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

The modifying effects of two natural products, curcumin and hesperidin, given during the initiation and postinitiation phases of oral carcinogenesis initiated with 4-nitroquinoline 1-oxide (4-NQO) were investigated in male F344 rats and compared with that of beta-carotene. At 6 weeks of age, rats were divided into experimental and control groups and fed the diet containing beta-carotene, hesperidin, or curcumin at a dose of 0.5 g/kg diet (500 ppm). At 7 weeks of age, all animals except those treated with each test chemical alone and control groups were given 4-NQO (20 ppm) in the drinking water for 8 weeks to induce oral cancer. Seven days after the 4-NQO exposure, groups of animals fed the diets containing test chemicals were switched to the basal diet and continued on this diet until the end of the study. Starting 1 week after the stop of 4-NQO exposure, the groups given 4-NQO and a basal diet were switched to the diets containing beta-carotene, hesperidin, and curcumin and maintained on these diets for 22 weeks. The other groups consisted of rats given 500 ppm beta-carotene, hesperidin, or curcumin alone or untreated rats. All animals were necropsied at the termination of the experiment (week 32). The incidences of tongue neoplasms and preneoplastic lesions, polyamine levels in the tongue tissue, and cell proliferation activity estimated by bromodeoxyuridine-labeling index and by morphometric analysis of silver-stained nucleolar organizer region proteins were compared among the groups. Feeding of curcumin and beta-carotene during the initiation and postinitiation phases and hesperidin at the initiation stage caused a significant reduction in the frequency of tongue carcinoma (41-91% reduction, P < 0.05) and the order of chemopreventive efficacy was curcumin > beta-carotene > hesperidin. The incidences of oral preneoplasia in rats fed the diets mixed with these compounds were also decreased (P < 0.05). There were no such lesions in rats treated with test compounds alone or those in an untreated control group. Dietary administration of these compounds significantly decreased the labeling index of bromodeoxyuridine and the number and area of silver-stained nucleolar organizer region proteins per cell nucleus that are proliferation biomarkers, of the tongue squamous epithelium (P < 0.05). In addition, polyamine levels in the oral mucosa were lowered in rats treated with 4-NQO and three test compounds when compared to those give 4-NQO alone (P < 0.05).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Chemoprevention of 4-nitroquinoline 1-oxide-induced oral carcinogenesis by dietary curcumin and hesperidin: comparison with the protective effect of beta-carotene. 806 59

The modifying effects of three doses of dietary protocatechuic acid (PCA) given the initiation and postinitiation phases of oral carcinogenesis initiated with 4-nitroquinoline 1-oxide (4-NQO) were investigated in male F344 rats. At 6 weeks of age, rats were divided into experimental and control groups and fed the diet containing PCA at various doses of 0 g/kg diet (basal diet alone), 0.5 g/kg diet (500 ppm), 1 g/kg diet (1000 ppm), and 2 g/kg diet (2000 ppm). At 7 weeks of age, all animals except PCA alone and control groups were given 4-NQO (20 ppm) in the drinking water for 8 weeks to induce oral cancer. Seven days after the 4-NQO exposure, groups of animals fed the PCA diets were switched to the basal diet and continued on this diet until the end of the study. Starting 1 week after the end of 4-NQO exposure, the groups given 4-NQO and a basal diet were switched to the diets containing PCA and maintained on these diets for 22 weeks. The other groups consisted of rats given 2000 ppm PCA alone or untreated rats. All animals were necropsied at the termination of the experiment (week 32). The incidences of tongue neoplasms and preneoplastic lesions, polyamine levels in the tongue tissue, and cell proliferation activity estimated by bromodeoxyuridine-labeling index and by morphometric analysis of silver-stained nucleolar organizer regions' protein were compared among the groups. Feeding of PCA at all doses during initiation or postinitiation phase significantly decreased the development of tongue neoplasms (squamous cell papilloma and carcinoma) and preneoplasia (hyperplasia and dysplasia) (P < 0.05). There were no such lesions in rats treated with 2000 ppm PCA alone or those in an untreated control group. Dietary administration of PCA also caused significant decreases in the labeling index of bromodeoxyuridine and the number and area of silver-stained nucleolar organizer regions per cell nucleus, known as cell proliferation indices, of the tongue squamous epithelium (P < 0.05). In addition, PCA exposure during either initiation or postinitiation phase decreased polyamine levels in the oral mucosa (P < 0.05). These results clearly indicated that PCA inhibited rat oral carcinogenesis in both initiation and postinitiation phases, when administered in these respective phases together with or following treatment with 4-NQO, and such inhibition might be related to suppression of cell proliferation by PCA.
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PMID:Chemoprevention of 4-nitroquinoline 1-oxide-induced oral carcinogenesis by dietary protocatechuic acid during initiation and postinitiation phases. 816 81

There are substantial variations in incidence and mortality from oral and pharyngeal cancer in Europe, with systematic tendencies towards increasing rates in most European countries, particularly in younger males. Most of the geographical differences are due to tobacco and alcohol consumption, which explain over three quarters of approximately 20,000 deaths from oral cancer registered every year in Europe, excluding the former Soviet Union. Nonetheless, dietary factors have an established and quantifiable role in oral carcinogenesis in Europe. Two studies showed a significant protective effect by vegetables and fresh fruit, which appeared particularly strong and consistent for fruit, but were not explained by measures of intake of beta-carotene or other micro-nutrients. Although it is not clear whether the observed associations simply reflected a generally poorer nutritional status of oral cancer cases, they open interesting perspectives for aetiological research and prevention, since about one in six oral cancers in European populations can be attributed to dietary deficiencies or imbalances.
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PMID:Diet and human oral carcinoma in Europe. 818 May 71

Extensive research has been carried out in experimental animals to demonstrate the anticancer activity of retinoids, carotenoids and tocopherol on oral cancer and oral precancerous leukoplakia. The anticancer properties of these micronutrients have been studied in experiments dealing with inhibition of carcinogenesis, prevention of oral cancer development and regression of established oral carcinoma. Synergism has been demonstrated in the anticancer activity of beta carotene and alpha tocopherol. Synergism has also been demonstrated between beta carotene and anticancer alkylating agents such as melphalan and cyclophosphamide. Micronutrients such as beta carotene have been found to inhibit both major phases of carcinogenesis--initiation and promotion. Animal studies of oral cancer inhibition, prevention and regression have been substantiated by tissue culture studies, using animal and human derived oral cancer cell lines and normal epithelial cells. Mechanisms of the anticancer activity of the micronutrients on experimental oral cancer have been explored. They include stimulation of elements of the immune system to kill cancer cells, and enhanced expression of heat-shock proteins and repressor genes such as P 53.
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PMID:Oral cancer inhibition by micronutrients. The experimental basis for clinical trials. 818 May 84

Understanding the pathogenesis of cancer may well lead to improved diagnostic tests, preventive treatment and management. This paper reviews the gene changes, the evidence implicating viruses in the aetiology of oral cancer, and the mechanisms whereby viruses may affect gene function and thereby contribute to carcinogenesis.
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PMID:Oral cancer: new insights into pathogenesis. 822 47

The most convincing evidence for a preventive role for any modality is obviously demonstration of incidence reduction produced by that modality. However, cancer prevention trials with cancer incidence as an endpoint have logistic problems rendering them essentially impossible to conduct for most malignancies. Hence a workable strategy often involves analysis of other, indirect lines of evidence to reach conclusions. For oral cancer, dietary epidemiologic evidence points to a protective role for foods rich in carotenoids. Other anti-oxidants, such as vitamin C, are also implicated. Similarly, laboratory evidence points to a carcinogenesis inhibitory role for both retinoids and carotenoids. Clinical studies have targeted premalignant lesions, i.e., oral leukoplakia. For over two decades the efficacy of retinoids, natural and synthetic, has been known. Nevertheless, it has been difficult to translate this into a recommendation for prevention because of the toxicity of retinoids. The synthetic retinoid most often used in these trials is 13-cis-retinoic acid. This compound is toxic even at very low doses (0.1 mg/kg/day), particularly when given over several weeks to months. Hence, although effective, it cannot be advocated for prevention or oral cavity cancer. Studies with nontoxic antioxidants, such as beta-carotene, are much more recent. Early results are promising in that beta-carotene, alone or in combination with other nutrients, can reverse oral leukoplakia without toxicity in short-term trials. Studies currently under way will demonstrate whether durable remissions can be obtained using this strategy. It should be emphasized that such long-term trials are problematic to conduct with the toxic retinoids because the risks of prolonged exposure to them outweighs the chance of cancer development in the usual leukoplakia lesion.
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PMID:Oral cancer prevention: the case for carotenoids and anti-oxidant nutrients. 823 10

In lymphocytes of 12 oral cancer patients (and two control groups) the frequencies of DNA single-strand breaks and DNA-protein cross-linking were determined by alkaline filter elution. We found elevated DNA elution rates, which must be interpreted as an increased strand breakage frequency. There were significant correlations between the DNA strand breakage frequency and smoking habits. Using the 32P-postlabelling assay we determined the DNA adduct level in lymphocytes of 23 oral cancer patients (and two control groups). No significant influence of smoking habit on the DNA adduct level could be detected. There was a significant correlation between the DNA adduct level and the gamma-glutamyltranspeptidase (GGT) value, suggesting systemic influences of alcohol drinking habits on the adduct level.
Carcinogenesis 1993 Nov
PMID:DNA strand breakage and DNA adducts in lymphocytes of oral cancer patients. 824 51

We have tested a range of normal, potentially malignant and malignant oral mucosal biopsies tissues by Southern blot hybridisation analysis for the simultaneous presence of HSV-1 and HPV type 16 DNA sequences, both of which have been implicated as risk factors in oral carcinogenesis. The results show that: (1) 2/4 patients with lichen planus, 2/4 patients with non-specific keratosis, 1/8 patients with oral carcinoma and 3/5 biopsy specimens of normal oral mucosa contained DNA sequences homologous to the HSV-1, Bam HI-G fragment. (2) HPV-16 homologous DNA sequences were detected in 3/4 patients with lichen planus, 4/4 non-specific keratosis, 4/8 oral carcinomas and in 3/5 biopsy specimens of normal oral mucosa. (3) Overall, only 5 patient biopsy specimens were positive for both HSV-1 and HPV-16 homologous DNA sequences; 2 lichen planus, 2 non-specific keratosis and 1 normal. The data cannot exclude a "hit and run" oncogenic mechanism for HSV but suggest that if HSV-1 and HPV-16 play a synergistic role in the development of oral cancer this may be an early event. Indeed, the data suggest HSV might be more frequently found in potentially malignant lesions than in carcinoma.
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PMID:Human herpes simplex-1 and papillomavirus type 16 homologous DNA sequences in normal, potentially malignant and malignant oral mucosa. 829 25

Cancer of the oral cavity accounts for almost 56,000 new cases in India each year totalling almost 30% of all cancer cases in the country. Despite the numerous advances in etiology and epidemiology, the mechanisms involved in oral carcinogenesis remain obscure. Current research has provided some provocative results, suggesting an association between human papillomavirus (HPV) and development of squamous cell tumors including oral cancer. Evidence has been presented showing HPV infection of the oral mucosa and its relation to neoplastic changes. However a clear cut association as is evident in the uterine cervix is not yet available. However, considering the many similarities between oral and cervical oncogenesis, many of the HPV induced changes in the cervix may also be applicable to the oral mucosa. This paper studies the evidence for the possible role of HPV infection in oral carcinogenesis, the uterine cervix as a model for HPV mediated carcinogenesis, and tries to determine if similar mechanisms could exist in both cases.
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PMID:Oral cancer and human papillomaviruses: is there a link? 838 58

The involvement of ADP-ribosylation has been investigated by comparing the extent of ADP-ribosylation in two different stages of oral cancer with that of the corresponding normal oral tissue. Poly(ADP-ribose) synthetase(PADPRS), the enzyme that is responsible for this type of posttranslational covalent modification, was assayed first by measuring 14C-ADP-ribose incorporation into different acceptor proteins of the tissue homogenate. The results clearly indicate an increase in PADPRS activity during oral carcinogenesis. After observing this increased pattern in total tissue, further experiments were conducted to check the extent of ADP-ribosylation in purified nuclei. The data of this experiment also indicates a progressive increase in the extent of ADP-ribosylation with increase in malignancy of oral tissue. Further analysis of an ADP-ribosylation of chromosomal proteins indicates that the increased pattern of ADP-ribosylation is mainly attributed to histones and not to non-histone chromosomal proteins. Our investigation suggests that ADP-ribosylation may play a role in oral cancer and may be used as a potential tumour marker.
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PMID:Increased ADP-ribosylation of histones in oral cancer. 840 95


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