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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The terminal differentiation, keratinization, of a rat bladder tumor cell line, NBT II, occurred in multicellular aggregates. After aggregation, these cells did not undergo a round of mitosis before keratinization. 5-Bromodeoxyuridine added to the monolayer cell culture 2 days before aggregation completely prevented this differentiation; it was ineffective when added at the time of cell aggregation. Vitamin A prevented the keratinization of NBT II cells in aggregates but did not inhibit aggregate formation; it enhanced the number of cells engaged in DNA synthesis. This model appears to be very useful for analyzing the mechanisms of terminal differentiation and its modulation by vitamin A in tumor cells.
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PMID:Keratinization and the effect of vitamin A in aggregates of a squamous carcinoma cell line NBT II. 615 20

Twenty-five patients with advanced squamous cell carcinoma of the head and neck were entered into this study. All patients had previously been irradiated and the majority had also undergone surgery for recurrent tumor. A low-dose regimen consisting of adriamycin, bleomycin, 5-fluorouracil, methotrexate, and vitamin A was prescribed, the median number of courses was four and a total of 95 were administered. Ten patients (40%) achieved objective responses (7 partial, 3 complete). The median duration of response was 14 weeks (range, nine to 60 weeks) with a median survival time of 38.5 weeks (range, eight to 72 weeks). The nonresponding patient group's survival time was significantly reduced (P = 0.002; median, 12 weeks; range, three to 40 weeks). The treatment was given on an outpatient basis and no serious hematologic toxic reactions were encountered. Mucositis was uncommon. This regimen produced an acceptable response rate without serious side-effects. The use of Vitamin A may have helped to prevent further impairment of the patient's nutritional status by ameliorating drug-induced mucositis.
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PMID:Advanced recurrent squamous cell carcinoma of the head and neck. Results of a chemotherapeutic regimen with adriamycin, bleomycin, 5-fluorouracil, methotrextate, and vitamin A. 615 69

Vitamin A is attracting increasing attention as a potential cancer chemopreventative agent. To investigate the effect of vitamin A on tumor establishment, growth and metastasis, rats were fed diets containing zero, adequate or excess (100X adequate) amounts of vitamin A prior to subcutaneous injection with transplantable hepatocellular carcinomas derived from solid tumors induced by N-2-fluorenylacetamide. When rats were injected at the same time the dietary regimen was begun, tumor growth was similar in both the deficient and adequate vitamin A groups with 20% less in the excess vitamin A group. However, when rats were injected 2 weeks post-initiation of the dietary regimen, tumors were fewer and appeared later under conditions of either vitamin A deficiency or excess. When rats were injected with a metastatic line 2 weeks following initiation of the dietary regimen, no metastases were observed in the animals fed excess vitamin A, but 60% had metastases in the deficient group and 75% in the adequate group. Results suggest that dietary extremes of vitamin A affect tumor establishment and growth and excess amounts prevent metastasis of transplantable hepatomas in the rat.
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PMID:Chemoprevention of tumor development and metastasis of transplantable hepatocellular carcinomas in rats by vitamin A. 624 1

In A-Jax mice, the appearance of MCA-induced sarcomas in delayed by Vitamin A application. Continuous uptake of drinking water containing 0.05% of a retinol palmitate emulsion leads to a significant inhibition. Administration of ethylnitrosourea (ENU) to pregnant Swiss mice on the 17th day of gravidity results in the formation of lymphoblastoid leukemias from the beginning of the 12th week after birth, 90% of the animals dying within 25 weeks. In this case, continuous addition of 0.1% retinol palmitate emulsion to drinking water leads to a dramatic reduction of the tumor risk to about 50%. By additional administration of proteolytic enzymes of animal and plant origin this risk can be further reduced. The lung adenomas developing to 100% in the animals are not influenced by this treatment. Vitamin A, added to drinking water, exerts a strong inhibitory effect on transplacentally induced leukemia.
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PMID:Experimental cancer prophylaxis. 635 37

In an initial effort to determine whether circulating retinol might promote differentiation of embryonal carcinoma (EC) cells in tumor form, we have assessed the ability of retinol to stimulate differentiation of cultured EC cells. We found that retinol induces several murine EC cell lines to differentiate in vitro. Differentiated derivatives were distinguishable from parental EC cells by morphology, cell surface antigenic properties and levels of secretion of plasminogen activator. Retinol effects could be seen at concentrations as low as 8.7 X 10(-8) M (0.025 microgram/ml). Only two of eight EC lines tested failed to differentiate in response to retinol: PCC4-aza1R, which dies at retinol concentrations above 3.5 X 10(-7) M; and PCC4(RA)-1, a mutant line derived from PCC4-aza1R cells, which also fails to differentiate in response to retinoic acid.
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PMID:Murine embryonal carcinoma cells differentiate in vitro in response to retinol. 668 58

Bovine aorta smooth muscle cells (SMC) incubated with a tumor-promoting phorbol ester, 12-O-tetradecanoylphorbol-13-acetate (TPA), released increased levels of prostaglandin I2 [measured as its stable hydrolytic product, 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha)], and this response was inhibited by all-trans-retinoic acid (RA) at concentrations as low as 17 nM. Retinol and retinyl acetate, at concentrations as high as 1.7 and 1.5 microM, respectively, did not inhibit the TPA-stimulated 6-keto-PGF1 alpha production. RA was not cytotoxic at 1.7 microM, as assayed by exclusion of trypan blue dye. Inhibition by RA was increased after preincubation of the SMC with RA prior to TPA stimulation. The inhibition of arachidonic acid (AA) metabolism by RA was not specific for TPA stimulation; RA inhibited prostaglandin production after SMCs were stimulated by serotonin; melittin; the Ca2+ ionophore, A23187; and fetal calf serum. RA had no effect on phorbol ester binding to SMC, nor did it inhibit increased 6-keto-PGF1 alpha production in SMC treated with exogenous AA. While RA inhibited TPA-stimulated production of 14C-labeled 6-keto-PGF1 alpha from [14C]AA-labeled cells, it did not inhibit the accumulation of [14C]AA in the culture medium. The data suggest that RA inhibits stimulated, rather than basal, levels of prostaglandin production. RA does not seem to act by inhibiting the deacylation of AA from cellular phospholipid pools, insofar as this is reflected in the accumulation of AA in the media, but may inhibit reactions at, or after, the generation of endoperoxides by cyclooxygenase.
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PMID:Inhibition of stimulated prostaglandin biosynthesis by retinoic acid in smooth muscle cells. 669 28

Zinc deficiency enhances experimental esophageal tumor induction. Vitamin A supplementation inhibits carcinogenesis in animals. Plasma zinc and plasma vitamin A levels are reduced in several human squamous cancers, but have not been studied in a US population with esophageal cancer. Therefore, we measured plasma zinc and vitamin A in patients with newly diagnosed esophageal cancer. In addition, we assessed hepatic and nutritional status and attempted to control for other factors known to influence plasma zinc and vitamin A levels. Plasma zinc and vitamin A were both significantly less in esophageal carcinoma than in age-matched healthy controls (plasma zinc 65.7 +/- 3.3 micrograms/dl [mean +/- SEM] in esophageal cancer versus 80.5 +/- 2.4 micrograms/dl in controls, P less than 0.01; plasma vitamin A 32.6 +/- 3.4 micrograms/dl in esophageal cancer versus 60.2 +/- 4.2 in controls, P less than 0.001). Overall, 15 of 17 patients with esophageal cancer had decreased plasma zinc and/or decreased plasma vitamin A. Our findings are compatible with a hypothesis that zinc or vitamin A deficiency may be co-factors in the induction of human esophageal carcinoma.
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PMID:Plasma zinc and vitamin A in human squamous carcinoma of the esophagus. 683 64

Retinol, 5 flavonoids, 3 steroids and 7 sweetening agents were studied for their effects on 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced early antigen (EA) of Epstein-Barr virus (EBV) in Raji cells. Concomitant treatment of Raji cells with TPA and retinol showed inhibition of EA induction. Among flavonoids, quercetin resulted in effective inhibition of EA induction by TPA and alpha-naphthoflavone showed the weakly inhibitory effect. None of the other flavonoids such as rutin, catechin and beta-naphthoflavone affected the induction of EBV-EA by TPA. beta-Estradiol obviously inhibited EBV-EA induction by TPA, but hydrocortisone did not show any inhibitory effect on it. Glycyrrhetinic acid, steviol, phyllodulcin and perrillartine also showed the remarkable inhibition of EBV-EA induction. On the other hand, glycyrrhizin and stevioside, glycosides of glycyrrhetinic acid and steviol, did not inhibit the induction of EBV-EA by TPA. Some of the inhibitors reported here may be effective on the inhibition of the in vivo tumor promotion by TPA.
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PMID:Inhibition of 12-O-tetradecanoylphorbol-13-acetate-induced induction in Epstein-Barr virus early antigen in Raji cells. 685 May 68

Retinoic acid induced lysozyme activity in mouse myeloid leukemia M1 cells. It also stimulated the synthesis and release of prostaglandins such as prostaglandin F2alpha, E2, and D2 by the cells. The particulate fraction of retinoic acid-treated M1 cells converted arachidonate to prostaglandins, and this conversion was almost completely inhibited by indomethacin. Retinol, retinal and retinyl acetate, but not the pyridyl analog of retinoic acid, also induced lysozyme activity and stimulated synthesis and release of prostaglandins. Indomethacin inhibited the induction of lysozyme activity by retinoic acid. The induction of lysozyme activity and the stimulation of prostaglandin E2 production were dependent on the concentration of retinoic acid. Kinetic studies showed that stimulation of prostaglandin E2 production by retinoic acid was followed by induction of lysozyme activity. The tumor promotor 12-O-tetradecanoyl-phorbol-13-acetate (TPA) and phorbol 12,13-didecanoate inhibited the induction of lysozyme activity by retinoic acid, but 4 alpha-phorbol didecanoate and phorbol did not. TPA and phorbol 12, 13-didecanoate, but not 4 alpha -phorbol didecanoate, also inhibited the stimulation of prostaglandin E2 production by retinoic acid. These results suggest that stimulation by retinoic acid of prostaglandin E2 production in M1 cells is a prerequisite for the induction of lysozyme activity. On the other hand, both retinoic acid and TPA inhibited the induction by dexamethasone of phagocytic activity, which is a typical functional marker of differentiation of M1 cells, without causing significant growth inhibition. Suboptimal concentrations of retinoic acid and TPA had synergistic inhibitory effects on the induction of phagocytic activity of M1 cells by dexamethasone.
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PMID:Stimulation by retinoic acid of prostaglandin production and its inhibition by tumor promoters in mouse myeloid leukemia cells. 694 53

Nutrition and cancer interact in a number of important ways and nutritional factors are increasingly recognized as relevant to both the prevention and treatment of cancer. The role of several nutrients in cancer development is considered briefly here. Deficiency of riboflavin (Vitamin B2) prolongs the survival of tumor-bearing animals, but may accelerate carcinogenesis caused by certain agents, as flavin cofactors are involved in drug and carcinogen metabolism. Deficiency of Vitamin A may enhance the development of tumors of epithelial origin, particularly lung. Evidence is accumulating that Vitamin A and/or its precursors, the B-carotenes, may possibly have an effect in chemoprevention of certain of these epithelial cancers both in animals and in man. The consumption of dietary fat among various nations is correlated closely with increased development of cancers of the breast, colon, and prostate, and possibly of other organs. Studies of migrant populations from Japan to the United States show changes in prevalence of stomach and colon cancer in the direction of the native United States population. Sources of nitrites are of concern because of their potential conversion to carcinogenic nitrosamines. Limitation of the delivery of nitrites may be difficult to accomplish so investigators are exploring the blockade of conversion of nitrites to nitrosamines. Nutrition should not be viewed as the sole means of cancer prevention and treatment but rather as a vital component of any treatment plan.
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PMID:Nutrition and cancer: state of the art relationship of several nutrients to the development of cancer. 718 45


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