Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0596263 (carcinogenesis)
 64,820 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of mild vitamin A deficiency or vitamin A supplementation on methylbenzylnitrosamine (MBN; CAS: 937-40-6)-induced esophageal carcinogenesis was examined in Sprague-Dawley rats. The animals were fed semipurified diets containing levels of retinyl acetate, which were adequate (2.2 mg/kg diet), deficient (0.30 mg/kg diet), or supplemented (29.9 mg/kg diet) with respect to vitamin A content. Carcinogen-treated rats received 2.5 mg MBN/kg (body wt) twice a week for 5 weeks; they were then sacrificed for evaluation of esophageal tumorigenesis 15 weeks later. Liver levels of retinol reflected vitamin A nutriture, but there were no clinical signs of deficiency or toxicity. There were no significant differences in the frequency or incidence of esophageal tumors (either carcinomas or papillomas) among the dietary groups. There was also no indication that either vitamin A deficiency or vitamin A supplementation influenced the formation of preneoplastic lesions. Although the time was short for the neoplastic development, tumors were observed. These data suggest that vitamin A is selective in tissues it may protect from cancer induction and that the esophagus is less involved than other tissues.
 ...
PMID:Effect of vitamin A nutriture on experimental esophageal carcinogenesis. 347 42

The effects of vitamins A, C, and E and of selenium on carcinogenesis are briefly summarized and updated. These vitamins and minerals were selected because they have been studied extensively in recent years with a variety of carcinogenesis models. The consumption of vitamin A and its precursors (carotenoids) has been negatively correlated with cancer at a number of sites, particularly the lung. Animal investigations on vitamin A involvement in carcinogenesis have generally been of three types: those assessing the effect of vitamin A deficiency, the effect of excess vitamin A, or the effect of supplementation with synthetic analogs of vitamin A. Vitamin A deficiency had no effect on salivary gland carcinogenesis, enhanced urinary bladder, lung, and liver carcinogenesis, and inhibited colon carcinogenesis. Excess of various forms of vitamin A enhanced or inhibited skin tumorigenesis, inhibited mammary carcinogenesis in rats (but not in mice), and carcinogenesis of the forestomach, liver, and urinary bladder (with one model, but not with another), or enhanced or did not influence lung carcinogenesis. Vitamin A analogs have enhanced or inhibited skin tumorigenesis, inhibited salivary gland, mammary, and urinary bladder carcinogenesis, enhanced tracheal and liver carcinogenesis, and either enhanced or inhibited pancreas carcinogenesis, depending upon the model employed. Although retinoids have been shown to inhibit carcinogenesis at many sites, numerous negative studies have been reported and some reports have indicated enhanced carcinogenesis. The most convincing evidence for the involvement of vitamin C in cancer prevention is the ability of ascorbic acid to prevent formation of nitrosamine and of other N-nitroso compounds. In addition vitamin C supplementation was shown to inhibit skin, nose, tracheal, lung, and kidney carcinogenesis, to either not influence or enhance skin, mammary gland, and colon carcinogenesis, and to enhance urinary bladder carcinogenesis, when given as sodium ascorbate, but not when given as ascorbic acid. Like vitamin C, vitamin E can inhibit nitrosation. Vitamin E was shown to inhibit skin, cheek pouch, and forestomach carcinogenesis, to enhance or inhibit colon carcinogenesis, and to have no effect on or to inhibit mammary gland carcinogenesis, depending upon the method of vitamin E administration or the level of dietary selenium or dietary fat. Selenium effects on carcinogenesis have been recently reviewed and the present discussion only updates this area by indicating that enhancement of carcinogenesis by dietary selenium supplements has been observed in the liver, pancreas, and skin.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Update on the effects of vitamins A, C, and E and selenium on carcinogenesis. 354 Sep 70

Retinoids clearly show both prophylactic and therapeutic effects against many kinds of neoplasm. Vitamin A deficiency and vitamin A excess, which are very different states clinically and metabolically, should be separately considered relative to carcinogenesis. The anticancer effects of retinoids and related compounds may be more closely related to their chemical structure than to their similarity to the structure and function of vitamin A. Retinoids act on cells and tissues in a number of ways. Although many interesting ideas have been proposed to clarify their mode of action, no single hypothesis adequately explains their many molecular interactions and responses. Investigation of early molecular interactions between retinoids and cells and the subsequent metabolism of retinoids in neoplastic and normal cells may aid in the clarification of their action as antineoplastic agents.
 ...
PMID:Some thoughts on the relationship between vitamin A and cancer. 359 30

The administration of N-nitrosodimethylamine (NDMA) and its endogenic synthesis from amidopyrine and sodium nitrite decreases in the liver the level of reduced glutathione, ascorbic acid, glutathione reductase and glutathione-S-transferase activities, the accumulation of oxidized glutathione as well as the damage of DNA. The gamma-glutamyltransferase activity, the marker of carcinogenesis, increased. The damaging action of NDMA under the influence of vitamin A deficiency increased, but the vitamin excess decreased the biochemical changes in the liver.
 ...
PMID:[Effect of vitamin A on the endogenous synthesis and system of N-nitrosodimethylamine detoxication in the rat liver]. 369 97

The effect of suboptimal levels of dietary vitamin A on diethylnitrosamine (DEN) carcinogenesis was studied in BALB/c and Swiss mice. Two different dietary regimens were employed to induce vitamin A deficiency and DEN was administered by gavage at 2 dose levels: 0.6 mg/kg as a single dose and 200 mg/kg in 4 divided doses. Shark liver oil (SLO) which was the main source of vitamin A in the standard diet, was deleted in one regimen and reduced to 25% in the other. The mice maintained on the former diet were given a high dose of DEN and those on the latter diet received a low dose. In both strains the deficient mice had a greater tumour incidence than those on standard diet with a marginal reduction in the latent period. At the low level of DEN there was shift in organotrophy, i.e. from liver in controls to lung in the vitamin-A-deficient mice of BALB/c strain. With the higher dose, lung adenomas predominated in deficient as well as control groups in both the strains. Forestomach carcinomas appeared in deficient mice and not in the controls.
 ...
PMID:Carcinogenicity of diethylnitrosamine in vitamin-A-deficient mice. 369 24

The present investigation shows the effect of vitamin A deficiency on the initiation and postinitiation phases of benzo(a)pyrene-induced lung carcinogenesis in male Wistar rats. Lung tumours were induced by giving three intratracheal instillations, one week apart, of 10 mg benzo(a)pyrene per instillation. Maximum tumour incidence (100%) and tumour burden per rat was found in rats which were kept on vitamin A deficient diet for 4 weeks prior to the first administration and 8 weeks after the last administration of benzo(a)pyrene. Rats in which vitamin A deficiency was terminated after the last administration of the carcinogen had 83% tumour incidence, whereas corresponding control pairfed animals had 39% incidence of tumours. These data represent the values obtained 32 weeks after the last administered dose of the carcinogen and indicate the role of vitamin A, both in the initiation as well as in the postinitiation phases of lung carcinogenesis.
 ...
PMID:The effect of vitamin A deficiency on the initiation and postinitiation phases of benzo(a)pyrene-induced lung tumourigenesis in rats. 407 46

The effects on tracheal glands of benzo[a]pyrene and of vitamin A deficiency were examined in explants derived from normal and vitamin A deficient hamsters, respectively. Both treatments caused hyperplasia and squamous metaplasia of the tracheal glands. It is suggested that a proportion of respiratory tract lesions may originate in tracheal glands.
Carcinogenesis 1983 Oct
PMID:Squamous metaplasia of tracheal submucosal glands induced by benzo[a]pyrene and vitamin A deficiency. 631 53

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.
 ...
PMID:Plasma zinc and vitamin A in human squamous carcinoma of the esophagus. 683 64

The biological mode of action of tumor promoters, exemplified by the phorbol esters, is a subject of intensive study in a number of laboratories. A few investigators have recently begun to examine the role of dietary nutrients in tumor promotion, but the available data are sparse and interpretation difficult. A few examples are provided to indicate that some nutrients may be important in the promotion of cancer. However, the fine dividing line between effects on initiation or on promotion, so clearly shown in the mouse two-stage skin cancer model, is not so clear as yet in models used for studies in nutritional carcinogenesis. The animal models for these studies have been primarily rats, mice and hamsters. These have shown that nutrients which appear to have promotion activity are zinc deficiency and 13-cis-retinoic acid for the esophagus; vitamin A deficiency and lipotrope deficiency for the forestomach, unsaturated fat and vitamin A deficiency for liver and colon, lipotrope deficiency for the liver; selenium for the liver. It is probably more correct at this early stage of investigation to consider the effects of nutrients acting either during the time of exposure to the carcinogen, or, after such exposure and when no detectable carcinogen is found in the animals tissues, rather than as promoters in the strict sense.
 ...
PMID:Promotion of gastrointestinal tract tumors in animals: dietary factors. 687 33

Retinoic acid (RA) plays an essential role in maintaining normal differentiation of tracheal epithelial cells. During vitamin A deficiency, tracheocytes undergo squamous metaplasia, an abnormal differentiation that can be reversed by RA. We used rat tracheal 2C5 cells to study the mechanism of inhibition of squamous differentiation by RA. 2C5 cells grown to confluence in the presence of serum underwent squamous differentiation as marked by an increase in their level of crosslinked envelope formation. The serum-induced crosslinked envelope formation was blocked by RA in 2C5 cells with an ED50 < 0.1 nM. However, the activity of the crosslinking enzyme, keratinocyte transglutaminase, did not correlate with the formation of crosslinked envelopes in 2C5 cells. Changes in biochemical markers of squamous differentiation such as an altered expression of specific cytokeratins also accompanied serum-induced squamous differentiation of 2C5 cells. The expression of the keratin squamous differentiation markers (i.e. K13) were inhibited by RA, although the ED50 for K13 expression was > 1 nM. The different dose responses for RA inhibiting differentiation markers suggests multiple mechanisms of regulation by RA. These results indicate that 2C5 cells remain responsive to differentiation factors such as RA and serum despite being an immortalized cell line.
Carcinogenesis 1994 Mar
PMID:The mechanism of the inhibition of squamous differentiation of rat tracheal 2C5 cells by retinoic acid. 750 32


<< Previous 1 2 3 4 Next >>