Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0699790 (colon cancer)
 28,837 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We examined the association between occupational and leisure physical activity and colorectal cancer in a cohort of male smokers. Among the 29,133 men aged 50-69 years in the Alpha-Tocopherol, Beta-Carotene Cancer Prevention study,152 colon and 104 rectal cancers were documented during up to 12 years of follow-up. For colon cancer, compared with sedentary workers, men in light occupational activity had a relative risk (RR) of 0.60 [95% confidence interval (CI), 0.34-1.04], whereas those in moderate/heavy activity had an RR of 0.45 (CI, 0.26-0.78; P for trend, 0.003). Subsite analysis revealed a significant association for moderate/heavy occupational activity in the distal colon (RR, 0.21; CI, 0.09-0.51) but not in the proximal colon (RR, 0.87; CI, 0.40-1.92). There was no significant association between leisure activity and colon cancer (active versus sedentary; RR, 0.82; CI, 0.59-1.13); however, the strongest inverse association was found among those most active in both work and leisure (RR, 0.33; CI, 0.16-0.71). For rectal cancer, there were risk reductions for those in light (RR, 0.71; CI, 0.36-1.37) and moderate/heavy occupational activity (RR, 0.50; CI, 0.26-0.97; P for trend, 0.04), and no association for leisure activity. These data provide evidence for a protective role of physical activity in colon and rectal cancer.
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PMID:Physical activity in relation to cancer of the colon and rectum in a cohort of male smokers. 1130 97

Estrogen used alone (estrogen replacement therapy [ERT]) or with the addition of progesterone (hormone replacement therapy [HRT]) is known to be effective in reducing menopausal symptoms including hot flashes, vaginal dryness and urinary symptoms. It has been traditionally contraindicated, however, in women with a previous diagnosis of breast cancer because of fear that it may increase the risk of recurrence. There are considerable basic scientific data but little methodologically strong observational data and none from randomized studies concerning the use of ERT in women with a prior diagnosis of breast cancer. From our knowledge of the physiology of breast cancer, however, estrogen and/or progestational agents should be used with caution in women with a previous diagnosis of breast cancer. There are currently many alternatives to ERT/HRT in the prevention of menopausal symptoms such as vitamin E, clonidine and selective serotonin reuptake inhibitor antidepressants such as venlafaxine. There are also a variety of other approaches to the prevention of osteoporosis and cardiovascular disease including bisphosphonates, diet, and exercise; and diet, exercise, and statins, respectively. Other suggested beneficial effects of estrogen such as colon cancer prevention can be approached by the use of aspirin or the non-steroidals. Several trials of ERT/HRT used for 2 years versus no therapy in menopausal women with a previous diagnosis of breast cancer are ongoing in Europe and Britain, and should give us stronger data as to the role of HRT in this setting.
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PMID:Hormone replacement in women with a history of breast cancer. 1152 54

The bioactive anthocyanins present in tart cherries, Prunus cerasus L. (Rosaceae) cv. Balaton, are cyanidin 3-glucosylrutinoside (1), cyanidin 3-rutinoside (2), and cyanidin 3-glucoside (3). Cyanidin (4) is the major anthocyanidin in tart cherries. In our continued evaluation of the in vivo and in vitro efficacy of these anthocyanins to prevent inflammation and colon cancer, we have added these compounds to McCoy's 5A medium in an effort to identify their degradation products during in vitro cell culture studies. This resulted in the isolation and characterization of protocatechuic acid (5), the predominant degradation product. In addition, 2,4-dihydroxybenzoic acid (6) and 2,4,6-trihydroxybenzoic acid (7) were identified as degradation products. However, these degradation products were not quantified. Compounds 5-7 were also identified as degradation products when anthocyanins were subjected to varying pH and thermal conditions. In cyclooxygenase (COX)-I and -II enzyme inhibitory assays, compounds 5-7 did not show significant activities when compared to the NSAIDs Naproxen, Celebrex, and Vioxx, or Ibuprofen, at 50 microM concentrations. However, at a test concentration of 50 microM, the antioxidant activity of protocatechuic acid (5) was comparable to those of the commercial antioxidants tert-butylhydroquinone (TBHQ), butylated hydroxytoluene (BHT), and butylated hydroxyanisole (BHA), and superior to that of vitamin E at 10 microM concentrations.
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PMID:Degradation products of cyanidin glycosides from tart cherries and their bioactivities. 1160 45

Alpha-tocopheryl succinate (alpha-TOS), a redox-inactive analogue of vitamin E, is a strong inducer of apoptosis, whereas alpha-tocopherol (alpha-TOH) lacks apoptogenic activity (J. Neuzil et al., FASEB J., 15: 403-415, 2001). Here we investigated the possible antineoplastic activities of alpha-TOH and alpha-TOS and further explored the potential of alpha-TOS as an antitumor agent. Using nude mice with colon cancer xenografts, we found that alpha-TOH exerted modest antitumor activity and acted by inhibiting tumor cell proliferation. In contrast, alpha-TOS showed a more profound antitumor effect, at both the level of inhibition of proliferation and induction of tumor cell apoptosis. alpha-TOS was nontoxic to normal cells and tissues, triggered apoptosis in p53(-/-) and p21(Waf1/Cip1(-/-)) cancer cells, and exerted a cooperative proapoptotic activity with tumor necrosis factor-related apoptosis-inducing ligand (Apo2 ligand) due to differences in proapoptotic signaling. Finally, alpha-TOS cooperated with tumor necrosis factor-related apoptosis-inducing ligand in suppression of tumor growth in vivo. Vitamin E succinate is thus a potent and highly specific anticancer agent and/or adjuvant of considerable therapeutic potential.
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PMID:Vitamin E succinate is a potent novel antineoplastic agent with high selectivity and cooperativity with tumor necrosis factor-related apoptosis-inducing ligand (Apo2 ligand) in vivo. 1189 20

Selenium and vitamin E are probably 2 of the most popular dietary supplements considered for use in the reduction of prostate cancer risk. This enthusiasm is reflected in the initiation of the Selenium and Vitamin E Chemoprevention Trial (SELECT). Is there sufficient evidence to support the use of these supplements in a large-scale prospective trial for patients who want to reduce the risk of prostate cancer? Results from numerous laboratory and observational studies support the use of these supplements, and data from recent prospective trials also add partial support. However, a closer analysis of the data reveals some interesting and unique associations. Selenium supplements provided a benefit only for those individuals who had lower levels of baseline plasma selenium. Other subjects, with normal or higher levels, did not benefit and may have an increased risk for prostate cancer. The concept that supplements reduce prostate cancer risk only in those at a higher risk and/or those with lower plasma levels of these compounds is supported by trials examining beta-carotene supplements. Smokers may be the only individuals who benefit, as has also been shown with vitamin E supplementation. In 4 recent prospective studies, vitamin E was found to reduce the risk of prostate cancer in past/recent and current smokers and those with low levels of this vitamin. Vitamin E supplements in higher doses (> or =100 IU) were also associated with a higher risk of aggressive or fatal prostate cancer in nonsmokers from a past prospective study. The dose of vitamin E in the SELECT trial (400 IU/day) is 8 times higher than what has been suggested to be effective (50 IU/day) by the largest randomized prospective trial in which the incidence rate of prostate cancer was used as an endpoint. Recent research also suggests that dietary vitamin E may be associated with a lower risk of prostate cancer than the vitamin E supplement. Additionally, recent results from all past cardiovascular prospective, randomized trials suggest that vitamin E shows little benefit for cardiovascular disease risk, especially at the dose being used in the SELECT trial. Other intriguing positive findings from past prospective studies of supplements suggest that aspirin and other nonsteroidal anti-inflammatory drugs have a role in reducing the risk of prostate cancer or other types of cancer (eg, colon cancer). It may be time to conduct a large costly trial to reconsider the use of selenium and vitamin E supplements for the reduction of prostate cancer risk. Some evidence for the use of these supplements exists, but serious embellishment of study findings may be leading to an inappropriate use of these supplements in a clinical setting.
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PMID:Selenium and vitamin E supplements for prostate cancer: evidence or embellishment? 1193 32

There are relatively few reports on the cancer chemopreventive effects of lycopene or tomato carotenoids in animal models. The majority, but not all, of these studies indicate a protective effect. Inhibitory effects were reported in two studies using aberrant crypt foci, an intermediate lesion leading to colon cancer, as an end point and in two mammary tumor studies, one using the dimethylbenz(a)anthracene model, and the other the spontaneous mouse model. Inhibitory effects were also reported in mouse lung and rat hepatocarcinoma and bladder cancer models. However, a report from the author's laboratory found no effect in the N-nitrosomethylurea-induced mammary tumor model when crystalline lycopene or a lycopene-rich tomato carotenoid oleoresin was administered in the diet. Unfortunately, because of differences in routes of administration (gavage, intraperitoneal injection, intra-rectal instillation, drinking water, and diet supplementation), species and strain differences, form of lycopene (pure crystalline, beadlet, mixed carotenoid suspension), varying diets (grain-based, casein based) and dose ranges (0.5-500 ppm), no two studies are comparable. It is clear that the majority of ingested lycopene is excreted in the feces and that 1000-fold more lycopene is absorbed and stored in the liver than accumulates in other target organs. Nonetheless, physiologically significant (nanogram) levels of lycopene are assimilated by key organs such as breast, prostate, lung, and colon, and there is a rough dose-response relationship between lycopene intake and blood levels. Pure lycopene was absorbed less efficiently than the lycopene-rich tomato carotenoid oleoresin and blood levels of lycopene in rats fed a grain-based diet were consistently lower than those in rats fed lycopene in a casein-based diet. The latter suggests that the matrix in which lycopene is incorporated is an important determinant of lycopene uptake. A number of issues remain to be resolved before any definitive conclusions can be drawn concerning the anticancer effects of lycopene. These include the following: the optimal dose and form of lycopene, interactions among lycopene and other carotenoids and fat soluble vitamins such as vitamin E and D, the role of dietary fat in regulating lycopene uptake and disposition, organ and tissue specificity, and the problem of extrapolation from rodent models to human populations.
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PMID:A review of animal model studies of tomato carotenoids, lycopene, and cancer chemoprevention. 1242 27

We conducted a prospective study on the association between supplemental vitamin E and colon cancer in 87,998 females from the Nurses' Health Study and 47, 344 males from the Health Professionals Follow-up Study. There was some suggestion that men with supplemental vitamin E intake of 300 IU/day or more may be at lower risk for colon cancer when compared with never users [multivariate relative risk (RR), 300-500 IU/day versus never users, 0.73 (95% confidence interval (CI), 0.52-1.03); >or=600 IU/day versus never users = 0.70 (95% CI = 0.38-1.29)], but CIs included 1. In women, there was no evidence for an inverse association between vitamin E supplementation and risk of colon cancer. Our findings do not provide consistent support for an inverse association between supplemental vitamin E and colon cancer risk. Considering the paucity of epidemiological data on this association, further studies of vitamin E and colon cancer are warranted.
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PMID:A prospective study on supplemental vitamin e intake and risk of colon cancer in women and men. 1243 6

Vitamin E, part of the body's primary lipid-soluble defense against free radicals and reactive oxygen molecules, has been suggested to reduce the risk for some cancers. However, the role of vitamin E in the etiology and prevention of colon cancer, especially in the highest risk group, the aged, is not clear. Thus, this study was conducted to elucidate the effect of vitamin E supplementation on susceptibility to colon cancer by examining azoxymethane (AOM)-induced aberrant crypt foci (ACF) formation, a surrogate biomarker of colon cancer. Young (3-4 mo) and old (19-20 mo) C57BL/6JNIA mice were fed either a control diet (30 mg dl-alpha-tocopheryl acetate/kg diet) or a vitamin E-supplemented diet (500 mg dl-alpha-tocopheryl acetate/kg diet) for 16 wk. After 6 wk of dietary supplementation, young and old mice were injected with saline or AOM weekly for 5 wk to receive the same total dose of AOM (2.2 mg) and killed 10 wk after the first AOM injection. Vitamin E supplementation had no effect on the number of AOM-induced ACF in young or old mice. In addition, vitamin E supplementation did not have an effect on splenocyte interferon-gamma, interluekin-6 and tumor necrosis factor-alpha levels, natural killer cell killing activity or colonic cell proliferation in young or old mice. Thus, alpha-tocopherol does not seem to affect the initiation and early promotion stages of AOM-induced colon carcinogenesis in young or old mice. Whether vitamin E supplementation might be effective in reducing AOM-induced colon tumors is unclear.
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PMID:Vitamin E supplementation does not alter azoxymethane-induced colonic aberrant crypt foci formation in young or old mice. 1256 95

Colon cancer incidence rates have risen sharply in Shanghai, China, since the early 1970s, and diet may have contributed to the rising incidence. To clarify the role of dietary factors for colon cancer in Shanghai, we analyzed data from a population-based case-control study of 931 cases (462 males and 469 females) and 1552 controls (851 males and 701 females) ages 30-74 years in Shanghai, China, from 1990-1993. Subjects were interviewed in person for a detailed history of dietary practices and food preferences by using a food-frequency questionnaire. Colon cancer risk was estimated by odds ratios (ORs) and 95% confidence intervals (CIs), adjusting for age, total energy, and other confounding factors. Risk for the highest versus the lowest quartile of intake was elevated for red meat (OR, 1.5; 95% CI, 1.0-2.1 for men and OR, 1.5; 95% CI, 1.0-2.2 for women), fish (OR, 1.7; 95% CI, 1.2-2.4 for men and OR, 1.2; 95% CI, 0.8-1.7 for women), and eggs (OR, 1.4; 95% CI, 1.0-1.9 for men and OR, 1.3; 95% CI, 0.9-1.9 for women), but was reduced for fresh fruit (OR, 0.7; 95% CI, 0.5-1.0 for men and OR, 0.6, 0.4-0.9 for women). High intake of preserved foods, whether animal or plant source, was associated with an excess risk of colon cancer (OR, 2.0; 95% CI, 1.5-2.9 for men and OR, 2.7; 95% CI, 1.9-3.8 for women). For dietary nutrients, risk generally declined with greater consumption of fiber and micronutrients common in fruit and vegetables, including vitamin C, carotene, and vitamin E. Intake of macronutrients in general was not significantly related to risk. Our findings suggest that diets high in fruit and antioxidant vitamins that are common in plant foods reduce the risk of colon cancer, whereas diets high in red meat, eggs, and preserved foods increase the risk.
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PMID:Dietary factors and risk of colon cancer in Shanghai, China. 1264 8

This study was conducted to investigate the role of the enzyme cyclooxygenase (COX) and its prostaglandin product PGE(2) in n-6 and n-3 polyunsaturated fatty acid (PUFA)-mediated effects on cellular proliferation of two human colorectal carcinoma cell lines. The long chain PUFAs eicosapentaenoic acid (EPA; 20:5n-3) and arachidonic acid (AA; 20:4n-6) both inhibited cell proliferation of Caco-2 cells compared with the long chain fatty acids alpha-linolenic acid (ALA; 18:3n-3) and linoleic acid (LA; 18:2n-6). Neither incubation with PGE(2) nor reduction in PGE(2) synthesis by EPA compared with AA led to differential effects on cell proliferation in Caco-2 cells. This suggests that n-6 and n-3 PUFA-mediated cell proliferation in Caco-2 cells is not regulated via PGE(2) levels. AA and EPA had no effect on growth of HT-29 colon cancer cells with a low COX activity. However, stimulation of COX-2 activity by IL-1 beta resulted in a decrease in cell proliferation and an induction of cytotoxicity by AA as well as by EPA. Both inhibition of the COX pathway by indomethacin as well as inhibition of direct lipid peroxidation by antioxidants such as vitamin E and C diminished the anti-proliferative effects of AA as well as EPA. Also, malondialdehyde, a product of lipid peroxidation and COX-activity was decreased by addition of vitamin E and partially decreased by indomethacin. These data support the hypothesis that growth inhibitory and cytotoxic effects of PUFAs with methylene-interrupted double bonds such as AA and EPA are due to peroxidation products that are generated during lipid peroxidation and COX activity.
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PMID:The role of cyclooxygenase in n-6 and n-3 polyunsaturated fatty acid mediated effects on cell proliferation, PGE(2) synthesis and cytotoxicity in human colorectal carcinoma cell lines. 1266 96


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