Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0025202 (melanoma)
 69,561 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A monoclonal antibody was raised against the highest molecular weight protein associated with microtubules (MAP-1). Its specific binding to MAP-1 was determined by immunoblotting of the gel electrophoretogram of microtubule proteins prepared from porcine brain. The antibody reacted only with MAP-1, not with MAP-2, tau or tubulin. Indirect immunofluorescent staining by this antibody showed bright intranuclear spots, the centrosome and the faint meshwork of the cytoplasm in several types of cultured mammalian cells; HeLa, PtK2, human skin fibroblasts, mouse melanoma cells, Chinese hamster ovary cells. The nuclear spots in the interphase cells, were replaced by diffuse enhanced fluorescence throughout the cell except for chromosomes during mitosis. They reappeared in late telophase, first in the cytoplasm, late in the nucleus. The punctate pattern of nuclear immunofluorescence was not affected by microtubule-depolymerizing agents. The result that it persisted on residual cell structures after extraction with a high salt concentration buffer containing Triton X-100 followed by digestion with DNase I and RNase A suggests that the antigen is associated with the nuclear skeleton.
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PMID:Monoclonal antibody against microtubule associated protein-1 produces immunofluorescent spots in the nucleus and centrosome of cultured mammalian cells. 636 13

The results of nonspecific immunotherapy with BCG vaccine in 98 cases of melanoma, breast cancer and other malignancies were used in evaluating the frequency and degree of side-effects and complications arising in cancer patients during this treatment. The procedure proved to be safe irrespective of patients' age. Prevention and treatment of side-effects such as fever, water-salt disorders, anorexia, interstitial hepatitis and promotion of tumor growth are discussed.
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PMID:[Treatment of the complications occurring in BCG vaccine immunotherapy of patients with malignant neoplasms]. 646 96

A direct cytotoxic effect of azelaic acid on melanocytes of human melanoma has been demonstrated. In view of a possible future therapeutic employment of this drug in the treatment of primary ocular melanoma, we investigated the route of choice of azelaic acid administration in rabbits. Our results evidenced a suden and direct blood absorption of topically (by retrobulbar injection) administered azelaic acid. This is in agreement with the high water solubility of azelaic acid sodium salt. These preliminary reports indicate that the elective route of azelaic administration in primitive eye melanoma is intravenously by continuous infusion.
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PMID:Distribution of radiolabelled azelaic cid in eye membranes and fluids of rabbits. 653 34

A salt-extractable low-molecular-weight fraction has been held responsible for the resistance of cartilage to invasion by malignant cells. To test this hypothesis, we have confronted in vitro fragments from bovine articular cartilage, from bovine nasal septum, from chick embryonic tibia, or from human knee meniscus with cells from the following malignant lines: LICR-HN-4 human squamous cell carcinoma; B16BL6 mouse melanoma; Hu-456 human transitional cell carcinoma; TE-85 and SAOS-2 human osteosarcoma; and MO4 mouse fibrosarcoma. Human embryo lung cells and chick embryonic heart cells were used as nonmalignant counterparts. Confronting cultures using living cartilage and cartilage extracted with 3 M guanidinium hydrochloride were examined light microscopically and ultrastructurally after 1 to 14 days. Neither invasion of malignant cells into the matrix of living or salt-extracted cartilage nor breakdown of collagen was observed in these cultures. In contrast, both malignant and nonmalignant cells occupied preexisting spaces in the matrix, namely, cut chondrocyte lacunae, cartilage canals, and fibrillation clefts. We concluded from these experiments that salt extraction did not alter the resistance of cartilage to invasion by malignant cells in vitro. This conclusion does not support the opinion that salt-extractable factors are solely responsible for the resistance of cartilage.
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PMID:Interaction of malignant cells with salt-extracted cartilage in vitro. 669 41

The treatment of mice bearing i.m. B16 melanoma with equitoxic dosages of the clinically used 5-(3,3-dimethyl-1-triazeno)-imidazole-4-carboxamide (DTIC) and of its benzenoid water-soluble analogue p-(3,3-dimethyl-1-triazeno)benzoic acid potassium salt (DM-COOK) prior to surgical tumor removal results in a remarkable proportion of cures, even when the treatment is started on already palpable tumors for which surgery alone is ineffective. The survival time of mice which are not cured is also significantly increased with DM-COOK. At the same time, DM-COOK does not affect artificial metastases or spontaneous metastases in mice undergoing surgery and treated with DM-COOK postoperatively. Inhibition of i.m. tumor growth in surgical experiments, and of s.c. tumors in mice not treated with surgery, is significant, although not as pronounced as is necessary to obtain significant prolongation of the life span of the host; the survival time of mice with s.c. tumors treated with both drugs is indeed not significantly increased. DM-COOK thus appears to exert selective antimetastatic effects, unrelated to cytotoxicity for tumor cells, against B16 melanoma in addition to those reported for Lewis lung carcinoma and M5 ovarian reticular cell sarcoma; its therapeutic usefulness is evidenced in adjuvant surgical experiments. DM-COOK, unlike DTIC, is devoid of hematological toxicity for the host. Since, in leukemic mice, it is at least as active as DTIC in increasing the life span of the treated animals, it appears to be an advantageous substitute for DTIC that could undergo preliminary clinical trial.
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PMID:Antimetastatic action and hematological toxicity of p-(3,3-dimethyl-1-triazeno)benzoic acid potassium salt and 5-(3,3-dimethyl-1-triazeno)imidazole-4-carboxamide used as prophylactic adjuvants to surgical tumor removal in mice bearing B16 melanoma. 669 62

The tyrosinase (EC 1.14.18.1) activity of cultured B-16 mouse melanoma cells (C2M) in the stationary phase depends greatly on whether the culture medium contains glucose or galactose. The activity in medium containing galactose was about ten times that in medium containing glucose at pH 7.2. This difference in tyrosinase activity was concluded to be due to a shift of balance between synthesis and degradation of the enzyme. Experiments were conducted with stationary phase cultures in the presence of cycloheximide. The melanoma cells did not synthesize tyrosinase in medium containing glucose in the stationary phase. But when they were cultured under identical conditions, except that glucose was replaced by galactose, they continued to synthesize tyrosinase. The rate of synthesis in medium containing galactose at pH 6.3 was one third of that in the same medium at about pH 7, in which the increase in specific activity of tyrosinase per day was about 30 nmoles/mg cell protein per hr. The rate of degradation of the enzyme was practically the same in medium containing glucose as in medium containing galactose, and largely depended on the pH of the culture medium. At pH 6.3, the half-life was about one third of that at pH 7.2, where it was about 1.8 days. The degradation at acidic pH values was much reduced by ammonium salt and was strongly inhibited by the protease inhibitor, leupeptin.
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PMID:Synthesis and degradation of tyrosinase in cultured melanoma cells. 677 69

Cytosol glucocorticoid receptor of hamster Malignant Melanoma No. 1 (MM1) was characterized by dextran-coated charcoal and sucrose gradient assays. MM1 contains a specific, saturable, high-affinity (Kd 2.5 nM; 73.3 fmol/mg cytosol protein) receptor for glucocorticoid. The receptor sedimented at 7 to 8S in low-salt buffer and 5.5S in 0.4 M KCl and was sensitive to proteolysis by trypsin. Glucocorticoid receptor was inactivated by 40% (NH4)2SO4. Addition of 20 mM molybdate to the homogenizing buffer prevented inactivation. Adrenalectomy increased MM1 receptor content without altering affinity. Chronic exposure of intact or adrenalectomized hamsters to gluco- and high-dose mineralocorticoid significantly decreased the amount of unbound glucocorticoid receptors available for binding. Exposure of intact hamsters to high doses of mineralocorticoid also decreased apparent receptor affinity. These results suggest that hamster MM1 contains a high-affinity cytosol receptor for glucocorticoids similar to that of other glucocorticoid-responsive tissues, which may mediate the action of adrenal steroids on tumor behavior.
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PMID:Effect of adrenal manipulation on glucocorticoid receptors in MM1 hamster melanoma. 707 6

A new polyelectrolyte was synthesized and evaluated for antitumor activity. The product is a derivative of ethylene/maleic anhydride copolymer of low molecular weight (Mn approximately equal to 1100). The anhydride groups were first converted to the half-amide, half-ammonium salt by reaction with ammonia. A percentage (14-25 wt %) of these groups was further converted to the imide by heating. The product, carboxyimamidate (Carbethimer, N-137) inhibited the growth of a number of solid tumors in vivo. Sensitive tumor models included Lewis lung carcinoma, Madison 109 lung carcinoma, M5076 ovarian tumor, colon carcinoma 26, B16 melanoma, and P815 mastocytoma. Activity was dose related between nontoxic dose levels of 300 and 2000 mg/kg ip.
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PMID:Carboxyimamidate, a low-molecular-weight polyelectrolyte with antitumor properties and low toxicity. 713 85

This paper reviews both minor and major adverse reactions caused by estrogenic substances (natural and synthetic, steroidal and nonsteroidal) of which diethylstilbestrol is the prototype of nonsteroidal synthetic estrogen. Minor side effects include nausea, breast tenderness, and excessive cervical secretions (most common), headache, and water and salt retention (less common and often eradicated by lowering estrogen dosage). Vertigo, yeast infections, depression, and photosensitivity are other minor effects. Major side effects are discussed in some detail. Major effects include those on the endocrine system (e.g., feminization in boys and men and precocious puberty in girls); breast tumors; endometrial carcinoma; ovarian tumors; hypertension; thromboembolism; blood clotting excesses; various metabolic effects (including lipid metabolism and carbohydrate metabolism alterations); liver changes (bile alterations and neoplasms); porphyria; melanoma; and effects on a fetus in situ during maternal estrogen administration. In general, lowering doses of estrogen should help eradicate or alleviate most of these effects.
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PMID:Clinical toxicology of estrogens. 741 28

The aim of this work was to study the in vitro effect of ozone on the 70 kDa family of inducible heat shock proteins (HSPs70). We also performed tests to investigate possible toxic effects of ozone at the different doses employed. In human haematic mononucleated cells ozone at doses up to 20 micrograms/ml had no toxic effects and induced biosynthesis of the HSPs70. Biosynthesis of these proteins was greater at 40 micrograms/ml. In murine macrophages testing with tetrazolium salt (MTT), neutral red, and 2-deoxy-D-[1-3H]glucose uptake and study of the cell morphology showed a remarkable resistance or no toxic effects at a dose of 100 micrograms/ml also. Melanoma B16 murine cells assayed with the MTT test demonstrated less resistance to the toxic effects of ozone than normal cells. These results provide indications relevant to the problems of ozone therapy.
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PMID:Effects of ozone on some biological activities of cells in vitro. 760 Feb 55


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