摘要:

AbstractIt is generally believed that breast cancer is a multistage process and that multiple and varying genetic events occur on the pathway to disease. We hypothesize that disease heterogeneity has an impact on our ability to identify risk factors. If a genetic alteration occurred in 50% of cases and a risk factor was associated only with that specific alteration, a risk estimate of 1.6 would be detected rather than the true risk estimate of 2.5 if analyses had been limited to those cases with the genetic alteration. Based on the literature we know that many genetic alterations occur in less than 50% of breast tumors. Thus, if environmental factors are related to some, but not all genetic alterations, we are decreasing our ability to identify potentially important risk factors. We therefore hypothesize that identification of dietary factors associated with breast cancer has been hampered by our inability to identify and capture the unique disease pathways which exist and contribute to the heterogeneity of common cancers such as breast cancer.

ISSN:0163-5581    

DOI:10.1080/01635589509514410

出版商:Taylor&Francis Group    

年代:1995

数据来源: Taylor

摘要:

AbstractThere has been little research concerning the health effects of whole grain intake in humans. We have synthesized 15 American and European case‐control and prospective studies of whole grain intake. Most subjects were middle aged or older. The studies employed disparate dietary methods, and the foods referred to and quantities eaten are ill defined. Nevertheless there is a striking consistency in reduced risk for colorectal and gastric cancers associated with intake of whole grain, also found in isolated studies of endometrial cancer and coronary heart disease. Because reduced risk was not associated with refined grain intake, these findings do not appear to be confounded by participant confusion concerning refined vs. whole grains. The independence of these findings from reduced risk associated with fruit and vegetable intake is not established. There should be further research to establish whether whole grain intake is protective against chronic disease.

ISSN:0163-5581    

DOI:10.1080/01635589509514411

出版商:Taylor&Francis Group    

年代:1995

数据来源: Taylor

摘要:

AbstractA scoring system was developed to help judge the scientific quality of observational epidemiologic studies linking diet with risk of cancer. The scoring system was developed from key headings used in developing research protocols and included questions under headings: three for case‐control studies (dietary assessment, recruitment of subjects, and analysis) and four for cohort studies (dietary assessment, definition of cohort, ascertainment, and analysis). Points were awarded for questions in each section, and a total score was derived.Interobserver variation was assessed for five case‐control and five cohort studies for 13 observers; 1 observer repeated the assessment of each paper. Absolute scores and ranking within observer were assessed. There was good agreement between observers in the ranking of studies. Papers that scored higher presented sufficient detail to enable the questions in the scoring system to be answered more easily. For some studies, the information required was either not collected or, if it was collected, not presented. In either case, the frequent lack of information available to judge papers raises questions about the editorial policy and review process of journals publishing dietary studies as much as it does about the scoring system.Applying the scoring system to a review of meat and cancer risk suggested that, taking the score into account, from what seemed like a large literature, there were relatively few studies that scored well (defined as a score>65%), but these studies tended to provide more consistent information.

ISSN:0163-5581    

DOI:10.1080/01635589509514412

出版商:Taylor&Francis Group    

年代:1995

数据来源: Taylor

摘要:

AbstractConjugated linoleic acid (CLA) is a minor fatty acid found predominantly in the form of triglycerides in beef and dairy products. Previous work by Ip and co‐workers showed that free fatty acid‐CLA at≤1% in the diet is protective against mammary carcinogenesis in rats. The present study verified that the anticancer activities of free fatty acid‐CLA and triglyceride‐CLA are essentially identical. This is an important finding, because it rules out a nonspecific free fatty acid effect. In terms of practical implication, we can continue the in vivo research with the less‐expensive free fatty acid‐CLA without compromising the physiological relevance of the data. A primary objective of this report was to investigate how the timing and duration of CLA feeding might affect the development of mammary carcinogenesis in the methylnitrosourea (MNU) model. We found that exposure to 1% CLA during the early postweaning and pubertal period only (from 21 to 42 days of age) was sufficient to reduce subsequent tumorigenesis induced by a single dose of MNU given at 56 days of age. This period incidentally corresponds to a time of active morphological development of the mammary gland to the mature state. In contrast to the above observation, a continuous intake of CLA was required for maximal inhibition of tumorigenesis when CLA feeding was started after MNU administration, suggesting that some active metabolite(s) of CLA might be involved in suppressing the process of neoplastic promotion/progression.

ISSN:0163-5581    

DOI:10.1080/01635589509514413

出版商:Taylor&Francis Group    

年代:1995

数据来源: Taylor

摘要:

AbstractDietary casein cooked at 180°C promotes the growth of aberrant crypt foci and colon cancer in rats initiated with azoxymethane. We speculated that promotion was due to a product that could be extracted by a solvent, such as 5‐hydroxymethyl‐2‐furaldehyde (HMF), with tumor‐promoting activity or the carcinogenic heterocyclic aromatic amines (HAA). This hypothesis was tested by extracting cooked casein with solvents and water. The extracts were then 1) assayed by high‐performance liquid chromatography for HMF and HAA, 2) measured for mutagenicity on a frame‐shift‐sensitive strain of Salmonella typhimurium, and 3) fed for 100 days to azoxymethane‐initiated rats to test the promoting effect on aberrant crypt foci. Data show that 1) no HMF or HAA was detected in cooked casein, 2) no mutagenicity was detected on strain TA98, with or without metabolic activation, and 3) promotion was not associated with the extracts but with the cooked casein residue. Therefore the promotion by cooked casein would not appear to be associated with a product that can be extracted by solvents.

ISSN:0163-5581    

DOI:10.1080/01635589509514414

出版商:Taylor&Francis Group    

年代:1995

数据来源: Taylor

摘要:

AbstractThe antiproliferative properties of lycopene, the major tomato carotenoid, were compared with those ofα‐andβ‐carotene. Lycopene, delivered in cell culture medium from stock solutions in tetrahydrofuran, strongly inhibited proliferation of endometrial (Ishikawa), mammary (MCF‐7), and lung (NCI‐H226) human cancer cells with half‐maximal inhibitory concentration of 1–2μ?;α‐andβ‐carotene were far less effective inhibitors. For example, in Ishikawa cells, a 4‐fold higher concentration ofα‐carotene or a 10‐fold higher concentration ofβ‐carotene was needed for the same order of growth suppression. The inhibitory effect of lycopene was detected after 24 hours of incubation, and it was maintained for at least three days. In contrast to cancer cells, human fibroblasts were less sensitive to lycopene, and the cells gradually escaped growth inhibition over time. In addition to its inhibitory effect on basal endometrial cancer cell proliferation, lycopene also suppressed insulin‐like growth factor‐I‐stimulated growth. Insulin‐like growth factors are major autocrinelparacrine regulators of mammary and endometrial cancer cell growth. Therefore, lycopene interference in this major autocrinelparacrine system may open new avenues for research on the role of lycopene in the regulation of endometrial cancer and other tumors.

ISSN:0163-5581    

DOI:10.1080/01635589509514415

出版商:Taylor&Francis Group    

年代:1995

数据来源: Taylor

摘要:

AbstractThe antioxidant and anticarcinogenic activities of soybean isoflavone extracts were investigated in female F344/N rats. Diethylnitrosamine (DEN, 15 mg/kg body wt) as a cancer initiator was injected intraperitoneally into 120 female F344/N rats at 10 days of age, and at weaning, phenobarbital (PB, 500 mg/kg diet) was fed to one‐half of the rats. Soybean isoflavones were extracted in acetone‐0.1 N HCl and analyzed by high‐performance liquid chromatography, and two levels of soybean isoflavones (920 and 1,840μmol/kg diet) were fed during PB treatment for 3 and 11 months. Control rats were fed diets without PB and with or without isoflavones. The effect of soybean isoflavone extract on hepatic glutathione peroxidase was measured, and development ofγ‐glutamyltransferase (GGT)‐positive (GGT+) and placental glutathione trans/erase (PGST)‐positive (PGST+) altered hepatic foci (AHF) was analyzed by computerized stereology. Soybean isoflavone extract providing 920 or 1,840μmol/kg diet normalized total hepatic glutathione peroxidase activity, which was suppressed about 17% by PB (p<0.05), and both doses of isoflavone extract suppressed PB promotion of hepatocarcinogenesis, decreasing the volume occupied by GGT+and PGST+AHF (p<0.05) after three months. After 11 months of PB promotion, isoflavone extract at 920μmol/kg diet decreased PGST+AHF compared with the PB‐fed group, but neither dose of isoflavone extract suppressed development of GGT+AHF compared with the group fed PB alone. Furthermore the control group fed isoflavone extract at 1,840μmol/kg diet showed greater development of GGT+and PGST+AHF than the group fed the basal diet alone. Therefore soybean isoflavones may be anticarcinogenic, but their margin of safety is relatively narrow, with a cancer‐promoting dose of 1,840μmol/kg in female F344/N rats initiated with DEN.

ISSN:0163-5581    

DOI:10.1080/01635589509514416

出版商:Taylor&Francis Group    

年代:1995

数据来源: Taylor

摘要:

AbstractAn association between meat eating and large bowel cancer risk has been shown in a variety of epidemiologic studies. One reason could be that meat is less well digested than other protein foods and leads to greater amounts of protein entering the large bowel and being metabolized by colonic bacteria to potential carcinogens. To test this hypothesis, five subjects with ileostomies were fed, for five days, a basal diet to which were added test meals of cheese, a small or a large fried beef steak, and a large steak with resistant starch (RS). Heal true nitrogen digestibility was similar for all five diets: control, 86.3% cheese, 89.4% low beef, 88.6% high beef, 89.6% and high beef + RS, 88.7%. Beef, at both low and high intake levels, was as well digested as cheese, suggesting that poor digestibility of meat does not explain the association between meat intake and large bowel cancer risk. Heal starch output on the high beef + RS diet was 27% greater than expected on the basis of the measurement of dietary RS in vitro (p = 0.002). Heal nitrogen output was strongly related to the amount of dietary nitrogen (p = 0.005 for linear trend), and this was confirmed by a meta analysis with eight other published studies. The relation between meat and large bowel cancer may reflect higher protein intakes in meat eaters or may be explained by other mechanisms.

ISSN:0163-5581    

DOI:10.1080/01635589509514417

出版商:Taylor&Francis Group    

年代:1995

数据来源: Taylor

摘要:

AbstractIt has previously been observed that allyl isothiocyanate, a compound naturally present in the diet, is more cytotoxic toward the human colorectal adenocarcinoma cell line HT29 in its control transformed state than after exposure to sodium butyrate or to dimethylformamide, which slow growth and induce differentiation (detransformation). In the present study, a range of other dietary compounds were assayed for such selective toxicity. These compounds were chosen as constituents of foodstuffs that have been identified from epidemiologic studies as being potentially antitumorigenic and also as having anticarcinogenic activity in experimental models. Benzyl and phenethyl isothiocyanate, benzyl thiocyanate, and quercetin showed decreased toxicity towards HT29 after detransformation of the cells by one or both treatments, whereas no change was observed in the sensitivity to diallyl sulfide or diallyl disulfide. It is proposed that the presence of such selectively toxic compounds in the diet may inhibit the development of tumors by interfering with the growth of preneoplastic lesions while having little effect on normal cells. The cumulative effects of these inhibitions may contribute to the chemopreventive properties of the parent foodstuffs observed in epidemiologic studies.

ISSN:0163-5581    

DOI:10.1080/01635589509514418

出版商:Taylor&Francis Group    

年代:1995

数据来源: Taylor

摘要:

AbstractPrevious work in breast cancer patients has indicated an inverse relationship between the risk of relapse and theα‐linolenic acid (18:3n‐3) level in adipose breast tissue. To determine whether lowα‐linolenic levels in patients with aggressive breast cancer resulted from lower 18:3n‐3 dietary intake and/or increased metabolism of stored 18:3n‐3, we analyzed the fatty acid composition of mammary adipose tissue during tumor growth in a rat model of mammary carcinogenesis. Rats were fed a diet containing 10% fat as rapeseed oil (in which 9% of total fatty acids is 18:3n‐3). One‐half of the rats received an injection of nitrosomethylurea (NMU) to initiate mammary tumors. In control and NMU‐treated groups, three to five animals were sacrificed every three weeks during the five‐month experimental time. Tumor growth was followed by weekly palpation of the animals and by the measure of total tumor mass and number in sacrificed rats. Mammary tumor and adipose tissues were sampled in sacrificed rats.We found that although mammary adipose tissue fatty acid profile changed throughout the experiment, there was no difference in fatty acid profile between control and NMU‐treated rats of the same age. In the NMU‐treated group, 18:3n‐3 level remained identical throughout the experimental period, irrespective of tumor burden. These data show that, in this model, mammary tumor growth does not modify stored fatty acid levels, including 18:3n‐3. This suggests that decreased 18:3n‐3 level in patients with poor prognosis is not a consequence of tumor burden but more likely depends on decreased dietary intake.

ISSN:0163-5581    

DOI:10.1080/01635589509514419

出版商:Taylor&Francis Group    

年代:1995

数据来源: Taylor