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Query: UMLS:C0596263 (carcinogenesis)
 64,820 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Serum retinol levels were measured in 356 women with neoplasms, inflammatory lesions or premalignant diseases of the genital tract. Significantly lower serum retinol level was found in ovarian carcinoma bearing patients (31.1 +/- 7.5) vs a control group (52.8 +/- 11.0 SD). We found too, that woman with benign neoplasms and inflammatory diseases of the genital tract, had lower serum retinol levels than a control group. On the basis of our study we present the hypothesis that low serum retinol level seems to be primarily due to carcinogenesis.
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PMID:Serum retinol levels in female genital tract cancers. 208 28

Painting and feeding of mice with 2mg of an extract from black pepper on 3 days a week for 3 months results in a significant increase of the number of tumor-bearing mice. Tumor incidence is reduced in those groups of experimental animals receiving 5 or 10mg Vitamin A-palmitate twice weekly for 3 months by feeding or painting during and subsequent to application of pepper extract. Feeding of mice with powder of black pepper in diet (50g/3kg food) has no impact on carcinogenesis.
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PMID:Carcinogenesis induced by black pepper (Piper nigrum) and modulated by vitamin A. 209 70

Vitamin A is known to be able to modulate cell growth and differentiation and to act as an inhibitor of the process of carcinogenesis in some experimental models. Here we have studied the effect of different concentrations of vitamin A on chemotactic and chemoinvasive behaviour of a metastatic osteosarcoma cell line. The cell proliferation was partially inhibited in the presence of 10(-5) M retinol after 4 days of incubation. Retinol effect on chemotactic and chemoinvasive activity of osteosarcoma cells seemed to be dose-dependent. The highest retinol concentration used (10(-5) M) had an inhibitory effect on migratory and invasive cell response. Lower retinol concentrations seemed to be able to enhance (10(-8) M) both chemotactic and chemoinvasive activity of osteosarcoma cells. Chemotaxis and chemoinvasion assays provide rapid and quantitative tools to study the "in vitro" behaviour of metastatic cells. Furthermore, they represent a mean to screen for drugs, hormones and other substances able to alter the metastatic phenotype.
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PMID:Effect of vitamin A on chemotactic and chemoinvasive behaviour of an osteosarcoma cell line. 239 Feb 27

Epidemiological and experimental research indicated some time ago that vitamins might act as protective agents in carcinogenesis. However, only more recently prospective studies proved a significant inverse correlation between certain vitamins and cancer at different site. The Basel Study (comprising 3756 healthy adult volunteers) is unique in its immediate measurement of the plasma vitamins at the time of the clinical assessment (1971-1973). The complete mortality follow-up allows testing of several hypotheses regarding the molecular basis of cancerogenesis. Among these mechanisms, aggressive oxygen species have been implicated. By analyzing plasma concentrations of essential antioxidants in cancer cases and survivors, we demonstrated a significantly negative inverse correlation between plasma beta-carotene and all cancer (n = 102, p less than .01), cancer of the lung (n = 37, p less than .01) and stomach (n = 17, p less than .05). Low retinol was related only to gastric cancer (p less than .01); low vitamin C and low vitamin E was related to all cancer and gastric cancer (p less than .05). The estimated antioxidant potential calculated as the molar product of vitamins C, E and beta-carotene showed a highly significant inverse correlation with all cancer and cancer of the lung and the stomach (p less than .01). These data and other newer studies strongly support the antioxidants in a role as natural inhibitors which may act on cancer initiation or promotion. Finally the convergence of results of the many epidemiological and experimental studies allow more soundly based conclusions with regard to dosage and time of vitamin intake in cancer.
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PMID:Preventive potential of antioxidative vitamins and carotenoids on cancer. 250 2

Squamous cell carcinomas were induced in hairless mice by repeated irradiations with UVB (280-320 nm, total dose 30 J/cm2) plus UVA (320-400 nm, total dose 168 J/cm2). The irradiated animals and non-irradiated controls were fed on diets with or without vitamin A supplementation (20,000 IU/kg). At the appearance of tumours, 30 to 43 weeks after the last irradiation, the vitamin A (retinol plus retinyl ester) concentrations in the serum, liver, epidermis and tumours and the retinol esterifying activities in microsomes from epidermis and tumours were measured. The liver and epidermal vitamin A concentrations were 2-3 times higher in vitamin A supplemented than in unsupplemented animals, but did not differ between tumour-bearing animals and non-irradiated controls receiving identical diets. The vitamin A concentration in the tumours was significantly lower than in perilesional epidermis. The largest difference (p less than 0.001) between the tumour and epidermal values was observed in the vitamin A supplemented group. The low vitamin A content of the tumours was entirely due to a marked (2 to 6-fold) reduction in the retinyl ester fraction. In contrast, the retinol content of the tumours was increased to twice that of normal epidermis. The activity of the esterifying enzyme, acyl-CoA:retinol acyltransferase (EC 2.3.1.76), was unchanged. The reason for the reduced retinyl ester concentration thus remains unclear. Still, it is possible that a disturbed interconversion of retinol to retinyl esters plays a role in murine photo-carcinogenesis.
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PMID:Decreased retinyl ester concentrations in UV-induced murine squamous cell carcinomas. 257 23

Over the past two decades, marked shifts have occurred in cancer mortality in the United States, the United Kingdom, and the Federal Republic of Germany. Stomach cancer mortality has declined sharply, while brain cancer and multiple myeloma increased nearly twofold for persons ages 75 to 84. Total cancer incidence in the United States, excluding lung cancer, has risen 27% since 1950, adjusted to the aging of the population. The origins of these trends are not known. The diet in the developed countries includes a number of naturally occurring, powerful anticarcinogens and carcinogens. To evaluate the role of these substances in the prevention and causation of human cancer, this paper reviews existing toxicologic and epidemiologic data. These data indicate that naturally occurring substances in food influence cancer initiation, promotion, progression, and demotion by a number of mechanisms, including (1) covalent binding to DNA of naturally occurring anticarcinogenic compounds to block the initiation of carcinogenesis; (2) induction of biotransforming enzymes such as cytochrome P450 and mixed-function oxidase (MFO) which can reduce carcinogenicity; (3) inhibition of tumor promotion by compounds such as retinol, tocopherol, and organosulfates found in garlic, onions, fruits, and vegetables; and (4) physical alteration of carcinogens by food constituents or by food preparation and handling so as to alter carcinogenicity. Systems have been proposed for estimating the relative ranking for humans of individually tested, experimental carcinogens, including some constituents of food. While qualitatively useful, such systems as the HERP Index do not take into account important interactions among naturally occurring and synthetic constituents in foods, nor do they permit examination of the possible role of evolved resistance. Common mixtures in food must be tested for carcinogenicity in human tissue cultures and in long-term rodent bioassays. Such studies need to examine whether the action of synthetic organic carcinogens may be inhibited by potent naturally occurring anticarcinogens.
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PMID:Natural anticarcinogens, carcinogens, and changing patterns in cancer: some speculation. 268 27

Retinoids that cause inhibition of methylcholanthrene-induced neoplastic transformation of C3H/10T1/2 cells enhance gap-junctional communication in carcinogen-initiated cells. Dose-response studies using retinoids of diverse structures and potency demonstrated a good correlation between these two events. Junctional permeability was enhanced by retinol and tetrahydrotetramethylnaphthalenyl propenylbenzoic acid (TTNPB) at concentrations from 10(-10) to 10(-6) M, and by retinoic acid between 10(-8) and 10(-6) M, the same concentrations that inhibited neoplastic transformation. Retinoic acid inhibited permeability at 10(-10) M, at which concentration transformation was enhanced. Retinoids caused similar alteration sin communication in parental 10T1/2 cells. Communication between initiated and 10T1/2 cells was not influenced by TTNPB. The tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA) inhibited junctional communication in initiated cells, in 10T1/2 cells and between these two cell lines. After repeated exposure of 10T1/2 cells to TPA only retinoid-enhanced communication was blocked; in contrast, basal communication became refractory. It is proposed that much of the chemopreventive action of retinoids can be explained by the enhanced junctional communication of growth regulatory signals.
Carcinogenesis 1989 Sep
PMID:Enhancement of gap junctional communication by retinoids correlates with their ability to inhibit neoplastic transformation. 276 67

Previous studies have shown that all-trans-retinoic acid fails to inhibit chemically induced transformation in 10T1/2 cells except at toxic levels, whereas retinol and many synthetic retinoids are potent inhibitors. In contrast, in many systems retinoic acid is a more effective modulator of differentiation and carcinogenesis than is retinol. In any attempt to explain this anomaly, we have studied the differential metabolism of retinoic acid and retinol by 10T1/2 cells and by their initiated and transformed derivatives, and have also reexamined these cells for the presence of retinoid-binding proteins. Whereas retinoic acid was depleted from the medium bathing 10T1/2 and initiated 10T1/2 cells within 48 h of treatment, retinol was concentrated 500-fold by these cells, and disappeared from the culture medium no faster than from cell-free medium. Retinoic acid metabolism by a number of transformed cell lines varied widely. There was no apparent correlation between metabolizing ability and transforming agent (methylcholanthrene, X-rays, fission spectrum neutrons, and plasmid oncogene transfection). Uptake of retinoic acid was seen in all cell lines and was not correlated with its metabolism. Retinol was metabolized minimally by all cell lines tested; metabolism of retinol was not correlated with retinoic acid metabolizing ability. Retinoic acid-induced growth inhibition and cytotoxicity were not correlated with metabolizing ability, suggesting that the rate of metabolism of retinoic acid is not a major determinant of its acute biological effects. Using sensitive radioimmunoassays, cellular retinoic acid- (CRABP) and retino-binding proteins (CRBP) were both detected in 10T1/2 and initiated 10T1/2 cells. CRABP levels of about 16 ng/10(6) cells were about 4-fold higher than CRBP levels. Therefore, lack of CRABP does not explain the failure of retinoic acid to inhibit carcinogen-induced transformation in these cells. These studies suggest that the inability of retinoic acid to inhibit transformation in the 10T1/2 cell system may be due to its rapid metabolism and clearance from the medium. On the other hand, the high cellular uptake and stability of retinol in these cells could be an important factor in the inhibition of neoplastic transformation by this retinoid.
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PMID:Differential uptake, binding, and metabolism of retinol and retinoic acid by 10T1/2 cells. 282 30

The results of a survey of a population with a high risk of oral and esophageal cancer and the outline of a chemoprevention scheme for persons found to have a precancerous condition of the mouth and esophagus are presented. Of a total of 1,569 men examined, 11% had preleukoplakia and leukoplakia of the mouth, and 60% of the 1,344 men in whom esophagogastroscopy was performed had chronic esophagitis. The relative risk of oral leukoplakia was highest (11.5) among men who smoke and use nass quid. The relative risk was also elevated for persons who only use nass quid (5.6) or who only smoke cigarettes (7.8). Nass use had no effect on the risk of esophagitis. A slight elevation of risk (1.9) of esophagitis was observed for current smokers and drinkers. Of the men from whom blood was drawn for analysis, 4%, 66%, and 86% had low levels of retinol, carotene, and riboflavin, respectively. The high prevalence of oral and esophageal precancerous conditions and low blood levels of riboflavin, carotene, and vitamin A observed in the surveyed population, as well as the existing evidence on the possible protective effect of these nutrients in carcinogenesis, provide an opportunity and a justification for the chemopreventive trial, with the regression of observed precancerous lesions as the end point of the study.
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PMID:Chemoprevention of oral and esophageal cancer in Uzbekistan, Union of Soviet Socialist Republics. 293 49

Retinol and retinoic acid were effective activators of oxygen consumption by human polymorphonuclear leucocytes (PMN) in micromolar concentrations. In contrast, retinyl acetate was ineffective as an activator. Retinol caused activation only after a lag time, the length of which depended on retinol concentration. Oxygen consumption was due to superoxide production by PMN. Superoxide production was observed as superoxide dismutase-inhibitable cytochrome c reduction. Previously, retinoids have been reported to inhibit PMN activation by phorbol myristate acetate, a tumour promoter. This retinoid-induced inhibition of PMN activation has been suggested to be a mechanism by which retinoids may protect against carcinogenesis in animals. However, the retinoid concentrations at which PMN inhibition was reported were much higher than those found to cause activation in this study. We found that retinoic acid slightly inhibited phorbol myristate acetate-activated superoxide production, but only at concentrations that caused activation. In contrast, activation by formyl-Met-Leu-Phe was effectively inhibited at a retinoic acid concentration that did not cause activation by itself.
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PMID:Retinoids activate superoxide production by polymorphonuclear leucocytes. 298 77


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