Effects of dietary fat and protein on DMH‐induced tumor development and immune responses

Nutter, Robert L.; Kettering, Janies D.; Aprecio, Raydolfo M.; Weeks, Douglas A.; Gridley, Daila S.

doi:10.1080/01635589009514055

Cited by 16 publications

(4 citation statements)

References 21 publications

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“…The colon was slit opened longitudinally and examined for tumors and the lengths of both the major and minor axes were recorded. Tumor volume was estimated using the formula for a sphere, V=4/3Πx (D/2) 3 , where D is the average of the major axis and the minor axis of the tumor [19,20].…”

Section: Methodsmentioning

confidence: 99%

Luteolin inhibits cell proliferation during Azoxymethane-induced experimental colon carcinogenesis via Wnt/ β-catenin pathway

Ashokkumar

Sudhandiran

2009

Invest New Drugs

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The protective role of Luteolin (LUT) against Azoxymethane (AOM)-induced mouse colon carcinogenesis has been documented earlier. The aim of this study is to investigate on the mechanism of chemopreventive action exhibited by LUT employing AOM-induced colon carcinogenesis in mice as an experimental model. LUT inhibited AOM-induced colon tumorigenesis by decreasing tumor incidence and size. LUT reduced the cell proliferation by decreasing the number of Argyrophillic nucleolar organizer region (AgNOR)/nucleus and Proliferating Cell Nuclear Antigen (PCNA) index. It was known that β-catenin is a key effector in Wingless and Int (Wnt) signaling pathway and 90% of colon tumors arise from mutations in this pathway. In this study, we show evidence that LUT inhibited colon carcinogenesis by decreasing AOM-induced cell proliferation through the involvement of β-catenin, Glycogen synthase kinase (GSK)-3β and cyclin D1, the key components in Wnt signaling pathway. In conclusion, the protective effect of LUT could be attributed to inhibition of AOM-induced cellular proliferation probably through the involvement of β-catenin, GSK-3β and cyclin D1.

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Section: Methodsmentioning

confidence: 99%

Luteolin inhibits cell proliferation during Azoxymethane-induced experimental colon carcinogenesis via Wnt/ β-catenin pathway

Ashokkumar

Sudhandiran

2009

Invest New Drugs

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“…Components in red meat or which are formed during the cooking of meat that may increase colorectal cancer risk include animal fat,17, 18 heme iron19, 20, 21 and heterocyclic amines (HCAs) 22, 23. In addition, human experimental studies have demonstrated that high red meat diets enhance the endogenous formation of N ‐nitroso compounds (NOCs),24, 25, 26, 27 which have been found to induce the formation of DNA adducts in human colonocytes 28.…”

mentioning

confidence: 99%

Red meat consumption and risk of cancers of the proximal colon, distal colon and rectum: The Swedish Mammography Cohort

Larsson

Rafter

Holmberg

et al. 2004

Intl Journal of Cancer

193

176

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Although there is considerable evidence that high consumption of red meat may increase the risk of colorectal cancer, data by subsite within the colon are sparse. The objective of our study was to prospectively examine whether the association of red meat consumption with cancer risk varies by subsite within the large bowel. We analyzed data from the Swedish Mammography Cohort of 61,433 women aged 40 -75 years and free from diagnosed cancer at baseline in [1987][1988][1989][1990]. Diet was assessed at baseline using a self-administered food-frequency questionnaire. Over a mean follow-up of 13.9 years, we identified 234 proximal colon cancers, 155 distal colon cancers and 230 rectal cancers. We observed a significant positive association between red meat consumption and risk of distal colon cancer (p for trend ‫؍‬ 0.001) but not of cancers of the proximal colon (p for trend ‫؍‬ 0.95) or rectum (p for trend ‫؍‬ 0.32). The multivariate rate ratio for women who consumed 94 or more g/day of red meat compared to those who consumed less than 50 g/day was 2. Although there is mounting support in the literature of an increased risk of colon or colorectal cancer associated with high consumption of red meat, 1,2 data for subsites within the colon are limited and conflicting. [3][4][5] Multiple lines of evidence indicate that proximal and distal colon cancers may have distinct etiologies. 6 -10 Cancers arising in the proximal and distal colon exhibit differences in incidence according to geographic region, age and sex. 7,10 Furthermore, there are various molecular and clinical differences between proximal and distal sites of the colon that may influence the susceptibility to environmental factors. 10 For example, differences between subsites exist in pH, 11 bacterial composition and bacterial metabolic capacity, 12,13 apoptotic index, 14 activity of ornithine decarboxylase 15 and expression of carcinogen metabolizing enzymes. 16 These differences underscore the need for separate analyses by subsite within the colon.Components in red meat or which are formed during the cooking of meat that may increase colorectal cancer risk include animal fat, 17,18 heme iron 19 -21 and heterocyclic amines (HCAs). 22,23 In addition, human experimental studies have demonstrated that high red meat diets enhance the endogenous formation of N-nitroso compounds (NOCs), 24 -27 which have been found to induce the formation of DNA adducts in human colonocytes. 28 The concentrations of the pro-mutagenic lesion O 6 -methyldeoxyguanosine, a marker of exposure to many NOCs, have been shown to be significantly greater in tissues from the distal colon and rectum than from the proximal colon. 29 A direct association of meat consumption with body iron stores has been found in many studies. 30 -32 In a nested case-control study, an increased colorectal cancer risk associated with high serum iron levels was restricted to the distal colon and rectum. 33 Thus, given these findings, a potential effect of diets high in red meat might be limited to cancers of t...

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“…Significant enhancement (P < 0.05) in CL was seen when either IFN-y or LPS was added to the samples regardless of which zymosan preparation was used. However, comparison of the three zymosans showed that our freshly prepared opsonized zymosan (22) significantly increased the baseline CL in the absence of the priming agents. This preparation also yielded the greater CL response with LPS priming.…”

Section: Resultsmentioning

confidence: 77%

“…For example, in the clnical setting CL quantitation is used to investigate phagocytic cell disorders (10,l I ) , serum opsonic activity (12,13), and the presence of immune complexes in sera ( 14,15). In our laboratories CL level has been measured under a variety of experimental conditions (16)(17)(18)(19)(20)(21)(22).…”

Section: Introductionmentioning

confidence: 99%

Phagocytic cell chemiluminescence using different zymosan preparations

Gridley

Lau

Tosk

1991

Clinical Laboratory Analysis

Self Cite

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This study compared the effectiveness of opsonized and unopsonized zymosan prepared in our laboratories with a commercially available opsonized preparation used for induction of luminol-dependent oxidative burst in phagocytic cells. The production of chemiluminescence (CL) by human whole blood, isolated human neutrophils, normal BALB c mouse splenocytes, and an immortal BALB c mouse macrophage cell line (J774A.1) was tested in an automated luminometer. Recombinant murine or human interferon-gamma (IFN-gamma) and lipopolysaccharide (LPS) were used as priming agents in some of the experiments. With human leukocytes and normal mouse spleen cells the laboratory-prepared zymosans (regardless of opsonization) induced equal or significantly greater CL than did the commercially prepared zymosan. In addition, greatly increased CL was evident with IFN-gamma- and LPS-primed neutrophils tested with our zymosans compared with the commercial preparation. These results suggest that effective zymosans capable of inducing strong, reproducible CL responses from several different phagocytic cell populations can be readily made in the laboratory.

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Effects of dietary fat and protein on DMH‐induced tumor development and immune responses

Cited by 16 publications

References 21 publications

Luteolin inhibits cell proliferation during Azoxymethane-induced experimental colon carcinogenesis via Wnt/ β-catenin pathway

Luteolin inhibits cell proliferation during Azoxymethane-induced experimental colon carcinogenesis via Wnt/ β-catenin pathway

Red meat consumption and risk of cancers of the proximal colon, distal colon and rectum: The Swedish Mammography Cohort

Phagocytic cell chemiluminescence using different zymosan preparations

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