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<title>American Journal of Clinical Nutrition Cancer</title>
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<description>American Journal of Clinical Nutrition RSS feed -- recent Cancer articles</description>
<prism:eIssn>1938-3207</prism:eIssn>
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<title>American Journal of Clinical Nutrition</title>
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<title><![CDATA[Conjugated linoleic acid intake and breast cancer risk in a prospective cohort of Swedish women [Cancer]]]></title>
<link>http://www.ajcn.org/cgi/content/short/90/3/556?rss=1</link>
<description><![CDATA[
<p><b>Background:</b> Studies in animals and in vitro suggest that conjugated linoleic acids (CLAs), a group of fatty acids found mainly in dairy products and in the meat of ruminants, have protective effects against mammary carcinogenesis. However, findings from epidemiologic studies on CLA intake in relation to breast cancer risk are sparse and inconsistent.</p>
<p><b>Objective:</b> The objective was to examine prospectively the association between CLA intake and the incidence of invasive breast cancer in the Swedish Mammography Cohort.</p>
<p><b>Design:</b> In 1987&ndash;1990, 61,433 cancer-free women completed a food-frequency questionnaire from which we estimated each woman's CLA intake. Cox proportional hazards models were used to estimate relative risks, adjusted for breast cancer risk factors.</p>
<p><b>Results:</b> During a mean follow-up of 17.4 y, 2952 incident cases of breast cancer were ascertained. In multivariate analyses, no significant association was observed between dietary CLA intake and risk of breast cancer, overall or by estrogen receptor (ER) and progesterone receptor (PR) status. The multivariate relative risks (95% CI) for the highest quintile of CLA intake (&ge;155.7 mg/d) compared with the lowest quintile (&lt;78.1 mg/d) were 1.04 (0.92, 1.17) for overall breast cancer, 1.09 (0.90, 1.31) for ER+/PR+ tumors, 1.09 (0.78, 1.53) for ER+/PR&ndash; tumors, and 0.84 (0.57, 1.24) for ER&ndash;/PR&ndash; tumors.</p>
<p><b>Conclusion:</b> The results provide no evidence of a protective effect of CLA against breast cancer development in women.</p>
]]></description>
<dc:creator><![CDATA[Larsson, S. C, Bergkvist, L., Wolk, A.]]></dc:creator>
<dc:date>Thu, 20 Aug 2009 10:03:27 PDT</dc:date>
<dc:identifier>info:doi/10.3945/ajcn.2009.27480</dc:identifier>
<dc:title><![CDATA[Conjugated linoleic acid intake and breast cancer risk in a prospective cohort of Swedish women [Cancer]]]></dc:title>
<dc:publisher>The American Society for Clinical Nutrition, Inc.</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>90</prism:volume>
<prism:endingPage>560</prism:endingPage>
<prism:publicationDate>2009-09-01</prism:publicationDate>
<prism:startingPage>556</prism:startingPage>
<prism:section>Cancer</prism:section>
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<item rdf:about="http://www.ajcn.org/cgi/content/short/90/3/561?rss=1">
<title><![CDATA[One-carbon metabolism-related nutrients and prostate cancer survival [Cancer]]]></title>
<link>http://www.ajcn.org/cgi/content/short/90/3/561?rss=1</link>
<description><![CDATA[
<p><b>Background:</b> Folate and other one-carbon metabolism nutrients may influence prostate cancer pathogenesis. Prior studies of these nutrients in relation to prostate cancer incidence have been inconclusive, and none have explored prostate cancer survival.</p>
<p><b>Objective:</b> The objective was to assess whether dietary intakes of folate, riboflavin, vitamin B-6, vitamin B-12, and methionine measured around the time of prostate cancer diagnosis are associated with prostate cancer survival.</p>
<p><b>Design:</b> This population-based prospective study comprised 525 men from &Ouml;rebro, Sweden, who received a diagnosis of incident prostate cancer between 1989 and 1994 and completed a self-administered food-frequency questionnaire. Record linkages to the Swedish Death Registry enabled all cases to be followed for up to 20 y after diagnosis, and the cause of death was assigned via medical record review. Cox proportional hazards regression was used to calculate multivariable hazard ratios (HRs) and 95% CIs. During a median of 6.4 y of follow-up, 218 men (42%) died of prostate cancer and 257 (49%) of other causes.</p>
<p><b>Results:</b> A comparison of the highest with the lowest quartile showed that vitamin B-6 intake was inversely associated with prostate cancer&ndash;specific death (HR: 0.71; 95% CI: 0.46, 1.10; <I>P</I> for trend = 0.08), especially in men with a diagnosis of localized-stage disease (HR; 0.05; 95% CI: 0.01, 0.26; <I>P</I> for trend = 0.0003). However, vitamin B-6 intake was not associated with improved prostate cancer survival among advanced-stage cases (HR: 1.04; 95% CI: 0.64, 1.72; <I>P</I> for trend = 0.87). Folate, riboflavin, vitamin B-12, and methionine intakes were not associated with prostate cancer survival.</p>
<p><b>Conclusion:</b> A high vitamin B-6 intake may improve prostate cancer survival among men with a diagnosis of localized-stage disease.</p>
]]></description>
<dc:creator><![CDATA[Kasperzyk, J. L, Fall, K., Mucci, L. A, Hakansson, N., Wolk, A., Johansson, J.-E., Andersson, S.-O., Andren, O.]]></dc:creator>
<dc:date>Thu, 20 Aug 2009 10:03:27 PDT</dc:date>
<dc:identifier>info:doi/10.3945/ajcn.2009.27645</dc:identifier>
<dc:title><![CDATA[One-carbon metabolism-related nutrients and prostate cancer survival [Cancer]]]></dc:title>
<dc:publisher>The American Society for Clinical Nutrition, Inc.</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>90</prism:volume>
<prism:endingPage>569</prism:endingPage>
<prism:publicationDate>2009-09-01</prism:publicationDate>
<prism:startingPage>561</prism:startingPage>
<prism:section>Cancer</prism:section>
</item>

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<title><![CDATA[Prospective study of meat intake and dietary nitrates, nitrites, and nitrosamines and risk of adult glioma [Cancer]]]></title>
<link>http://www.ajcn.org/cgi/content/short/90/3/570?rss=1</link>
<description><![CDATA[
<p><b>Background:</b> The hypothesis that nitrosamine exposure may increase the risk of glioma has been circulating for several decades, but testing it has been difficult because of the ubiquitous nature of nitrosamine exposure. Diet has been the focus of many studies because it can substantially influence nitrosamine exposure, mostly from the endogenous formation of nitrosamines based on intake of nitrite and nitrate.</p>
<p><b>Objective:</b> The objective was to examine the relation between intakes of meats, nitrate, nitrite, and 2 nitrosamines [nitrosodimethylamine (NDMA) and nitrosopyrolidine (NPYR)] and glioma risk in a prospective analysis.</p>
<p><b>Methods:</b> Data from 3 US prospective cohort studies were combined for this analysis; 335 glioma cases were diagnosed during &le;24 y of follow-up. Dietary intake was assessed with food-frequency questionnaires. Nitrate, nitrite, and nitrosamine values were calculated based on published values of these nutrients in various foods over different periods in time. Cox proportional hazards models were used to estimate incidence rate ratios (RRs) and 95% CIs. Estimates from each cohort were pooled by using a random-effects model.</p>
<p><b>Results:</b> Risk of glioma was not elevated among individuals in the highest intake category of total processed meats (RR: 0.92; 95% CI: 0.48, 1.77), nitrate (RR: 1.02; 95% CI: 0.66, 1.58), nitrites (RR: 1.26; 95% CI: 0.89, 1.79), or NDMA (RR: 0.88; 95% CI: 0.57, 1.36) compared with the lowest category. No effect modification was observed by intake of vitamins C or E or other antioxidant measures.</p>
<p><b>Conclusion:</b> We found no suggestion that intake of meat, nitrate, nitrite, or nitrosamines is related to the risk of glioma.</p>
]]></description>
<dc:creator><![CDATA[Michaud, D. S, Holick, C. N, Batchelor, T. T, Giovannucci, E., Hunter, D. J]]></dc:creator>
<dc:date>Thu, 20 Aug 2009 10:03:27 PDT</dc:date>
<dc:identifier>info:doi/10.3945/ajcn.2008.27199</dc:identifier>
<dc:title><![CDATA[Prospective study of meat intake and dietary nitrates, nitrites, and nitrosamines and risk of adult glioma [Cancer]]]></dc:title>
<dc:publisher>The American Society for Clinical Nutrition, Inc.</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>90</prism:volume>
<prism:endingPage>577</prism:endingPage>
<prism:publicationDate>2009-09-01</prism:publicationDate>
<prism:startingPage>570</prism:startingPage>
<prism:section>Cancer</prism:section>
</item>

<item rdf:about="http://www.ajcn.org/cgi/content/short/90/3/578?rss=1">
<title><![CDATA[A human, double-blind, placebo-controlled, crossover trial of prebiotic, probiotic, and synbiotic supplementation: effects on luminal, inflammatory, epigenetic, and epithelial biomarkers of colorectal cancer [Cancer]]]></title>
<link>http://www.ajcn.org/cgi/content/short/90/3/578?rss=1</link>
<description><![CDATA[
<p><b>Background:</b> Diet is an important factor in colorectal carcinogenesis; thus, dietary supplements may have a role in colorectal cancer prevention.</p>
<p><b>Objective:</b> The objective was to establish the relative luminal, epithelial, and epigenetic consequences of prebiotic, probiotic, and synbiotic dietary supplementation in humans.</p>
<p><b>Design:</b> This was a randomized, double-blind, placebo-controlled, 4-wk crossover trial of resistant starch and <I>Bifidobacterium lactis</I>, either alone or as a combined synbiotic preparation, in 20 human volunteers. Rectal biopsy, feces, and serum samples were collected. The rectal mucosal endpoints were DNA methylation at 16 CpG island loci and <I>LINE-1</I>, epithelial proliferation (Ki67 immunohistochemistry), and crypt cellularity. The fecal endpoints were short-chain fatty acid concentrations, pH, ammonia, and microbiological profiles (by denaturing gradient gel electrophoresis and sequencing). Serum endpoints were a panel of cytokines and high-sensitivity C-reactive protein.</p>
<p><b>Results:</b> Seventeen subjects completed the entire study. The synbiotic intervention fostered a significantly different fecal stream bacterial community than did either the prebiotic (<I>P</I> = 0.032) or the probiotic (<I>P</I> = 0.001) intervention alone, in part because of a greater proportion of patients harboring fecal <I>Lachnospiraceae</I> spp<I>.</I> These changes developed in the absence of any significant differences in fecal chemistry. There were no differences in epithelial kinetics.</p>
<p><b>Conclusions:</b> This synbiotic supplementation with <I>B. lactis</I> and resistant starch, in the doses used, induced unique changes in fecal microflora but did not significantly alter any other fecal, serum, or epithelial variables. This trial was registered in the Australian New Zealand Clinical Trials Registry at www.anzctr.org.au as ACTRN012606000115538.</p>
]]></description>
<dc:creator><![CDATA[Worthley, D. L, Le Leu, R. K, Whitehall, V. L, Conlon, M., Christophersen, C., Belobrajdic, D., Mallitt, K.-A., Hu, Y., Irahara, N., Ogino, S., Leggett, B. A, Young, G. P]]></dc:creator>
<dc:date>Thu, 20 Aug 2009 10:03:27 PDT</dc:date>
<dc:identifier>info:doi/10.3945/ajcn.2009.28106</dc:identifier>
<dc:title><![CDATA[A human, double-blind, placebo-controlled, crossover trial of prebiotic, probiotic, and synbiotic supplementation: effects on luminal, inflammatory, epigenetic, and epithelial biomarkers of colorectal cancer [Cancer]]]></dc:title>
<dc:publisher>The American Society for Clinical Nutrition, Inc.</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>90</prism:volume>
<prism:endingPage>586</prism:endingPage>
<prism:publicationDate>2009-09-01</prism:publicationDate>
<prism:startingPage>578</prism:startingPage>
<prism:section>Cancer</prism:section>
</item>

<item rdf:about="http://www.ajcn.org/cgi/content/short/90/2/354?rss=1">
<title><![CDATA[Fish consumption and markers of colorectal cancer risk: a multicenter randomized controlled trial [Cancer]]]></title>
<link>http://www.ajcn.org/cgi/content/short/90/2/354?rss=1</link>
<description><![CDATA[
<p><b>Background:</b> Diet is a major factor in the etiology of colorectal cancer, with high fish consumption possibly decreasing colorectal cancer risk, as was shown in several observational studies. To date, no intervention trials have examined the possible beneficial effects of fish intake on colorectal cancer risk.</p>
<p><b>Objective:</b> The objective was to investigate the effects of a 6-mo intervention with oil-rich or lean fish on apoptosis and mitosis within the colonic crypt.</p>
<p><b>Design:</b> In a multicenter, randomized, controlled intervention trial, patients with colorectal polyps, inactive ulcerative colitis, or no macroscopic signs of disease were recruited (<I>n</I> = 242) and randomly allocated to receive dietary advice plus either 300 g oil-rich fish (salmon) per week (<I>n</I> = 82), 300 g lean fish (cod) per week (<I>n</I> = 78), or only dietary advice (DA) (<I>n</I> = 82). Apoptosis and mitosis were measured in colonic biopsy samples collected before and after intervention (<I>n</I> = 213).</p>
<p><b>Results:</b> The total number of apoptotic cells per crypt did not increase in the salmon or cod group: &ndash;0.10 (95% CI: &ndash;0.36, 0.16) and &ndash;0.06 (95% CI: &ndash;0.32, 0.20), respectively, compared with the DA group. The total number of mitotic cells per crypt decreased nonsignificantly in the salmon group (&ndash;0.87; 95% CI: &ndash;2.41, 0.68) and in the cod group (&ndash;1.04; 95% CI: &ndash;2.62, 0.53) compared with the DA group. Furthermore, the distribution of mitosis within the crypt did not significantly change in either group.</p>
<p><b>Conclusion:</b> An increase in the consumption of either oil-rich or lean fish to 2 portions weekly over 6 mo does not markedly change apoptotic and mitotic rates in the colonic mucosa. This trial was registered at www.clinicaltrials.gov as NCT00145015.</p>
]]></description>
<dc:creator><![CDATA[Pot, G. K, Majsak-Newman, G., Geelen, A., Harvey, L. J, Nagengast, F. M, Witteman, B. J., van de Meeberg, P. C, Timmer, R., Tan, A., Wahab, P. J, Hart, A. R, Williams, M. P, Przybylska-Phillips, K., Dainty, J. R, Schaafsma, G., Kampman, E., Lund, E. K]]></dc:creator>
<dc:date>Mon, 20 Jul 2009 10:02:05 PDT</dc:date>
<dc:identifier>info:doi/10.3945/ajcn.2009.27630</dc:identifier>
<dc:title><![CDATA[Fish consumption and markers of colorectal cancer risk: a multicenter randomized controlled trial [Cancer]]]></dc:title>
<dc:publisher>The American Society for Clinical Nutrition, Inc.</dc:publisher>
<prism:number>2</prism:number>
<prism:volume>90</prism:volume>
<prism:endingPage>361</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>354</prism:startingPage>
<prism:section>Cancer</prism:section>
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