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ascorbate/сарком

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Ascorbate stabilizes the differentiated state and reduces the ability of Rous sarcoma virus to replicate and to uniformly transform cell cultures.

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In primary avian tendon cells, Rous sarcoma virus can coexist or completely take over the cell. Infection, at high multiplicity or under conditions that promote high virus production (no ascorbate and high serum concentrations), results in almost complete oncogenic transformation of the culture.

The influence of sodium ascorbate, menadione sodium bisulfite or pyridoxal hydrochloride on the toxic and antineoplastic action of N-methylformamide in P 388 leukemia or M 5076 sarcoma in mice.

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The toxicity of daily subcutaneously applied 500 mg/kg N-methylformamide (NMF) during a period of 8 days in female CD-mice was ameliorated when 100 mg/kg sodium ascorbate, 60 mg/kg menadione bisulfite or 80 mg/kg pyridoxal hydrochloride were applied simultaneously. The comparison of the daily s.c.

Redox active metals and H2O2 mediate the increased efficacy of pharmacological ascorbate in combination with gemcitabine or radiation in pre-clinical sarcoma models.

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Soft tissue sarcomas are a histologically heterogeneous group of rare mesenchymal cancers for which treatment options leading to increased overall survival have not improved in over two decades. The current study shows that pharmacological ascorbate (systemic high dose vitamin C achieving ≥ 20mM

H-ras mutations in rat urinary bladder carcinomas induced by N-[4-(5-nitro-2-furyl)-2-thiazolyl]formamide and sodium saccharin, sodium ascorbate, or related salts.

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Male F344 rats were fed 0.2% N-[4-(5-nitro-2-furyl)-2-thiazoly]formamide for 6 weeks and then fed 3% or 5% sodium saccharin, 5% sodium ascorbate, 3.12% calcium saccharin, 1.34% sodium chloride, 5.2% calcium saccharin plus 1.34% sodium chloride, or basal diet alone for 72 weeks. Protein and DNA were

[The inhibitory effect of ascorbic acid on the estrogen-stimulated promotion of uterine sarcoma development in mice].

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The administration of estradiol propionate after the discontinuation of 1,2-dimethylhydrazine (DMH) treatment increased the incidence of uterine sarcoma in CBA mice from 32.5 (DMH alone) to 62.5%. The addition of the ascorbic acid (0.3% solution in drinking water) to estradiol propionate was

Modifying effect of ascorbic acid and sodium ascorbate on the promoting stage of uterine sarcomogenesis induced in CBA mice by 1,2-dimethylhydrazine and estradiol-dipropionate.

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Administration of estradiol-dipropionate (EP) after the cessation of 1,2-dimethylhydrazine (DMH) treatment increased the incidence of uterine sarcomas in CBA mice from 32.5 (DMH alone) to 62.5%. Ascorbic acid (AA) (0.3% in drinking water) given simultaneously with EP decreased the tumour incidence

[Effect of ascorbate on the permeation and photosensitizing activity of hematoporphyrin derivative (HPD) in tumor].

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OBJECTIVE To determine the depth of permeation and concentration of HPD in tumor tissue which had been immersed in HPD in the presence and absence of ascorbic acid, and to examine its photosensitizing effect. METHODS Solid S-180 sarcoma of 1 cm3 in size was excised from tumor-bearing mice and

Reticulum cell sarcoma: two complete 'spontaneous' regressions, in response to high-dose ascorbic acid therapy. A report on subsequent progress.

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In 1975, we reported the remarkable case of a 42-year-old man with histologically proven widely disseminated reticulum cell sarcoma who, in a remarkably short time, appeared to enjoy not one, but two, complete spontaneous regressions of his fatal illness. Both these regressions coincided exactly in

Altered production of the active oxygen species is involved in enhanced cytotoxic action of acylated derivatives of ascorbate to tumor cells.

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Our previous study shows that 6-O-acyl derivatives of L-ascorbic acid inhibits more markedly cell growth of mouse Ehrlich carcinoma than ascorbic acid. The present study shows that 6-O-palmitoyl ascorbic acid but not ascorbic acid prolongs the lifespan of mice into which tumors such as Meth A

Tempicol-2 (4-hydroxy-4-(2-picolyl)-2,2,6,6-tetramethylpiperidine-1-oxyl), a stable free radical, is a novel member of nitroxide class of antioxidants and anticancer agents.

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As a part of our studies on the chemical, biochemical and pharmacological characteristics of the newly synthesized antioxidants, nitroxide derivatives, we designed a novel nitroxide, named Tempicol-2. Its capacity to act as antioxidant of potential pharmacological application was tested in three

Experimental evidence for the existence of the passive antitumor defense system formed by the synergistic action of certain small substances of the circulatory system.

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In AIDS, only a few types of tumors (mainly Kaposi's sarcoma and non-Hodgkin's lymphoma) increase in incidence despite global abnormalities in the immune system. In addition, the reason for the higher incidence of these tumors is not immunosuppression but other agents. This shows that the immune

A mixture of amino acids and other small molecules present in the serum suppresses the growth of murine and human tumors in vivo.

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Previously we have hypothesized that the small molecules which are selectively accumulated in cancer cells might participate in a non-immunological antitumor surveillance mechanism. We demonstrated earlier that a mixture of experimentally selected substances ("active mixture", AM: L-arginine,

Catalytic properties of lysyl hydroxylase from cells synthesizing genetically different collagen types.

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Crude preparations of lysyl hydroxylase were extracted from chick-embryo tendons synthesizing exclusively type I collagen, chick-embryo sterna synthesizing exclusively type II collagen and HT-1080 sarcoma cells synthesizing exclusively type IV collagen. No differences were found in the Km values for

Primary avian tendon cells in culture. An improved system for understanding malignant transformation.

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Primary avian tendon (PAT) cells which maintain their differentiated state in culture are rapidly transformed by Rous sarcoma virus. By criteria of morphology, increased rate of 2-deoxyglucose uptake, and loss of density dependent growth control, PAT cells transform as well as their less

Vitamin C preferential toxicity for malignant melanoma cells.

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Vitamin C has been suggested and disputed as an anti-cancer agent. For cells in culture, no preferential effect against any type of cancer has yet been demonstrated. Our aim here is to show that vitamin C is selectively toxic to at least one type of malignant cell--a melanoma--at concentrations that
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