efficiencies are not always those with optimal target cell binding specificities. As a consequence, virus pseudotyping has been developed to endow transfection competent viruses with improved cell binding specificities and affinities. We have hypothesized that
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