beta-carotene has been researched along with Leukoplakia--Oral* in 40 studies
11 review(s) available for beta-carotene and Leukoplakia--Oral
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Chemoprevention of oral cancer in leukoplakia patients: A systematic review and meta-analysis.
The systematic review and meta-analysis of published randomised controlled trials (RCTs) was conducted to review the effectiveness of current chemopreventive agents in the treatment of oral leukoplakia lesions (OPLs) and prevention of their progression to oral cancer. Material was identified through a retrospective literature search of the electronic PubMed database, Embase and Cochrane Library between 2008 and 2016.Eight RCTs were included for systematic review. The pooled estimate showed a 14% greater chance of responding for those randomised to interventions compared with placebo (Risk Ratio [RR] 1.14, 95% confidence interval [CI] 0.72 to 1.81). The CI from individual studies overlapped. The results suggested that there were no significant differences in comparing clinical responses between chemopreventive agents with placebo in treatment of OPLs. It is time to investigate new agents for oral cancer chemoprevention. Topics: Antineoplastic Agents; beta Carotene; Chemoprevention; Erlotinib Hydrochloride; Humans; Isotretinoin; Leukoplakia, Oral; Mouth Neoplasms; Precancerous Conditions; Provitamins; Tea; Treatment Outcome; Vitamin A; Vitamins | 2017 |
Systematic review of randomized trials for the treatment of oral leukoplakia.
Oral leukoplakia is a relatively common oral lesion that, in a varying proportion of cases, undergoes malignant transformation. The aim of this review was to assess the effectiveness of treatments for leukoplakia. Randomized controlled trials (RCTs) enrolling patients with a diagnosis of oral leukoplakia were identified by searching biomedical databases, hand-searching relevant oral medicine journals, and contacting oral medicine experts through a European mailing list. The methodological quality of included studies was assessed on the basis of the method of allocation concealment, blindness of the study, and loss of participants. Data were analyzed by calculating relative risk. Malignant transformation of leukoplakia, demonstrated by histopathological examination, was the main outcome considered. Secondary outcomes included clinical resolution of the lesion and variation in dysplasia severity. Six RCTs were included in the review. Vitamin A and retinoids were tested in four RCTs; the other agents tested were bleomycin, mixed tea, and beta carotene. Malignant transformation was recorded in just two studies: none of the treatments tested showed a benefit when compared with placebo. Treatment with beta carotene and vitamin A or retinoids was associated with better rates of clinical remission, compared with placebo or absence of treatment. Whenever reported, a high rate of relapse was a common finding. Side effects of variable severity were often described; however, interventions were well accepted by patients since drop-out rates were similar between treatment and control groups. It is noteworthy that the possible effectiveness of surgical interventions, including laser therapy and cryotherapy, has apparently never been studied by means of an RCT. To date, in conclusion, there is no evidence of effective treatment in preventing malignant transformation of leukoplakia. Treatments may be effective in the resolution of lesion; however, relapses and adverse effects are common. Topics: Antineoplastic Agents; beta Carotene; Bleomycin; Cell Transformation, Neoplastic; Humans; Leukoplakia, Oral; Meta-Analysis as Topic; Neoplasm Recurrence, Local; Outcome Assessment, Health Care; Phytotherapy; Randomized Controlled Trials as Topic; Research Design; Retinoids; Tea | 2002 |
Chemoprevention in head and neck cancer.
Topics: Anticarcinogenic Agents; Antioxidants; beta Carotene; Carcinoma, Squamous Cell; Cell Transformation, Neoplastic; Chemoprevention; Head and Neck Neoplasms; Humans; Leukoplakia, Oral; Retinoids; Tea | 2001 |
Antioxidants in oral cancer prevention.
I present evidence in support of a chemopreventive role for the so-called antioxidant nutrients, beta-carotene and vitamin E, against oral cavity cancer. This evidence is from laboratory studies, animal model systems, epidemiologic surveys, intervention trials involving reversal of premalignant changes, and prevention of malignancies in particularly high-risk subjects. Because agents proposed for disease prevention are meant to be used widely without close medical supervision, almost any toxicity is unacceptable. beta-Carotene and vitamin E fulfill this criterion for a suitable chemopreventive agent. In several epidemiologic studies, low intakes of vitamin E, carotenoids, or both have been associated with a higher cancer risk. Smoking, a major risk factor, results in lower beta-carotene concentrations in plasma and oral mucosal cells. In several laboratory and animal model systems, beta-carotene and other antioxidant nutrients are inhibitors of oral cavity carcinogenesis. beta-Carotene and vitamin E can produce clinical regression of oral leukoplakia, a premalignant lesion for oral cancer. The design and limitations of such studies in oral leukoplakia are discussed. Cancer incidence reduction trials in high-risk groups have targeted prevention of second malignancies in patients cured of a primary oral cancer. These trials are in progress. The data thus far are supportive of a significant preventive role for these nutrients in oral cancer. Topics: Animals; Antioxidants; beta Carotene; Carotenoids; Humans; Leukoplakia, Oral; Mouth Neoplasms; Vitamin E | 1995 |
Emerging role of beta-carotene and antioxidant nutrients in prevention of oral cancer.
beta-carotene and other antioxidant nutrients, such as vitamin E, are well suited for widespread preventive use because they are nontoxic and easily given in supplement form. Intervention trials designed to show a reduction of cancer incidence in the general population are logistically and practically impossible for most types of cancer, including cancer of the oral cavity. Thus evidence for chemoprevention must be indirect, using laboratory and animal models, epidemiologic surveys, and trials showing reversal of premalignant lesions or cancer prevention in high-risk groups. In several animal models, beta-carotene and other antioxidant nutrients inhibit oral carcinogenesis. Epidemiologic studies consistently relate low intake of these nutrients with high cancer risk. Smokers have lower beta-carotene levels in plasma and oral mucosal cells than nonsmokers. Eight clinical trials have now shown that beta-carotene and vitamin E produce regression of oral leukoplakia, but chemoprevention studies in oral leukoplakia have limitations, which we review. All available evidence supports a significant role for antioxidant nutrients in preventing oral cancer. Topics: Animals; Antioxidants; beta Carotene; Carotenoids; Clinical Trials as Topic; Humans; Leukoplakia, Oral; Mouth Neoplasms; Vitamin E | 1995 |
Chemoprevention of oral cancer: beta-carotene and vitamin E in leukoplakia.
The most definitive and direct way to show that a putative chemoprevention agent actually prevents cancer would be to demonstrate a reduction in cancer incidence in a clinical trial. From a practical standpoint this approach is not feasible for most cancers. Therefore, it becomes necessary to draw conclusions on chemopreventive activity through consideration of indirect lines of evidence, one of which is activity in premalignant lesions such as leukoplakia. As a corollary, it must be emphasized that the goal of undertaking chemoprevention trials in oral leukoplakia is to develop approaches for the prevention of oral cancer. Because the risk of cancer in the usual leukoplakia lesion is low, only non-toxic agents should be tested in this setting and they should be suited for eventual use in a prevention setting. Beta-carotene and vitamin E, unlike the retinoids, fulfill the criteria for a suitable chemopreventive agent and several lines of evidence point to a preventive role for them against oral cancer. These include laboratory in vitro and animal model findings, but the strongest evidence comes from epidemiologic studies which uniformly suggest protection by beta-carotene against head and neck cancer. Much like the retinoids, but without toxicity, beta-carotene and vitamin E can produce regression of oral leukoplakia, a premalignant lesion for oral cancer, as has now been shown in eight clinical trials, five with beta-carotene alone, one with vitamin E alone and two that used these agents as part of combinations.(ABSTRACT TRUNCATED AT 250 WORDS) Topics: Animals; beta Carotene; Carotenoids; Clinical Trials as Topic; Drug Combinations; Humans; Leukoplakia, Oral; Mouth Neoplasms; Vitamin E | 1994 |
Chemoprevention strategies in lung carcinogenesis.
Chemoprevention entails using specific agents to suppress carcinogenesis and thereby prevent the development of primary or second primary cancers. Because the concept of chemoprevention in patients with or at risk of lung cancer is new, ongoing clinical trials are based on data from epidemiologic and preclinical research, as well as on results of chemoprevention studies in head and neck cancer. The latter studies have provided a model for such studies in lung cancer, considering the two diseases have a similar etiology and biology of field carcinogenesis. Beta-carotene, natural vitamin A, and the retinoids may be effective chemopreventive agents. However, chronic administration of such agents may be required to prevent the development of cancer. Results of chemoprevention trials in head and neck cancer have demonstrated effective inhibition of the development of second primary tumors with the synthetic retinoid 13-cis-retinoic acid; investigators are hopeful this will be repeated in patients with lung cancer. Results of ongoing phase III trials and continued advances in the epidemiologic and biologic study of lung carcinogenesis should contribute to future research in this area. Topics: beta Carotene; Carotenoids; Head and Neck Neoplasms; Humans; Isotretinoin; Leukoplakia, Oral; Lung Neoplasms; Neoplasms, Second Primary; Risk Factors; Vitamin A | 1993 |
Chemoprevention of aerodigestive epithelial cancers.
Topics: Alcohol Drinking; Animals; Anticarcinogenic Agents; beta Carotene; Carcinoma, Squamous Cell; Carotenoids; Cell Differentiation; Clinical Trials as Topic; Cricetinae; Diet; Drug Screening Assays, Antitumor; Head and Neck Neoplasms; Humans; Leukoplakia, Oral; Mesocricetus; Respiratory Tract Neoplasms; Smoking; United States; Vitamin A | 1992 |
Precancerous lesions of the mouth.
Leukoplakia is the only important precancerous lesion of the mouth. The epidemiology of oral leukoplakia has been well established in white adults in the United States. There is a hole in the epidemiologic literature, however, on leukoplakia in American minority populations. Recent literature has begun to address the issue of the pathophysiology of leukoplakia, its causes and treatment, and predicting its malignant transformation. Computerized image analysis, retinoid compounds, beta-carotene, and laser surgery are contributing to advances in these lines of research. Though leukoplakia is often seen in patients who use smokeless tobacco products, it is usually benign and reversible if use of the tobacco product is discontinued. The direction of current research in leukoplakia studies eventually should lead to an understanding of the nature and cure of this ubiquitous lesion. Topics: beta Carotene; Carotenoids; Humans; Laser Therapy; Leukoplakia, Oral; Plants, Toxic; Tobacco, Smokeless | 1991 |
Potential role of beta-carotene in prevention of oral cancer.
Recent data suggests that retinoids and carotenoids may be effective in reversing a putative "field cancerization" defect in the epithelium at risk for oral cancer. Animal experiments have shown that these compounds can inhibit cancer formation. Several clinical trials have demonstrated the ability of retinoids to reverse oral leukoplakia. However, toxicities associated with retinoids at the doses used in these studies limits their potential for chemoprevention. Because of its lack of toxicity, beta-carotene is a very attractive agent for chemoprevention. It suppresses micronuclei in exfoliated oral mucosal cells from subjects at risk for oral cancer and recently has been shown to be active in reversing leukoplakia. Another area under investigation is the possibility of preventing second primary tumors in patients cured of their initial cancer who have an increased risk of developing new cancers of the upper acrodigestive tract. Topics: Animals; beta Carotene; Carotenoids; Humans; Leukoplakia, Oral; Mouth Neoplasms; Retinoids | 1991 |
Remission of precancerous lesions in the oral cavity of tobacco chewers and maintenance of the protective effect of beta-carotene or vitamin A.
Participants in the intervention trials were fishermen (Kerala, India), who chewed tobacco-containing betel quids daily before and throughout the study period. Frequency of oral leukoplakia, micronuclei in oral mucosal cells, and alterations in nuclear textures were used as endpoints. Administration of vitamin A (60 mg/wk) for 6-mo resulted in complete remission of leukoplakias in 57% and a reduction of micronucleated cells in 96% of tobacco-chewers. beta-carotene (2.2 mmol/wk) induced remission of leukoplakia in 14.8% and reduction of micronucleated cells in 98%. Vitamin A completely suppressed and beta-carotene suppressed by 50% formation of new leukoplakia within the 6-mo trial period. After withdrawal of vitamin A or beta-carotene treatment, oral leukoplakias reappeared, frequency of micronuclei in oral mucosa increased, and nuclear textures reverted to those present before the administration of chemo-preventive agents. The protective effect of the original treatment could be maintained for at least 8 additional months by administration of lower doses of vitamin A or beta-carotene. Topics: Areca; beta Carotene; Carotenoids; Humans; Leukoplakia, Oral; Mouth Neoplasms; Plants, Medicinal; Plants, Toxic; Precancerous Conditions; Tobacco, Smokeless; Vitamin A | 1991 |
16 trial(s) available for beta-carotene and Leukoplakia--Oral
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p53 and ki67 as biomarkers in determining response to chemoprevention for oral leukoplakia.
We performed a randomized controlled chemoprevention trial of oral leukoplakia by administrating a low dose of beta-carotene and vitamin C supplements. 17% of subjects in the experimental arm (4/23) demonstrated clinical remission (complete or partial response) at completion of the trial. The objective of this study was to determine whether baseline expression of p53 and ki67 demonstrated any differences between those responding or not responding to our intervention. A secondary objective was to elucidate any relationship between dietary factors and clinical responses.. For this biomarker study, we included all subjects in the experimental group (n = 23) who were non-smokers. Among 16 who completed the trial for 1 year of supplementation, there were four responders and 12 non-responders at 1-year follow-up. Following immuno-staining for p53 and ki67, the percentage of positive cell nuclei were analyzed as labeling index (LI).. Expression of p53 was greater in basal layers than in para-basal layers. Mean para-basal LI of p53 was higher in non-responding (26.0) than in responding subjects (11.2) (P = 0.028). ki67 LIs were not significantly different in the two groups.. Expression of p53 was inversely related to clinical response to the supplements. Other biomarkers that may recognize subject's responsiveness to chemoprevention require further study. Topics: Aged; Ascorbic Acid; beta Carotene; Biomarkers; Dietary Supplements; Female; Humans; Ki-67 Antigen; Leukoplakia, Oral; Male; Treatment Outcome; Tumor Suppressor Protein p53 | 2017 |
Treatment of oral leukoplakia with a low-dose of beta-carotene and vitamin C supplements: a randomized controlled trial.
Management of oral leukoplakia-a potentially malignant disorder-is currently not evidence-based. Of the few randomized trials that have been reported, most have negative data. Therefore, a multi-centre, randomized, double-blind controlled trial (RCT) was undertaken to evaluate the use of low-dose beta-carotene combined with vitamin C supplements for the treatment and to prevent malignant transformation of oral leukoplakia. 46 Japanese participants with oral leukoplakia were allocated randomly either to an experimental arm (10 mg day(-1) of beta-carotene and 500 mg day(-1) of vitamin C) or placebo arm (50 mg day(-1) of vitamin C). Current or ex-smokers within 3 months of cessation were excluded. The supplements were continued over a period of 1 year. The primary endpoint was clinical remission at 1-year and the likelihood of malignant transformation during a 5-year follow-up period as a secondary endpoint. The overall clinical response rate in the experimental arm was 17.4% (4/23) and 4.3% (1/23) in the placebo arm (p = 0.346). During the median 60-month follow-up period, two subjects in the experimental arm and three in the control arm developed oral cancer. Under the intention-to-treat principle, relative risk by supplementing with beta-carotene and vitamin C was 0.77 (95%CI: 0.28-1.89) (p = 0.580) by the Cox proportional hazards model. No unfavorable side-effects were noted. Beta-carotene (10 mg day(-1) ) and vitamin C were neither effective for clinical remission, nor for protection against the development of cancer. Data from this RCT does not support the hypothesis that chemoprevention with this treatment is effective for oral leukoplakia. Topics: Adult; Aged; Ascorbic Acid; beta Carotene; Cell Transformation, Neoplastic; Dietary Supplements; Disease Progression; Female; Follow-Up Studies; Humans; Leukoplakia, Oral; Male; Middle Aged; Risk Factors; Treatment Outcome | 2015 |
DeltaNp63 overexpression, alone and in combination with other biomarkers, predicts the development of oral cancer in patients with leukoplakia.
The risk of malignant transformation of oral preneoplastic lesion (OPL) is difficult to assess. DeltaNp63 is an early oncoprotein associated with mucosal tumorigenesis. The purpose of this study was to assess DeltaNp63 expression in OPL and its role as a marker of oral cancer risk.. DeltaNp63 expression was determined using immunohistochemistry in 152 OPL patients included in a clinical trial comparing retinyl palmitate alone or plus beta-carotene with low-dose 13-cis-retinoic acid. The associations between DeltaNp63 expression as well as DeltaNp63 expression with other potential risk factors for oral cancer development were analyzed.. DeltaNp63 expression was positive in 41 (27%) patients, clusters of intraepithelial inflammatory cells (EIC) were noted in 37 (26%) patients, and podoplanin (previously reported) was positive in 56 (37%) patients. Significantly more patients whose lesions were DeltaNp63 positive or exhibited EIC developed oral cancers. In the multicovariate analysis including age, treatment, and histologic status as cofactors, positive DeltaNp63 expression was associated with an increased hazard ratio of 3.308 (95% confidence interval, 1.663-6.580; P = 0.0007). Patients whose lesions showed positive DeltaNp63, podoplanin, and EIC had the highest oral cancer risk with a hazard ratio of 4.372 (95% confidence interval, 1.912-9.992; P = 0.0005) and 61% oral cancer development rate at 5 years compared with 15% of other OPL patients (P < 0.0001).. DeltaNp63 overepression in OPL is associated with increased oral cancer risk. Together, DeltaNp63, podoplanin, and EIC may be used as biomarkers to identify OPL patients with substantially high oral cancer risk. Topics: Antineoplastic Combined Chemotherapy Protocols; beta Carotene; Biomarkers, Tumor; Carcinoma, Squamous Cell; Diterpenes; Female; Follow-Up Studies; Gene Expression Regulation, Neoplastic; Genetic Predisposition to Disease; Humans; Inflammation; Isotretinoin; Leukoplakia, Oral; Male; Membrane Glycoproteins; Middle Aged; Mouth Neoplasms; Prognosis; Retinyl Esters; Trans-Activators; Transcription Factors; Tumor Suppressor Proteins; Up-Regulation; Vitamin A | 2009 |
Beta-carotene produces sustained remissions in patients with oral leukoplakia: results of a multicenter prospective trial.
Beta-Carotene has been reported to produce regressions in patients with oral leukoplakia, a premalignant lesion. However, previous studies have all been of short duration, with clinical response as the end point.. To evaluate the duration of response and the need for maintenance therapy in subjects who respond to beta-carotene.. In this multicenter, double-blind, placebo-controlled trial, subjects were given beta-carotene, 60 mg/d, for 6 months. At 6 months, responders were randomized to continue beta-carotene or placebo therapy for 12 additional months.. Fifty-four subjects were enrolled in the trial, with 50 being evaluable. At 6 months, 26 subjects (52%) had a clinical response. Twenty-three of the 26 responders completed the second, randomized phase. Only 2 (18%) of 11 in the beta-carotene arm and 2 (17%) of 12 in the placebo arm relapsed. Baseline biopsies were performed in all patients, with dysplasia being present in 19 (38%) of the 50 evaluable patients. A second biopsy was obtained at 6 months in 23 subjects who consented to this procedure. There was improvement of at least 1 grade of dysplasia in 9 (39%), with no change in 14 (61%). Nutritional intake was assessed using food frequency questionnaires. There was no change in carotenoid intake during the trial. Responders had a lower intake of dietary fiber, fruits, folate, and vitamin E supplements than did nonresponders. Beta-carotene levels were measured in plasma and oral cavity cells. Marked increases occurred during the 6-month induction. However, baseline levels were not restored in subjects taking placebo for 6 to 9 months after discontinuation of beta-carotene therapy.. The activity of beta-carotene in patients with oral leukoplakia was confirmed. The responses produced were durable for 1 year. Topics: Aged; Alcohol Drinking; Antioxidants; beta Carotene; Diet; Double-Blind Method; Female; Humans; Leukoplakia, Oral; Male; Middle Aged; Remission Induction; Smoking; Treatment Outcome | 1999 |
Long-term supplementation with alpha-tocopherol and beta-carotene and prevalence of oral mucosal lesions in smokers.
To assess the effect of alpha-tocopherol and beta-carotene supplementation on the prevalence of oral mucosal lesions in smokers.. An end-point examination of a random sample of participants in a controlled trial for 5-7 years (Alpha-Tocopherol Beta-Carotene Cancer Prevention Study) in Helsinki, Finland.. A total of 409 white male cigarette smokers, aged 55-74 years who received either alpha-tocopherol (50 mg per day) or beta-carotene (20 mg per day) supplementation, both of these or placebo capsules.. Clinical examination of oral mucosae, histological examination of lesions showing leukoplakia and cytological examination of buccal epithelium. Statistical analysis using Fisher's exact test.. No statistically significant differences were found between the study groups either in the prevalence of oral mucosal lesions or in the cells of unkeratinized epithelium. Leukoplakia was present in 24 (5.9%) of the subjects. Seven lesions showed dysplasia.. The present study on oral health does not support the hypothesis that alpha-tocopherol or beta-carotene supplementation plays an essential role in preventing oral mucosal changes in smokers. Topics: Aged; beta Carotene; Dietary Supplements; Humans; Leukoplakia, Oral; Male; Middle Aged; Mouth Diseases; Mouth Mucosa; Smoking; Vitamin E | 1998 |
Beta-carotene concentration in buccal mucosal cells with and without dysplastic oral leukoplakia after long-term beta-carotene supplementation in male smokers.
To measure the beta-carotene concentration in buccal mucosal cells in smoking men who had received long-term beta-carotene (BC) supplementation in a controlled trial. To assess the association of cellular BC on the prevalence of dysplasia in oral leukoplakia.. An end-of-trial examination of a part of subjects in the Alpha-Tocopherol, Beta Carotene Cancer Prevention Study.. 343 men who for 5-7 years had received BC (20 mg/d) or alpha-tocopherol (AT) (50 mg/d), or both of these or placebo. BC concentration of buccal mucosal cells was compared in the subjects with BC supplementation (n = 173) to that of those without it (n = 170). Oral mucosae were examined clinically and lesions showing leukoplakia histopathologically.. Mean (s.d.) BC concentration in buccal mucosal cells was 7.7 (10.3)mg/kg protein in the subjects who received BC compared to 1.1 (1.7) mg/kg protein in those who did not. The BC concentration in the cells of supplemented subjects correlated with their serum BC levels (P < 0.001). AT supplementation had no effect on BC concentration nor was daily amount of smoking statistically significantly associated with the BC concentration in buccal cells. Altogether 17 subjects showed oral leukoplakia, 7 had dysplasia. In these 7 subjects, the BC concentration in buccal mucosal cells did not differ statistically significantly compared to subjects with only hyperkeratosis (n = 10) (F-test, P = 0.74).. After long-term BC supplementation, BC concentration in oral mucosal cells was 7-fold greater than without supplementation. There was no evidence to support an association between cellular BC concentration and precancerous lesions among the few subjects having them in their oral mucosae. Topics: Aged; beta Carotene; Humans; Leukoplakia, Oral; Male; Middle Aged; Mouth Mucosa; Mouth Neoplasms; Smoking | 1998 |
Chemoprevention of oral leukoplakia with vitamin A and beta carotene: an assessment.
We conducted a double-blind placebo-controlled trial to evaluate the chemopreventive potential of either vitamin A alone or beta carotene alone in subjects with oral leukoplakia in Kerala, India. We randomised 160 fishermen and women with oral precancerous lesions to receive oral vitamin A (retinyl acetate 300,000 IU/week x 12 months, n = 50), or beta carotene (360 mg/week x 12 months, n = 55), or placebo (n = 55). Blood, saliva and urine samples were collected at baseline and at exit to study serum micronutrients and mutagenicity assays. Biopsies of the mucosal lesions at entry were performed for histopathological exclusion of malignancy. The subjects were examined once every 2 months to establish clinical response of lesions and toxicity, if any. The results are based on 43 complaint subjects on placebo, 42 on vitamin A and 46 on beta carotene. The complete regression rates were: 10% in the placebo arm, 52% with vitamin A and 33% with beta carotene (P < 0.0001). Homogeneous leukoplakias and smaller lesions responded better than non-homogeneous and larger lesions. No major toxicities were observed. Half of the responders with beta carotene and two thirds with vitamin A relapsed after stopping supplementation. Serum beta carotene concentration increased substantially with beta carotene administration while with vitamin A supplementation there was no change in serum retinol levels. In the vitamin A treated group there was a significant decrease in serum alpha tocopherol. Vitamin A administration resulted in a significant remission of oral leukoplakia without any side effects of prolonged vitamin A supplementation. The results of this study, as well as those from previous studies, appear to provide strong supporting evidence to justify long term trials with vitamin A in subjects with high-risk leukoplakias with oral cancer as an endpoint. Topics: Adult; Anticarcinogenic Agents; beta Carotene; Diterpenes; Double-Blind Method; Female; Humans; Leukoplakia, Oral; Male; Micronutrients; Middle Aged; Mouth Neoplasms; Mutagenicity Tests; Retinyl Esters; Treatment Outcome; Vitamin A | 1997 |
Evaluation of chemoprevention of oral cancer with Spirulina fusiformis.
The blue-green microalgae Spirulina, used in daily diets of natives in Africa and America, have been found to be a rich natural source of proteins, carotenoids, and other micronutrients. Experimental studies in animal models have demonstrated an inhibitory effect of Spirulina algae on oral carcinogenesis. Studies among preschool children in India have demonstrated Spirulina fusiformis (SF) to be an effective source of dietary vitamin A. We evaluated the chemopreventive activity of SF (1 g/day for 12 mos) in reversing oral leukoplakia in pan tobacco chewers in Kerala, India. Complete regression of lesions was observed in 20 of 44 (45%) evaluable subjects supplemented with SF, as opposed to 3 of 43 (7%) in the placebo arm (p < 0.0001). When stratified by type of leukoplakia, the response was more pronounced in homogeneous lesions: complete regression was seen in 16 of 28 (57%) subjects with homogeneous leukoplakia, 2 of 8 with erythroplakia, 2 of 4 with verrucous leukoplakia, and 0 of 4 with ulcerated and nodular lesions. Within one year of discontinuing supplements, 9 of 20 (45%) complete responders with SF developed recurrent lesions. Supplementation with SF did not result in increased serum concentration of retinol or beta-carotene, nor was it associated with toxicity. This is the first human study evaluating the chemopreventive potential of SF. More studies in different settings and different populations are needed for further evaluation. Topics: Adult; beta Carotene; Carotenoids; Cyanobacteria; Female; Food, Fortified; Humans; India; Leukoplakia, Oral; Male; Middle Aged; Mouth Neoplasms; Remission Induction; Vitamin A | 1995 |
A clinical trial of antioxidant supplements in the treatment of oral leukoplakia.
Seventy-nine patients with oral leukoplakia that was histologically verified as either hyperkeratosis or epithelial dysplasia with hyperkeratosis were enrolled in an antioxidant supplementation program for the treatment of the oral lesions. The patients received 30 mg of beta-carotene, 1000 mg of ascorbic acid, and 800 IU of alpha-tocopherol per day for 9 months. Clinical improvement of the oral lesion was noted in 55.7% of the patients and was more likely to occur in patients who reduced their use of alcohol or tobacco (p = 0.0056). Although risk-factor reduction was important, approximately half of the patients who did not alter their exposure to either alcohol or tobacco showed clinical improvement. The antioxidant supplementation significantly increased serum and tissue levels of beta-carotene, ascorbic acid, and alpha-tocopherol, but these changes did not correlate strongly with clinical improvement. Topics: Adult; Aged; Aged, 80 and over; Alcohol Drinking; Antioxidants; Ascorbic Acid; beta Carotene; Carotenoids; Female; Humans; Leukoplakia, Oral; Male; Middle Aged; Risk Factors; Smoking; Treatment Outcome; Vitamin E | 1994 |
Micronuclei, a biomarker for chemoprevention trials: results of a randomized study in oral pre-malignancy.
Biomarkers are being sought that could serve as surrogate end points for chemoprevention trials. Micronuclei, cytoplasmic fragments of DNA, have been proposed as a biomarker and studied in oral pre-malignancy. This study evaluated micronuclei frequency in a randomized chemoprevention trial of oral pre-malignancy. A recent clinical trial evaluated the responses of pre-malignant oral lesions to 3 months of therapy with isotretinoin followed by 9 months of either low-dose isotretinoin or beta-carotene. For 57 study participants, micronuclei were counted in mucosal scrapings of the lesion and in normal-appearing mucosa at baseline and following 3 months and 12 months of therapy. Micronuclei counts were higher in scrapings from the lesion than in the normal-appearing mucosa. Following 3 months of isotretinoin, the micronuclei counts in scrapings of the lesion were significantly reduced. With treatment, the mean micronuclei count declined at 3 months. In a randomized comparison, both isotretinoin and beta-carotene maintained the suppression of micronuclei. The change in micronuclei count was not associated with the clinical or histological response to treatment. Chemoprevention treatment with isotretinoin led to a reduction in frequency of micronuclei, a marker of recent DNA injury, which was then maintained by both isotretinoin and beta-carotene. Topics: beta Carotene; Biomarkers, Tumor; Carotenoids; Cell Transformation, Neoplastic; Female; Humans; Isotretinoin; Leukoplakia, Oral; Male; Micronuclei, Chromosome-Defective; Middle Aged; Mouth Mucosa; Mouth Neoplasms; Precancerous Conditions; Remission Induction; Statistics, Nonparametric | 1994 |
Chemoprevention of oral leukoplakia and chronic esophagitis in an area of high incidence of oral and esophageal cancer.
This intervention trial carried out in Uzbekistan (former USSR) in an area with a high incidence of oral and esophageal cancer involved random allocation of 532 men, 50 to 69 years old, with oral leukoplakia and/or chronic esophagitis to one of four arms in a double-blind, two-by-two factorial design, with active arms defined by the administration of (a) riboflavin; (b) a combination of retinol, beta-carotene, and vitamin E; or (c) both. Weekly doses were 100,000 IU of retinol, 80 mg of vitamin E, and 80 mg of riboflavin. The dose of beta-carotene was 40 mg/d. Men in the trial were followed for 20 months after randomization. The aim of the trial was to determine whether treatment with these vitamins or their combination could affect the prevalence of oral leukoplakia and/or protect against progression of oral leukoplakia and esophagitis, conditions considered to be precursors of cancer of the mouth and esophagus. A significant decrease in the prevalence odds ratio (OR) of oral leukoplakia was observed after 6 months of treatment in men receiving retinol, beta-carotene, and vitamin E (OR = 0.62; 95% confidence interval (CI): 0.39 to 0.98). After 20 months of treatment, no effect of vitamin supplementation was seen when the changes in chronic esophagitis were compared in the four different treatment groups, although the risk of progression of chronic esophagitis was lower in the subjects allocated to receive retinol, beta-carotene and vitamin E (OR = 0.65; 95% CI: 0.29 to 1.48) A secondary analysis not based on the randomized design revealed a decrease in the prevalence of oral leukoplakia in men with medium (OR = 0.45; 95% CI: 0.21 to 0.96) and high (OR = 0.59; 95% CI: 0.29 to 1.20) blood concentrations of beta-carotene after 20 months of treatment. Risk of progression of chronic esophagitis was also lower in men with a high blood concentration of beta-carotene, odds ratios being 0.30 (95% CI: 0.10 to 0.89) and 0.49 (95% CI: 0.15 to 1.58) for medium and high levels, respectively. A decrease in risk, also statistically not significant, was observed for high vitamin E levels (OR = 0.39; 95% CI: 0.14 to 1.10). These results were based on levels of vitamins in blood drawn after 20 months of treatment. Topics: Aged; beta Carotene; Carotenoids; Chronic Disease; Double-Blind Method; Esophageal Neoplasms; Esophagitis; Humans; Incidence; Leukoplakia, Oral; Male; Middle Aged; Mouth Neoplasms; Odds Ratio; Precancerous Conditions; Prevalence; Riboflavin; Risk Factors; Uzbekistan; Vitamin A; Vitamin E; Vitamins | 1993 |
Comparison of low-dose isotretinoin with beta carotene to prevent oral carcinogenesis.
High-dose isotretinoin therapy has been determined to be an effective treatment for leukoplakia. However, a high rate of relapses and toxic reactions led us to conduct a trial of a much lower dose of isotretinoin in the hope of maintaining a response and limiting toxicity.. In the first phase of the study, 70 patients with leukoplakia underwent induction therapy with a high dose of isotretinoin (1.5 mg per kilogram of body weight per day) for three months; in the second phase, patients with responses or stable lesions were randomly assigned to maintenance therapy with either beta carotene (30 mg per day) or a low dose of isotretinoin (0.5 mg per kilogram per day) for nine months.. In the first phase, the rate of response to high-dose induction therapy in the 66 patients who could be evaluated was 55 percent (36 patients). The lesions of seven patients progressed, and therefore they did not participate in the second phase of the trial. Of the 59 patients included in the second phase, 33 were assigned to beta carotene therapy and 26 to low-dose isotretinoin therapy; these two groups did not differ significantly in prognostic factors. Of the 53 patients who could be evaluated, 22 in the low-dose isotretinoin group and 13 in the beta carotene group responded to maintenance therapy or continued to have stable lesions (92 percent vs. 45 percent, P < 0.001). In situ carcinoma developed in one patient in each group, and invasive squamous-cell carcinoma in five patients in the beta carotene group. Toxicity was generally mild, though greater in the group given low-dose isotretinoin therapy.. When preceded by high-dose induction therapy, low-dose isotretinoin therapy was significantly more active against leukoplakia than beta carotene and was easily tolerated. Topics: Adult; Aged; Aged, 80 and over; beta Carotene; Carcinoma, Squamous Cell; Carotenoids; Female; Head and Neck Neoplasms; Humans; Immunologic Factors; Isotretinoin; Leukoplakia, Oral; Male; Middle Aged; Mouth Neoplasms; Remission Induction | 1993 |
Treatment of oral leukoplakia with beta-carotene.
Over the past few years, beta-carotene has progressively gained ground as a drug chosen in the treatment of oral leukoplakias, thus making it possible to reduce the use of 13-cis-retinoic acid, which was shown by many studies to be highly toxic while beta-carotene has proved to have no significant side effects and hence to be much more suitable in oral premalignancy. In 1989, a phase II study of patients showing oral leukoplakias and treated with beta-carotene (90 mg/day) was begun. A total of 23 patients (aged between 17 and 85) were included in the study and 18 (8 male and 10 female) were evaluated. Eight patients (44.4%) had objective responses (6 complete, 2 partial). Four CR and a PR appeared unexpectedly within 2-7 months after the end of the therapy. The lesions were macroscopically and histologically examined at entry; in the evaluated patients, two types of alterations were found: atypical hyperplasia (16 patients) and dysplasia (2 patients). No signs of significant toxicity were detected; only in 1 patient treatment had to be interrupted for 1 week. The results of this study show the fair efficacy of beta-carotene against oral leukoplakias, but further confirmations through controlled clinical studies are needed. Topics: Adult; Aged; beta Carotene; Carotenoids; Drug Evaluation; Female; Humans; Leukoplakia, Oral; Male; Middle Aged; Risk Factors; Smoking | 1992 |
Beta-carotene didn't prevent cancer: what's up doc?
Topics: beta Carotene; Carotenoids; Dose-Response Relationship, Drug; Humans; Leukoplakia, Oral; Neoplasms; Tretinoin | 1991 |
Management of oral mucosal dysplasia with beta-carotene retinoic acid: a pilot cross-over study.
Mucosal dysplasia in the head and neck region is recognized to be a precancerous lesion. Between January 1983 and December 1987, a pilot study was conducted at the Manitoba Cancer Treatment and Research Foundation to determine the effects of beta-carotene and cis-retinoic acid on mucosal dysplasias. Eighteen patients were treated with a "cross-over" regimen. The overall response to treatment was 61%, with 33.3% complete responses. Patients who smoked had a significantly better response than nonsmokers. The response rate for 9 of 11 smokers was 81.2%, and 2 of 7 nonsmokers or 28.6% responded to this protocol. The beneficial effect of these drugs should be established by prospective, randomized trial in high risk populations. Topics: Adult; Aged; Aged, 80 and over; beta Carotene; Carotenoids; Drug Evaluation; Erythroplasia; Female; Humans; Leukoplakia, Oral; Lichen Planus; Male; Middle Aged; Mouth Diseases; Mouth Mucosa; Pilot Projects; Precancerous Conditions; Prospective Studies; Smoking; Tretinoin; Vitamin A | 1991 |
Remission of oral leukoplakias and micronuclei in tobacco/betel quid chewers treated with beta-carotene and with beta-carotene plus vitamin A.
Fishermen from Kerala (India) who chewed tobacco-containing betel quids daily (17.2 +/- 9.6 quids per day) and had well-developed oral leukoplakias with elevated frequencies of micronucleated cells participated in a short-term intervention trial. Beta-carotene (180 mg/week) (Group I), beta-carotene (180 mg/week) plus vitamin A (100,000 IU/week) (Group II), and placebo (Group III) capsules were given twice weekly for 6 months under strict supervision. The remission of oral leukoplakias, the inhibition of new leukoplakias, and the reduction of micronucleated oral mucosal cells were recorded at the 3rd and 6th months of the trial period. After 3 months, the frequency of micronucleated cells was significantly reduced in Group I (from 4.09% to 1.1% in areas of leukoplakia, and from 4.1% to 1.0% in the normal mucosa). At this time, remission of oral leukoplakias did not differ significantly from that observed in the placebo group. After 6 months of treatment, remission of leukoplakias in Group I (14.8%) and Group II (27.5%) differed significantly from that seen in Group III (3.0%). The development of new leukoplakias during the 6-month period was strongly inhibited in Group II (7.8%), and to a lesser degree in Group I (14.8%), as compared to Group III (21.2%). During the trial period, all participants continued to chew tobacco-containing betel quids in their accustomed manner. Thus, remission and inhibition of new oral leukoplakias and reduction of micronucleated mucosal cells occurred in the groups receiving beta-carotene and beta-carotene plus vitamin A during the continuous presence of carcinogens derived from tobacco and areca nut. Topics: Areca; beta Carotene; Carotenoids; Female; Humans; Leukoplakia, Oral; Male; Nicotiana; Plants, Medicinal; Plants, Toxic; Time Factors; Tobacco, Smokeless; Vitamin A | 1988 |
13 other study(ies) available for beta-carotene and Leukoplakia--Oral
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Diet and risk of oral potentially malignant disorders in rural Sri Lanka.
While the protective role of antioxidant nutrients against cancer is well established, data on Asian diets in patients with oral cancer are meagre.. A total of 1029 subjects over 30 years of age were investigated on their dietary practices in the Sabaragamuwa province (Sri Lanka) in 2006-07. Data collection tools were an interviewer-administered questionnaire, a three-day food diary and an examination of the oral cavity. Subjects identified with Oral Potentially Malignant Disorders (OPMD) and disease-free controls were analysed in a case-control fashion. Among the OPMDs, those with leukoplakia were separately considered. A further subgroup analysis was undertaken for β-carotene-rich foods. The analysis was stratified by portions of fruit/vegetables consumed as five or more portions and two or more portions daily.. A low BMI (<18.5) was a significant independent risk factor for the development of OPMD. More than half of both cases and controls consumed less than two portions of fruit/vegetables per day and only 20 subjects consumed more than five portions per day. Intake of more than two portions per day of β-carotene-containing fruits/vegetables significantly reduced the risk of having an OPMD and leukoplakia (OR = 0.5; 95% CI, 0.3-0.9). The significant differences observed with BMI and fruits/vegetables were attenuated when adjusted for betel quid chewing, smoking and alcohol use.. This study discloses prevailing under-nutrition in this rural population with very low daily consumption of fruit/vegetables. Cancer preventive properties in their diets are limited and are swamped by the known carcinogenic agents associated with use of betel quid, tobacco and alcohol. Topics: Adult; Alcohol Drinking; Areca; beta Carotene; Body Mass Index; Capsicum; Case-Control Studies; Cross-Sectional Studies; Diet; Diet Records; Female; Fruit; Humans; Leukoplakia, Oral; Male; Mouth Neoplasms; Precancerous Conditions; Recommended Dietary Allowances; Risk Factors; Rural Health; Smoking; Sri Lanka; Surveys and Questionnaires; Tea; Thinness; Vegetables; Vitamins | 2013 |
Serum antioxidant micronutrients and the risk of oral leukoplakia among Japanese.
A population-based case-control study was designed for the investigation of any association between serum micronutrient levels and oral leukoplakia. Out of a total of 9536 subjects over the age of 40 years who participated in the oral mucosal screening programme in Tokoname city, 48 cases detected with oral leukoplakia (38 male:10 female) were recruited. For each case, four controls matched by age and sex were selected from the same cohort. We examined the fasting serum levels of retinol, alpha-tocopherol, zeaxanthin and lutein, cryptoxanthin, lycopene and carotenoids (alpha-carotene and beta-carotene) by high-performance liquid chromatography. Among males with leukoplakia mean serum lycopene and beta-carotene levels (0.175+/-0.202, 0.357+/-0.295 micromol/l) were significantly lower than those of controls (0.257+/-0.252, 0.555+/-0.408 micromol/l) (P<0.05, P<0.005). Logistic regression analysis with leukoplakia as the dependent variable showed that high serum levels of beta-carotene were related to low risk of oral leukoplakia (odds ratio 0.160, 95% C.I.: 0.029-0.866, P<0.05). There were no significant differences in any of the serum nutrients estimated in female subjects. Our results suggest for the first time that high serum levels of beta-carotene may provide protection against oral precancer for the Japanese male. Topics: Adult; Analysis of Variance; Antioxidants; beta Carotene; Case-Control Studies; Female; Humans; Japan; Leukoplakia, Oral; Logistic Models; Male; Mouth Neoplasms; Smoking; Vitamin A; Vitamin E | 2000 |
Retinol dietary intake and oral leukoplakia development.
To investigate the clinical outcome of unbalanced diet in patients with oral precancerosis and to assess a possible relationship between dietary factors and the development of oral leukoplakia, a case-control study was carried out within a cohort of 53 subjects treated at our Centre in October-November 1997. Enrolled subjects and suitable controls underwent a careful interview on their own alimentary habits with a particular interest in retinol and carotenoids major sources. An individual qualitative and quantitative assessment of retinol-equivalents dietary intake, yielding average values for each group, allowed to compare the cohorts and to relate data also to tobacco use and to the severity of histopathological findings. Case levels were always significantly lower than controls (P<0.001), disregarding smoking, whilst no difference resulted between smokers and non smokers within the same groups. No statistical influence seemed to link alimentary vitamin A to the development of oral dysplasia but this work strengthen the epidemiological opinion that specific dietary factors are of great importance in oral oncology. Topics: Adult; Aged; Aged, 80 and over; beta Carotene; Carotenoids; Case-Control Studies; Cohort Studies; Dairy Products; Diet; Eggs; Feeding Behavior; Female; Fruit; Humans; Leukoplakia, Oral; Male; Middle Aged; Reference Values; Smoking; Vegetables; Vitamin A | 1998 |
Serum vitamins' status in oral leucoplakias--a preliminary study.
Vitamins, such as A, beta carotene, C, E, B12 and folate, are the micronutrients with the strongest evidence of having a link to cancer prevention and control. Deficiency of these vitamins at the dietary, systemic or mucosal level will interact with tobacco use and increase the risk of oral precancerous lesions. The objective of this study was to (1) establish the baseline circulating levels of these vitamins in our normal population with and without tobacco use and (2) compare these levels with the values obtained in cases of oral leucoplakias. 50 normal controls with 25 each in chewers and non-chewers, matched for age and sex, were selected. 50 cases of oral leucoplakias (clinically detectable white patches) from the field constituted the study group. Simultaneous measurement of serum vitamin B12 and folate were carried out by radioassay. The other serum vitamins were estimated spectrophotometrically. Except for serum vitamin E, all the other serum vitamin levels were significantly decreased in oral leucoplakias compared to the controls. Cancer chemopreventive agents acting as inhibitors of both initiation and promotion, as analysed in our population, is promising for further intervention trials. Topics: Ascorbic Acid; beta Carotene; Carotenoids; Case-Control Studies; Folic Acid; Humans; Leukoplakia, Oral; Plants, Toxic; Tobacco, Smokeless; Vitamin A; Vitamin B 12; Vitamin E; Vitamins | 1996 |
Beta-carotene and lung cancer?
Topics: Adult; Aged; Aged, 80 and over; Antioxidants; beta Carotene; Cardiovascular Diseases; Contraindications; Humans; Leukoplakia, Oral; Lung Neoplasms; Male; Middle Aged; Randomized Controlled Trials as Topic; Vitamin A; Vitamin E | 1996 |
[A clinical and microscopic evaluation of the leukoplakia of oral mucosa].
The authors present methods of treatment of 90 patients with leukoplakia of oral mucosa. In 60 cases tissue material taken from focus of leukoplakia, has been tested in microscope. In 8 cases the cancer has been identified. Using method of Carr-Price, the level of vit. A and beta-karoten has been appointed. Topics: beta Carotene; Humans; Leukoplakia, Oral; Mouth Mucosa; Vitamin A | 1996 |
Screening at a health fair to identify subjects for an oral leukoplakia chemoprevention trial.
Screening examinations were conducted at a Chinese community health fair in Houston, Texas, to identify individuals with oral leukoplakia for a chemoprevention trial of oral-cavity squamous cell carcinoma. All 161 volunteer participants were interviewed regarding age, smoking habits, and betel-nut and alcohol use. The screening included an examination of the oral cavity, oropharynx, and neck. One participant had a 1-mm area of oral leukoplakia on the right lateral surface of the oral tongue. Eighteen participants had other head and neck abnormalities. Only 12 participants (7.5%) were active smokers, and eight (5%) reported a prior history of smoking. One participant reported prior betel-nut use. The mean age was 55 years. The authors conclude that a venue such as this has a low yield for screening and recruitment of high-risk individuals for chemoprevention of oral-cavity squamous cell carcinoma, that generally health-conscious individuals attend health fairs, and that only a small percentage volunteer for oral screening. Topics: Adult; Aged; beta Carotene; Carcinoma, Squamous Cell; Carotenoids; China; Female; Health Fairs; Humans; Leukoplakia, Oral; Male; Middle Aged; Mouth Neoplasms; Smoking; Texas; Vitamin A | 1995 |
Biologic modifiers and chemoprevention of cancer of the oral cavity.
Topics: beta Carotene; Carcinoma, Squamous Cell; Carotenoids; Cell Transformation, Neoplastic; Head and Neck Neoplasms; Humans; Immunologic Factors; Isotretinoin; Leukoplakia, Oral; Mouth Neoplasms | 1993 |
The effects of 13-cis-retinoic acid and beta-carotene on cellular immunity in humans.
Deficiency of vitamin A and/or its precursors has been associated with increased cancer risk in animals and humans. Therapeutic trials of vitamin A and related compounds have demonstrated activity in several cancerous and precancerous conditions. The authors measured the effects of a retinoid, 13-cis-retinoic acid, and a carotenoid, beta-carotene, on the human immune system in vivo in conjunction with their use in ongoing clinical trials. Immune cell subpopulations were analyzed by quantifying the expression of markers using flow cytometric study. Both compounds produced significant effects on immune cell populations. 13-cis-Retinoic acid resulted in an increase in the percentage of peripheral blood lymphoid cells expressing surface markers for T-helper cells with only minimal effect on natural killer cell marker expression. In contrast, beta-carotene produced an increase in the percentage of cells expressing natural killer cell markers with smaller effect on T-helper markers. Modest increases in the percentage of cells expressing Ia antigen, transferrin, and interleukin-2 receptors were produced by both drugs. These results suggest that retinoids and carotenoids can produce major changes in immune cellular marker expression in vivo in humans at doses relevant to their potential clinical use. Topics: Adult; Aged; Barrett Esophagus; beta Carotene; Carotenoids; Humans; Immunity, Cellular; Killer Cells, Natural; Leukoplakia, Oral; Male; Middle Aged; T-Lymphocyte Subsets; T-Lymphocytes; T-Lymphocytes, Helper-Inducer; Tretinoin | 1991 |
Evaluation of risk factors in smokeless tobacco-associated oral lesions.
Smokeless tobacco (ST) users and nonusers were recruited to evaluate the contribution of various risk factors (ST use, cigarettes, alcohol, and diet) in the development of oral mucosal lesions. Ninety-eight ST users with no lesion, 29 ST users with an oral lesion, and 33 nonusers were enrolled in the study. ST users with lesions, when compared with users with no lesion, were more likely to have used snuff than chewing tobacco (p = 0.01) and to have used more ST (p less than 0.01). Alcohol consumption, dietary intake of beta-carotene, and serum levels of beta-carotene were not related to an increased risk of lesion development. Our findings showed that the only significant risk factor for ST-associated oral lesions was the extent of ST exposure. Of 127 ST users, 29 (22.8%) had an oral lesion at the time of examination. Of these lesions, 23 (79.3%) were hyperkeratotic and 6 (20.7%) were epithelial dysplasia. Topics: Adolescent; Adult; Aged; Alcohol Drinking; beta Carotene; Carotenoids; Chromatography, High Pressure Liquid; Epithelium; Humans; Leukoplakia, Oral; Lip Diseases; Middle Aged; Plants, Toxic; Risk Factors; Smoking; Socioeconomic Factors; Tobacco, Smokeless | 1991 |
Beta-carotene didn't prevent cancer: what's up doc?
Topics: beta Carotene; Carotenoids; Leukoplakia, Oral; Publishing | 1990 |
Beta-carotene didn't prevent cancer: What's up, doc.
Topics: beta Carotene; Carotenoids; Diet; Humans; Leukoplakia, Oral; Neoplasms; Tretinoin | 1990 |
Chemopreventive trials with vitamin A and beta-carotene: some unresolved issues.
The administration of beta-carotene (180 mg/week) plus vitamin A (100,000 IU/week) or vitamin A alone (200,000 IU/week) to chewers of betel quids in Kerala, India led to a reduction in the frequency of micronucleated buccal mucosal cells, a remission of oral leukoplakia, and an inhibition of the development of new leukoplakias. The advantages of this test system include a profound knowledge of exposure levels to tobacco-specific nitrosamines, areca nut-specific nitrosamines, and reactive oxygen species (ROS)-generating polyphenolics; the ease of quantitating micronuclei in exfoliated buccal mucosal cells and oral leukoplakia by noninvasive procedures; and solid information on the incidence of preneoplastic lesions and carcinomas. Some practical issues such as the level of nontoxic beta-carotene which could maintain the reduced frequency of micronucleated cells and the remission of oral leukoplakias for prolonged periods of time, the logistics of distributing beta-carotene to the many millions of smokeless tobacco users who are at elevated risk for oral cancer, and the possibility of using beta-carotene in the form of sweet potatoes or red palm oil, which could contain an economical source of beta-carotene for developing countries in which most of the tobacco chewers live, still remain unresolved. Topics: Antineoplastic Combined Chemotherapy Protocols; Areca; beta Carotene; Carotenoids; Humans; India; Leukoplakia, Oral; Micronuclei, Chromosome-Defective; Plants, Medicinal; Vitamin A | 1989 |