Showing papers in "Nutrition and Cancer in 1992"
TL;DR: It would appear that major public health benefits could be achieved by substantially increasing consumption of fruit and vegetable consumption, and in particular in cancers of the esophagus, oral cavity, and larynx, for which 28 of 29 studies were significant.
Abstract: Approximately 200 studies that examined the relationship between fruit and vegetable intake and cancers of the lung, colon, breast, cervix, esophagus, oral cavity, stomach, bladder, pancreas, and ovary are reviewed. A statistically significant protective effect of fruit and vegetable consumption was found in 128 of 156 dietary studies in which results were expressed in terms of relative risk. For most cancer sites, persons with low fruit and vegetable intake (at least the lower one-fourth of the population) experience about twice the risk of cancer compared with those with high intake, even after control for potentially confounding factors. For lung cancer, significant protection was found in 24 of 25 studies after control for smoking in most instances. Fruits, in particular, were significantly protective in cancers of the esophagus, oral cavity, and larynx, for which 28 of 29 studies were significant. Strong evidence of a protective effect of fruit and vegetable consumption was seen in cancers of the pancreas and stomach (26 of 30 studies), as well as in colorectal and bladder cancers (23 of 38 studies). For cancers of the cervix, ovary, and endometrium, a significant protective effect was shown in 11 of 13 studies, and for breast cancer a protective effect was found to be strong and consistent in a meta analysis. It would appear that major public health benefits could be achieved by substantially increasing consumption of these foods.
3,250 citations
TL;DR: A protective effect of turmeric is document on BP-induced forestomach and DMBA-induced skin tumors in mice, which is dose and time dependent.
Abstract: The anticarcinogenic effect of dietary turmeric on benzo[a]pyrene-(BP) induced forestomach neoplasia and 7,12-dimethylbenz[a]anthracene (DMBA)-induced skin tumorigenesis in female Swiss mice was evaluated. To further elucidate the mechanism of antineoplastic action of turmeric, its effect on the hepatic cytochrome b5, cytochrome P-450, glutathione, and glutathione S-transferase activities was studied in female Swiss mice. Turmeric (2% or 5%) in the diet significantly inhibited the BP-induced forestomach tumors, and this response was dose and time dependent. The 2% turmeric diet significantly suppressed DMBA-induced skin tumors in mice. The 5% turmeric diet for seven consecutive days resulted in a 38% decrease in the hepatic cytochrome b5 and cytochrome P-450 levels. Glutathione content was increased by 12%, and the glutathione S-transferase activity was enhanced by 32% in the liver. Our results document a protective effect of turmeric on BP-induced forestomach and DMBA-induced skin tumors in mice.
300 citations
TL;DR: The study demonstrated the feasibility of achieving cancer prevention with the use of a selenium-rich food system and showed that diallyl disulfide was more active than dially l sulfide or allyl methyl sulfide.
Abstract: The anticarcinogenic activities of regular (soil‐grown) garlic and selenium‐enriched garlic (cultivated in the greenhouse) were evaluated using the 7,12‐dimethylbenz[&]anthracene‐(DMBA) induced mammary tumor model in rats. In Experiment 1, milled regular garlic powder was added to the basal AIN‐76A diet at 20 g/kg. The results from different schedules of supplementation suggested that a continuous treatment, which started before DMBA and persisted for the entire duration of the study, was most effective in tumor suppression. In Experiment 2, selected allyl group‐containing sulfides that are normal constituents of garlic extract were given by gavage in three single doses immediately before DMBA. Several structurally related compounds were found to be protective during the initiation phase in the mammary cancer model. Although the present study was not designed specifically to elucidate the structure‐activity relationship with respect to sulfur chain length or alkyl versus alkenyl substitution, our...
208 citations
TL;DR: The overall conclusion on present evidence is that alcohol, particularly beer consumption, is an etiologic factor for colon and rectal cancer for females and males.
Abstract: The relationship between alcohol consumption and colorectal cancer in humans has been examined in 52 major studies in the past 35 years. An association was found in five of the seven correlational studies. An elevated risk was found in about half of the 31 case‐control studies and, of these, in 9 of the 10 studies using community controls but in only 5 of the 17 studies using hospital controls (p = 0.008), suggesting that the absence of association when hospital controls are used is due to a high prevalence of alcohol consumption/alcohol‐related illness in the hospital controls. Of the 14 cohort studies, an association with alcohol was found in 10, while in 3 of the 4 cohort studies in which an association was not found the alcohol data obtained were somewhat restricted. A positive dose‐response effect was found in two of three cohort studies and in all four case‐control studies with community controls in which this effect was examined. In both case‐control and cohort studies, the association was...
191 citations
TL;DR: The present study confirms the presence of a moderate adverse effect of high intake of foods of animal origin, chiefly milk, while it suggests that a diet rich in fresh fruit and vegetables does not convey a protection.
Abstract: The relationship between intake of various indicator foods and beverages and risk of prostatic cancer was assessed in 271 cases of prostatic cancer and 685 hospital controls recruited in two areas of northern Italy, the province of Pordenone and the greater Milan area. Increased risks were found for more frequent intake of meat [odds ratio (OR) in the highest vs. lowest consumption fertile = 1.4, 95% confidence interval (CI) 1.0–2.0], milk (OR = 1.6, 95% CI 1.1–2.4), fresh fruit (OR = 1.4, 95% CI 1.0–2.1), and vegetables (OR = 1.4, 95% CI 0.9–2.2). After allowance for the reciprocal confounding effect of various dietary habits, only frequent intake of milk seemed to be a significant independent indicator of prostatic cancer risk. There was also a clue that the unfavorable influence of frequent intake of a few food items (i.e., meat, fish, liver, ham and salami, milk and butter, and retinol) may be greater or restricted to older individuals (i.e., ≥70 yrs of age). In conclusion, the present study ...
161 citations
TL;DR: This database will allow researchers to examine the relationship between dietary GSH and risk of cancers and other diseases, and show that dairy products, cereals, and breads are generally low in GSH; fruits and vegetables have moderate to high amounts of G SH; and freshly prepared meats are relatively high in G SH.
Abstract: Glutathione (GSH) is an antioxidant and anticarcinogen that is present in plant and animal tissues that form the bulk of the human diet. Recent studies show that GSH is absorbed intact in rat small intestine and that oral GSH increases plasma GSH concentration in humans. To provide a database for epidemiological studies of dietary intake of GSH and risk of diseases in humans, we have measured the content of GSH in the foods listed in the National Cancer Institute's Health Habits and History Questionnaire. Foods were purchased in the Atlanta area and prepared as most commonly consumed in the United States. GSH analyses were performed using a high‐performance liquid chromatography technique with a method of additions to correct for losses during sample preparation. A separate set of samples was run after treatment with dithiothreitol to measure the total of GSH and its disulfide forms (GSH,). The results show that dairy products, cereals, and breads are generally low in GSH; fruits and vegetables h...
155 citations
TL;DR: The cancer protective effects of flaxseed suggested by a previous short-term study were tested in a long-term tumorigenesis experiment and it was speculated that the effect may be related to the lignans enterolactone and enterodiol produced in such large quantities on the ingestion ofFlaxseed.
Abstract: The cancer protective effects of flaxseed suggested by our previous short‐term study were tested in a long‐term tumorigenesis experiment. Feeding rats 5% flaxseed flour supplemented in a high‐fat diet at the promotional stage of tumorigenesis, i.e., after 7,12‐dimethyl‐benz[a]anthracene administration, significantly reduced by 66.7% the size of the tumors that occurred. Although flaxseed feeding at the initiation stage also tended to reduce the number of tumors per tumor‐bearing animal, significant differences were seen only between the group fed flaxseed throughout the experiment and the promotional group. Therefore the effect of flaxseed on mammary tumorigenesis is not consistent. Although it was speculated that the effect may be related to the lignans enterolactone and enterodiol produced in such large quantities on the ingestion of flaxseed, further studies are required to clarify the role of lignans and other flaxseed constituents in mammary tumorigenesis.
149 citations
TL;DR: Although in northern Italy tea was consumed daily by only a limited proportion of the population, this integrated series of studies offers further reassuring evidence on the relationship between tea and cancer risk.
Abstract: The relationship between tea consumption and cancer risk has been analyzed using data from an integrated series of case-control studies conducted in northern Italy between 1983 and 1990. The dataset included 119 histologically confirmed cancers of the oral cavity and pharynx, 294 of the esophagus, 564 of the stomach, 673 of the colon, 406 of the rectum, 258 of the liver, 41 of the gallbladder, 303 of the pancreas, 149 of the larynx, 2,860 of the breast, 567 of the endometrium, 742 of the ovary, 107 of the prostate, 365 of the bladder, 147 of the kidney, 120 of the thyroid, and a total of 6,147 controls admitted to hospital for acute nonneoplastic conditions unrelated to long-term dietary modifications. Multivariate relative risks (RR) for tea consumption were derived after allowance for age, sex, area of residence, education, smoking, and coffee consumption. All the estimates for tea consumption were close to unity, the highest values being 1.4 for rectum, gallbladder, and endometrium. There was no association with cancers of the oral cavity (RR = 0.6), esophagus (RR = 1.0), stomach (RR = 1.0), bladder (RR = 0.8), kidney (RR = 1.1), prostate (RR = 0.9), or any other site considered. Although in northern Italy tea was consumed daily by only a limited proportion of the population, this integrated series of studies offers further reassuring evidence on the relationship between tea and cancer risk.
139 citations
TL;DR: A high intake of vegetables including cruciferous vegetables, beta-carotene- and vitamin C-containing foods, and fish appears to be protective for nonmelanocytic skin cancer, and this deserves further study, as does the possible etiologic relevance of the low serum levels of beta- carotene and vitamin A.
Abstract: A case-control study was conducted in Melbourne, Australia of 88 consecutive males admitted for the surgical removal of a nonmelanocytic skin cancer (histologically confirmed basal cell carcinoma and squamous cell carcinoma) and of 88 male control patients admitted for small elective surgical procedures. In both cases and controls, previous diet, alcohol consumption, and smoking habit were investigated and serum beta-carotene and vitamin A levels were measured. A statistically significant inverse relationship was found between the risk of skin cancer and a high intake of fish (p = 0.05); vegetables in general (p < 0.001); beans, lentils, or peas (p < 0.001), carrots, silverbeet (Swiss chard), or pumpkin (p < 0.001); cruciferous vegetables (cabbage, brussel sprouts, or broccoli) (p < 0.001); and beta-carotene- and vitamin C-containing foods (p = 0.004). Cases had a lower mean serum level of beta-carotene (p < 0.001) and vitamin A (p = 0.02) than controls. The incidence of skin cancer in the study was inversely related to the level of serum beta-carotene (p < 0.0001). The correlation coefficient between dietary beta-carotene/vitamin C and serum beta-carotene was 0.22 (p = 0.04). Smoking and alcohol consumption showed no statistically significant association with the risk of nonmelanocytic skin cancer. The results were similar for both cell types. A high intake of vegetables including cruciferous vegetables, beta-carotene- and vitamin C-containing foods, and fish appears to be protective for nonmelanocytic skin cancer, and this deserves further study, as does the possible etiologic relevance of the low serum levels of beta-carotene and vitamin A.
135 citations
TL;DR: Results provide quantitative documentation that alcohol drinking, tobacco smoking, and education, three of the major determinants of cancer risks, were also correlates of dietary patterns and, hence, may exert an important confounding or modifying effect on the diet and cancer relationship.
Abstract: Differences in the frequency of consumption of 30 selected foods and in the estimated intake of total calories and selected nutrients in relation to alcohol drinking, tobacco smoking, and education were described using information obtained from 1,774 controls of a case-control study of digestive tract cancers conducted in northern Italy. Heavy alcohol consumption, tobacco smoking, and lower level of education were associated with a diet poorer in several aspects, including lower consumption of fresh fruit and green vegetables and higher intake of specific indicator foods, such as sausages and canned meat. For instance, the mean number of portions of fresh fruit per week was 10.5 among male nondrinkers vs. 9.0 among heavy drinkers, 10.4 among male nonsmokers vs. 8.1 among heavy smokers, and 8.8 in less educated individuals vs. 10.7 among those more educated. Consequently, intake of beta-carotene, ascorbic acid, and calcium tended to be inversely related to alcohol and tobacco and directly related to education. Most associations were stronger in males, for whom alcohol consumption was also more common in less educated individuals. Calorie intake was directly related to alcohol consumption, largely reflecting calories provided by alcohol itself. However, alcohol drinking was also directly related to fat consumption. In both sexes, there was a strong positive correlation between cigarette smoking and coffee drinking. These results provide quantitative documentation that alcohol drinking, tobacco smoking, and education, three of the major determinants of cancer risks, were also correlates of dietary patterns and, hence, may exert an important confounding or modifying effect on the diet and cancer relationship.
111 citations
TL;DR: The results of the present study suggest that the green tea preparation from Sikkim may be a good source for the isolation of EGCG and that this compound may have significant potential as a cancer chemopreventive agent.
Abstract: Recently, we and others showed that the components of green tea may be useful cancer chemopreventive agents. It has been suggested that (‐)‐epigallocatechin‐3‐gallate (EGCG), the major constituent in green tea, may possess antitumor‐promoting and/or anticarcinogenic effects in rodent tumor bioassay systems. During the chemical analysis of various green tea products, we found a traditionally preserved preparation of green tea used by tribes in the Himalayan region of Sikkim, India that was rich in EGCG. EGCG was isolated from this tea product, and its inhibitory effects were evaluated against the binding of topically applied 3H‐labeled polycyclic aromatic hydrocarbons (PAHs) to epidermal DNA and 12‐O‐tetra‐decanoylphorbol‐13‐acetate (TPA) caused induction of epidermal ornithine decarboxylase (ODC) activity in Sencar mice, the short‐term markers of tumor initiation and tumor promotion, respectively. Preapplication of EGCG resulted in significant inhibition (p < 0.05) in the binding of [3H] PAH to e...
TL;DR: The objective of this paper is to discuss the effect of dietary phytosterols on cholesterol and bile acid metabolism and how these effects may lead to a decreased risk for colon cancer development.
Abstract: Epidemiological and experimental studies have shown that increased intake of plant foods and decreased meat consumption are correlated with a decreased risk for colon cancer. Many components of plant foods are suggested to mitigate colon carcinogenesis, including vitamins, minerals, and dietary fiber. Phytosterols are a common component of plant foods consumed in relatively large quantities by vegetarians, who are at lower risk for colon cancer development than individuals on a Western diet low in phytosterols. In addition, phytosterols have been shown experimentally to inhibit colon cancer development. Dietary cholesterol, although structurally similar to the phytosterols, is correlated etiologically to the incidence of colon cancer, with changes in serum cholesterol levels and fecal bile acid profiles suggested to increase susceptibility to colon tumorigenesis. The objective of this paper is to discuss the effect of dietary phytosterols on cholesterol and bile acid metabolism and how these effects may lead to a decreased risk for colon cancer development.
TL;DR: Seven dietary patterns were identified among control subjects in the Western New York Diet Study by application of principal components analysis to data from a 95-item food frequency interview and three were associated positively with fat and energy consumption; they elevated risk for colon cancer and accounted for more risk than did the specific nutrients.
Abstract: Seven dietary patterns were identified among control subjects in the Western New York Diet Study (1975-1986) by application of principal components analysis to data from a 95-item food frequency interview. The results of case-control analyses of colon cancer risk for these patterns are presented. Cases were matched with neighborhood controls on the bases of age and sex; 205 colon case-control male and 223 female pairs were obtained. The dietary patterns and intakes of energy, total fat, and dietary fiber were examined with logistic regression for their individual contributions to risk. In males, three of these dietary patterns were associated positively with fat and energy consumption; they elevated risk for colon cancer and accounted for more risk than did the specific nutrients. Control for energy and fat intakes allowed the protective influences of additional dietary patterns to be expressed. No patterns elevated risk in women; two patterns were protective for colon cancer. Controlling for energy and fat intake enhanced the protection afforded by one of these patterns but had no influence on that of the other. Measures of foods rather than single nutrients may be more inclusive of dietary exposures to risk as well as being related more directly to underlying health behaviors. Therefore they may be better able to account for risk in diseases with multiple causation.
TL;DR: Mice treated with Se showed no signs of toxicity and had significantly less skin damage by UV irradiation, as indicated by reduced inflammation and pigmentation and by later onset and lesser incidence of skin cancer.
Abstract: This study was conducted to determine whether oral and/or topical selenium (Se) supplementation can reduce the incidence of acute and/or chronic damage to the skin (i.e., sunburn and pigmentation and/or skin cancer, respectively) induced by ultraviolet (UV) irradiation in mice. Groups of 38 BALB:c female mice or 16 Skh:2 hairless pigmented mice were treated with 1) lotion vehicle, 2) 0.02% L-selenomethionine (SeMet) lotion, or 3) vehicle and 1.5 ppm SeMet in the drinking water. Within each group, 30 BALB:c mice or 12 Skh:2 mice were given UV irradiation (Westinghouse FS 40 bulbs) three times per week in doses of 0.575 and 0.24 J/cm2, respectively. The animals' weights and food intakes and the Se concentrations of skin and liver were measured. Skin biopsies were taken from the backs and abdomens of all animals to evaluate the relative amounts of Se and the damage by UV irradiation. Skin pigmentation was scored, and the total number of clinically detectable skin tumors per animal was counted weekly. Results showed that the skin Se concentrations in areas of application of the lotion containing SeMet were greater than those of animals given comparable oral doses, while the Se concentrations of untreated skin and liver were similar to those of animals receiving oral Se. Mice treated with Se showed no signs of toxicity and had significantly less skin damage by UV irradiation, as indicated by reduced inflammation and pigmentation and by later onset and lesser incidence of skin cancer.
TL;DR: Comparisons between Groups I and II showed that this reduction in tumor burden was mainly due to a decrease in tumor mass; however, the animals treated with limonin 17-beta-D-glucopyranoside exhibited a 55% decrease in average tumor burden.
Abstract: Limonin 17-beta-D-glucopyranoside, nomilin 17-beta-D-glucopyranoside, and nomilinic acid 17-beta-D-glucopyranoside, three limonoid glucosides isolated from oranges, were tested for cancer chemopreventive activity. Eighty female Syrian hamsters were divided into four equal groups. The left buccal pouches of the animals in each group were pretreated topically with two applications of water (Group I) or a 3.5% solution of limonin 17-beta-D-glucopyranoside (Group II), nomilin 17-beta-D-glucopyranoside (Group III), or nomilinic acid 17-beta-D-glucopyranoside (Group IV). After this initial treatment, the left buccal pouches of 16 hamsters from each group were painted five times per week. Two or three times per week the pouches were treated with a 0.5% solution of the carcinogen 7,12-di-methylbenz[a]anthracene (DMBA) dissolved in mineral oil. On alternate days, the pouches were treated with water (Group I) or a 3.5% solution of limonin 17-beta-D-glucopyranoside (Group II), nomilin 17-beta-D-glucopyranoside, or nomilinic acid 17-beta-D-glucopyranoside. The 16 remaining animals were used as controls. These hamsters were treated five times per week, one day with mineral oil and the next with either water (Group I) or one of the 3.5% solutions of the limonoid glucosides (Groups II-IV). After 15 weeks (71 applications), the hamsters were killed. Multiple tumors were common in the animals treated with DMBA; however, the animals treated with limonin 17-beta-D-glucopyranoside exhibited a 55% decrease in average tumor burden. Further comparisons between Groups I and II showed that this reduction in tumor burden was mainly due to a decrease in tumor mass.(ABSTRACT TRUNCATED AT 250 WORDS)
TL;DR: A case-control study to examine the influence of dietary factors on the risk of developing lung cancer among women who have never smoked cigarettes indicated a strong protective effect associated with total vegetable consumption and intake of carotene.
Abstract: A case-control study was conducted to examine the influence of dietary factors on the risk of developing lung cancer among women who have never smoked cigarettes. This study included 124 cases of histologically confirmed carcinoma of the lung and 263 community-based controls. Dietary data were collected utilizing the reduced version of the National Cancer Institute (Block) food frequency questionnaire. The results of this analysis, adjusted for age, education, and total calories, indicated a strong protective effect associated with total vegetable consumption and intake of carotene. Individuals in the highest quartile of vegetable consumption experienced the greatest decreased risk with an odds ratio (OR) of 0.2, [confidence interval (CI) 0.1-0.5]. The effect of all vegetables combined was greater than that of green and yellow vegetables alone (highest quartile OR 0.4, CI 0.2-0.7). Similarly, the protective effect of total carotene (highest quartile OR 0.3, CI 0.1-0.6) was somewhat greater than that of beta-carotene alone (highest quartile OR 0.4, CI 0.2-0.8). Retinol intake was not associated with a decreased risk of lung cancer in our population. There was an inverse association between lung cancer risk and vitamin C intake, which was not significant, although a statistically significant trend was noted.
TL;DR: Higher intake of dietary sodium was associated with increased risk among both age groups, and the trends were statistically significant, suggesting the importance of diet in the etiology of bladder cancer.
Abstract: We present the dietary epidemiology of bladder cancer while controlling for a number of lifestyle and environmental risk factors in a study of 351 white male cases with histologically confirmed transitional cell carcinoma of the bladder and 855 white male controls selected from Erie, Niagara, and Monroe counties of western New York from 1979 to 1985. Usual diet was estimated by comprehensive interviews with use of a detailed food frequency questionnaire. An increased risk of bladder cancer was associated with higher kilocalorie intake, but only among those under 65 years of age, with the strongest pattern associated with fat intake. Further analyses of fat, carbohydrates, and protein, with adjustment for total kilocalories, resulted in a positive association of risk with fat intake and a decreasing risk with higher protein intake. Of the vitamins, carotenoid consumption appeared to decrease risk with increased consumption for those under 65 years of age. No significant differences between cases and controls were seen for intake of calcium, retinol, thiamin, riboflavin, niacin, vitamin C, vitamin D, and vitamin E. After adjustment for kilocalories and other confounders, higher intake of dietary sodium was associated with increased risk among both age groups, and the trends were statistically significant. The importance of diet in the etiology of bladder cancer is suggested by our findings.
TL;DR: The data suggest that low serum alpha-tocopherol was associated with CIN I/III, although the adjusted OR was not statistically significant, and low serum ascorbic acid and red blood cell folate were not associated with cervical dysplasia.
Abstract: American Indian women in the Southwest have high rates of cervical cancer and cervical dysplasia in contrast to low rates of cancers for other sites. Despite their high rates of cervical disease, no published information has specifically examined risk factors for cervical cancer or cervical dysplasia among American Indian women. We carried out a pilot case‐control study of cervical dysplasia in southwestern American Indian women to examine the relationship of dietary intake of vitamin C, folacin, vitamin E, carotenoids, and retinol with cervical cytological abnormalities. Twenty‐four‐hour dietary recalls were collected from women with cervical dysplasia (n = 42) and women with normal cervical cytologies (n = 58). Macro‐ and micronutrient intake was estimated from these recalls utilizing food and nutrient data from the USDA Survey Nutrient Database. Although mean differences between cases and controls were not statistically significant for any of the micronutrients examined, women with low intake ...
TL;DR: In a hospital-based case-control study, 290 oral cancer cases and 133 esophageal cancer cases were queried as to smoking status, alcohol consumption, and dietary exposures, including vitamin supplement history, and vitamin E use appeared to exert a protective effect.
Abstract: In a hospital‐based case‐control study, 290 oral cancer cases and 133 esophageal cancer cases were queried as to smoking status, alcohol consumption, and dietary exposures, including vitamin supplement history. Among oral cancer cases, vitamin E use appeared to exert a protective effect. Vitamins C and E had protective effects among esophageal cancer cases. When stratified by smoking status, the protective effect of vitamin C use in esophageal cancer was significant only among current smokers, as was vitamin B use. A reduced risk of oral cancer was correlated with multivitamin use and increasing vegetable consumption, as was vegetable/fruit consumption and vitamin C supplementation. Among esophageal cancer cases, increasing meat consumption and vitamin C use were associated with a significantly reduced cancer risk.
TL;DR: It is suggested that diets low in carotenoids and high in fat may increase risk and the strong association between tobacco and alcohol and laryngeal cancer is demonstrated and the effect modification by smoking is demonstrated.
Abstract: A case-control study among white men in western New York was conducted from 1975 through 1985 to examine diet and other risk factors for laryngeal cancer. Incident pathologically confirmed cases (250) and age- and neighborhood-matched controls (250) were interviewed to determine usual diet and lifetime use of tobacco and alcohol. Cigarettes were strongly associated with risk; pipes and cigars were not. Beer and hard liquor but not wine were associated with increased risk. Dietary fat and carotenoids were related to risk in opposite ways. The upper quartile odds ratio for dietary fat was 2.40 [95% confidence interval 1.26, 4.55], and the upper quartile odds ratio for carotenoids was 0.51 (0.26, 1.01). There was effect modification by smoking. Carotenoids were most negatively associated with risk among the lightest smokers, whereas dietary fat was most positively associated with risk among the heaviest smokers. Total calories, protein, and retinol were associated with increased risk; there was no relationship between laryngeal cancer and vitamin C, vitamin E, carbohydrate, or dietary fiber. This study again demonstrates the strong association between tobacco and alcohol and laryngeal cancer and also suggests that diets low in carotenoids and high in fat may increase risk.
TL;DR: It is demonstrated that EA localizes preferentially in lung tissues and confirmed that EA administered orally can inhibit lung tumorigenesis and demonstrate that EA in cyclodextrin doubles the level of EA in lung tissue.
Abstract: Ellagic acid (EA), derived from fruit ellagitannins, is known to be antimutagenic and anticarcinogenic in various animal tumor models. In this study, EA at a dose of 4 g/kg diet inhibited multiplicity of tumors induced by 4‐(methylnitrosamino)‐I‐(3‐pyridyl)‐I‐butanone (NNK) in A/J mice by 54%. This inhibition was dose related between 0.06 and 4.0 g/kg diet. In contrast, two related compounds, esculin and esculetin, had no effect on lung tumorigenesis. The biodistribution of EA was studied as a function of dose and time after gavage of EA. The levels of EA in the lung were directly proportional to the dose of EA between 0.2 and 2.0 mmol. The maximum level of EA, corresponding to 21:3 nmol/g, was observed 30 minutes after gavage with 2.0 mmol of EA/kg body wt, which corresponds to only 70 ppm of the administered dose. The levels in liver tissues were 10‐fold lower and reached a maximum 30 minutes after gavage. At this interval, the blood level of EA was 1 nmol/ml. The inclusion of EA in cyclodextri...
TL;DR: It is shown that RRR‐α‐tocopheryl succinate (TS) inhibits HL‐60 cell proliferation and induces the HL‐ 60 cells to differentiate toward a functionally deficient macrophage‐like cell.
Abstract: HL‐60 human promyelocytic leukemia cells can be induced to differentiate to granulocytes by retinoic acid and dimethyl sulfoxide or monocyte‐macrophages by phorbol esters and 1,25‐dihydroxyvitamin D3. These studies show that RRR‐α‐tocopheryl succinate (TS) inhibits HL‐60 cell proliferation and induces the HL‐60 cells to differentiate toward a functionally deficient macrophage‐like cell. TS at (15 μg/ml) was found to suppress HL‐60 cell proliferation by 63% and 89% at 24 and 48 hours, respectively. This suppression of proliferation, however, is not permanent and requires the presence of TS. HL‐60 cells treated for 48 hours with TS (15 μg/ml) were found to be blocked in the G2/M phase of the cell cycle. HL‐60 cells blocked in the G2/M cell cycle phase by TS expressed normal levels of the transferrin receptor. TS‐treated HL‐60 cells exhibited binucleated morphological appearance; however, the cells did not exhibit chemo‐taxis, phagocytosis, or changes in the expression of the cell surf ace markers, ...
TL;DR: The results show that the intrinsic antimutagenic and anticarcinogenic properties of the carotenoids are not significantly influenced by their conversion to vitamin A.
Abstract: Four carotenoids, canthaxanthin, β ‐carotene, 8'‐apo‐ β ‐carotenal, and 8'‐apo‐ β ‐carotene methylester were tested for their ability to suppress the mutagenicity of 1‐methyl‐3‐nitro‐1‐nitrosoguanidine and benzo[a]pyrene (BP) in Salmonella typhimurium tester strain TA 100. The anticarcinogenic efficacy of the four carotenoids was further assessed in the BP‐induced forestomach tumor model in female Swiss mice. The effect of dietary palm oil was also examined in BP‐induced neoplasia in the female Haffkine Swiss mouse strain. Canthaxanthin, s‐carotene, 8'‐apo‐s‐carotenal, and 8'‐apo‐s‐carotene methylester showed a dose‐dependent decrease in the mutagenicity compared with 1‐methyl‐3‐nitro‐1‐nitrosoguanidine and BP in strain TA 100. In the BP‐induced forestomach tumor model, all four carotenoids showed a similar significant anticarcinogenic effect. Dietary administration of palm oil showed a dose‐dependent antitumor activity in the animals. Our results show that the intrinsic antimutagenic and anticar...
TL;DR: It is shown that colonic cancerous tissue contains high levels of ROM, which may play an important role in the pathogenesis of colon cancer.
Abstract: Reactive oxygen metabolites (ROM) have been postulated to contribute to the development of various carcinomas, including colon cancer. Indeed, the effects of ROM scavengers are being tested for chemoprevention of adenocarcinoma of the colon. However, there has been no evidence to indicate that high levels of ROM are indeed present in cancerous tissue. In this study, we used a chemiluminescence probe to estimate ROM levels in cancerous and neighboring noncancerous colonic tissues from seven patients with colon cancer. Cancerous tissues contained significantly (p < 0.05) more luminol‐enhanced chemiluminescence (4,808 ± 2,282 counts/min/mg protein) than neighboring noncancerous tissues (2,175 ± 1,111). The addition of an ROM scavenger, catalase (2, 4, and 8 μg/ml), to the tissue suspension inhibited chemiluminescence produced by both noncancerous (—74%, —85%, and —71%) and cancerous (—11%, —61%, and — 53 %) tissues. This study shows that colonic cancerous tissue contains high levels of ROM, which ma...
TL;DR: The present investigation did not provide any support for the hypothesis that a high-fat diet is a survival determinant for breast cancer patients.
Abstract: The relationship between the occurrence of breast cancer and dietary intake, in particular a high‐fat diet, has attracted much attention in recent years. In addition, the prognosis of breast cancer patients on the basis of dietary intake is also an interesting subject. The present study utilized breast cancer patients whose dietary intake was carefully assessed about one decade previously in a case‐control study to determine whether dietary intake was indeed related to the patients’ prognosis. The study included 212 patients who underwent a surgical operation between 1975 and 1978. They were followed‐up until 1987, and a total of 47 breast cancer deaths were certified. The 5‐ and 10‐year relative survival rates were 78.5% and 75.3%, respectively. The older patients tended to ingest smaller amounts of all nutrients, except animal fat from fish. Height was significantly correlated with total animal protein intake, whereas there was no significant correlation between body mass index and intake of an...
TL;DR: The ability of these three unlignified cell-wall preparations to adsorb the hydrophobic environmental mutagen 1,8-dinitropyrene was studied and these findings are consistent with the hypothesis that the composition of the dietary fiber determines its adsorptive properties and that there may be important differences between the major dietary fibers of South Pacific and European food plants.
Abstract: The incidence of colorectal cancer is lower in Polynesian populations of the South Pacific than in European populations. This difference in incidence of the disease may be, at least partly, related to diet. Dietary fiber is believed to protect against colorectal cancer, and one of the ways it may act is by adsorbing mutagens that are carcinogenic. Very little is known about the chemical composition or the ability to adsorb mutagens of these dietary fibers from South Pacific food plants. In contrast to European food plants, which are mostly dicotyledons, South Pacific food plants are mainly monocotyledons. We isolated cell walls (dietary fiber) from the three edible parts of taro (Colocasia esculenta), which is a monocotyledon and a major South Pacific food plant. The ability of these three unlignified cell-wall preparations to adsorb the hydrophobic environmental mutagen 1,8-dinitropyrene was studied. The greatest adsorption occurred with walls from leaf blade, followed by petiole and corm walls, although the differences were not major. The amount of adsorption was intermediate between the low adsorption previously found with unlignified dicotyledon walls (from the flesh of potato tubers and immature cabbage leaves) and the much higher adsorption found with unlignified walls from monocotyledons of the grass and cereal family (Poaceae) (from leaves of seedling Italian ryegrass). These data are consistent with the monosaccharide compositions of the taro wall preparations, which were more similar to those of unlignified walls of dicotyledons than to unlignified walls of the Poaceae. These findings are consistent with the hypothesis that the composition of the dietary fiber determines its adsorptive properties and that there may be important differences between the major dietary fibers of South Pacific and European food plants.
TL;DR: The results suggest that promotion of N-nitrosomethylbenzylamine-induced esophageal tumors by ethanol may in part result from increased lipid peroxidation and that vitamin E reduces carcinogenicity of NMBzA or ethanol promoter effects by inhibiting lipidperoxidation.
Abstract: Promotion of chemically induced esophageal cancer by ethanol may include the generation of highly reactive free radicals and thus may be preventable by the antioxidant vitamin E. In the present study, female C57BL/6 mice received N‐nitrosomethylbenzylamine (NMBzA, 0.2 mg/kg ig) three times a week for three weeks. After this esophageal carcinogenic treatment, mice were fed a nutritionally adequate liquid diet with 30% of the calories supplied by ethanol or an isocaloric carbohydrate with or without supplemental α‐tocopherol (142 mg/kg diet). As a marker of in vivo lipid peroxidation, exhaled ethane was collected and measured 24 hours “before”; the mice were killed after 20 weeks of dietary treatment. Hepatic malondial‐dehyde, lipid fluorescence, and conjugated dienes were determined as markers of products of lipid peroxidation and serum aminotransferases as indexes of liver toxicity. Hepatic liver concentrations of vitamins A and E and the size and frequency of esophageal tumors were also assessed...
TL;DR: These data are relevant in the consideration of primary prevention of colorectal cancer in Australia, but their general application needs to be approached with caution in view of major differences in the genetic background and the dietary practices in various regions of the world.
Abstract: From the data obtained in a large comprehensive population‐based case‐control study of colorectal cancer (The Melbourne Colorectal Cancer Study), attributable risk was calculated for a family history of colorectal cancer in near relatives for diet (when ≥5 of the 11 previously determined dietary risk factors were present) and for beer consumption (for rectal cancer only). The attributable risk was 11% in the presence of a family history of colorectal cancer and 46% in the presence of five or more dietary risk factors. The attributable risk for rectal cancer in the presence of beer consumption was 31% in males and 11% in females. These data are relevant in the consideration of primary prevention of colorectal cancer in Australia, but their general application needs to be approached with caution in view of major differences in the genetic background and the dietary practices in various regions of the world and in view of the uncertainty of what is achievable change, especially for dietary practices.
TL;DR: The results indicate that the sustained development of AFB1-induced preneoplastic foci depends on a high protein intake and suggest that low protein intake inhibits lesion development.
Abstract: The effects of sequential alterations in the feeding of two levels of dietary protein (5% and 20% casein) on the postinitiation development of aflatoxin B1- (AFB1) induced gamma-glutamyl transpeptidase-positive (GGT+) preneoplastic foci were examined. Weanling male Fischer 344 rats fed AIN-76A diet (20% protein) were administered 10 intragastric doses of AFB1 (1 dose/day during the 14-day dosing period excluding weekends) at 250 micrograms/kg body wt (initiation). After AFB1 tissue clearance, rats were randomly assigned to dietary treatment groups. During the next 12 weeks (promotion), they developed AFB1-induced GGT+ preneoplastic lesions. The 12-week promotion period was subdivided into four three-week periods, during which rats were fed isocaloric diets containing 20% casein during all four periods (20:20:20:20), 5% casein during all four periods (5:5:5:5), or sequentially altered casein levels (20:5:20:5 and 5:20:5:20). Rats were killed at 3,6,9, and 12 weeks to examine the dependence of GGT+ foci development on protein intake. Animals fed 5% casein diets developed significantly fewer (p < 0.01) GGT+ foci than animals fed 20% casein diets despite greater total caloric intake. Similarly, in the intervention groups, preneoplastic development was enhanced when the 20% casein diet was fed and inhibited when the 5% casein diet was fed. These results indicate that the sustained development of AFB1-induced preneoplastic foci depends on a high protein intake. Alternatively, these results suggest that low protein intake inhibits lesion development.
TL;DR: It was concluded that the inhibitory effect of vitamin E in combination with selenium on tumorigenesis might be causally related to reduction of carcinogen treatment associated with lipid peroxidation, the latter presumably playing an important role in DMBA-induced mammary carcinogenesis.
Abstract: The effects of combined dietary vitamin E supplementation and a relatively low increase in selenium levels on 7,12-dimethylbenz[a]anthracene (DMBA) induction of lipid peroxidation in the short term and development of mammary tumors in the long term were investigated in female Sprague-Dawley rats. Control animals were fed the basal diet (20 mg/kg vitamin E and 0.6 mg/kg selenium) throughout the experiment. Three other groups received a high vitamin E diet (235 mg/kg vitamin E and 0.6 mg/kg selenium) at different times, the first two from three weeks after DMBA treatment and the other throughout the experiment. When the vitamin E diet with selenium supplementation was applied until three weeks after DMBA or until the termination of the experiment, tumor yields (tumors per rat) were significantly inhibited compared with the control group. On the other hand, delaying the supplementation of vitamin E until three weeks postcarcinogen produced no prophylactic effect. The elevation of lipid peroxidation levels observed immediately after DMBA administration was also significantly inhibited in both mammary fat pads and livers of animals in the high vitamin E group. It was therefore concluded that the inhibitory effect of vitamin E in combination with selenium on tumorigenesis might be causally related to reduction of carcinogen treatment associated with lipid peroxidation, the latter presumably playing an important role in DMBA-induced mammary carcinogenesis.