Prévention

Nutrition et prévention

Menée sur 330 femmes ménopausées, cette étude randomisée évalue l'effet d'une supplémentation en calcium et vitamine D pendant un an sur la densité mammaire

Vitamin D and calcium supplementation and one-year change in mammographic density in the Women's Health Initiative Calcium and Vitamin D Trial
• Cancer Epidemiology Biomarkers & Prevention, sous presse, 2012 (résumé)

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Menée sur 330 femmes ménopausées, cette étude randomisée évalue l'effet d'une supplémentation en calcium et vitamine D pendant un an sur la densité mammaire

“Vitamin D and calcium supplementation and one-year change in mammographic density in the Women's Health Initiative Calcium and Vitamin D Trial”

• Bertone-Johnson, Elizabeth R.;McTiernan, Anne;Thomson, Cynthia A.;Wactawski-Wende, Jean;Aragaki, Aaron K.;Rohan, Thomas E.;Vitolins, Mara Z.;Tamimi, Rulla M.;Johnson, Karen C.;Lane, Dorothy;Rexrode, Kathryn M.;Peck, Jennifer D.;Chlebowski, Rowan T.;Sarto, Gloria;Manson, JoAnn E.

Background: Calcium and vitamin D may be inversely related to breast cancer risk, in part by affecting mammographic density. However, results from previous, mostly cross-sectional studies have been mixed, and there have been few randomized clinical trials of the effect of calcium and vitamin D supplementation on change in mammographic density. Methods: We assessed the effect of one year of supplementation on mammographic density in 330 postmenopausal women enrolled in the Women's Health Initiative Hormone Therapy (HT) and Calcium and Vitamin D (CaD) trials. Women were randomized to receive 1000 mg/day of elemental calcium carbonate plus 400 IU/day of vitamin D3 or placebo. Results: After approximately one year, mammographic density decreased 2% in the CaD supplementation group and increased 1% in the placebo group (ratio of means = 0.97; 95% confidence interval (CI) = 0.81-1.17). Results suggested potential interaction by HT use (P = 0.08). Among women randomized to HT placebo, the ...

Mots clés : Sein; Prévention (Nutrition et prévention)

Menée in vitro et à l'aide d'une xénogreffe, cette étude montre que la monocilline II peut inhiber la croissance des cellules tumorales du sein en bloquant les voies de signalisation de la protéine kinase MAPK et la phosphorylation de la thréonine 160 de la kinase CDK2

Monocillin II Inhibits Human Breast Cancer Growth Partially by Inhibiting MAPK Pathways and CDK2 Thr160 Phosphorylation
• ChemBioChem, sous presse, 2012 (résumé)

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Menée in vitro et à l'aide d'une xénogreffe, cette étude montre que la monocilline II peut inhiber la croissance des cellules tumorales du sein en bloquant les voies de signalisation de la protéine kinase MAPK et la phosphorylation de la thréonine 160 de la kinase CDK2

“Monocillin II Inhibits Human Breast Cancer Growth Partially by Inhibiting MAPK Pathways and CDK2 Thr160 Phosphorylation”

• Wei, Huanhuan;Xu, Liangxiong;Yu, Min;Zhang, Ling;Wang, Huijie;Wei, Xiaoyi;Ruan, Yuanyuan

Twenty-two β-resorcylic acid lactones (RALs) were evaluated for cytotoxicity against human breast cancer cells to find their structure–activity relationship (SAR). Monocillin II, a trans-enone RAL without epoxy and conjugated dienone, was found to have higher activity in inhibiting tumor cell growth in both in vitro experiment and in vivo nude xenografted mice model than its analogue radicicol, an anticancer lead compound. We demonstrated for the first time that monocillin II could arrest breast cancer cell cycle in G1 phase, which might partially be the result of its inhibition effect on the phosphorylation of the Thr160 residue of cyclin dependent kinase 2 (CDK2), a key enzyme in cell-cycle regulation. Moreover, monocillin II exhibited inhibition of heat shock protein 90 (Hsp90) and depleted its target proteins, Raf-1 and A-Raf, which are involved in Ras/Raf/MEK/ERK mitogen-activated protein kinase (MAPK) pathway. Remarkably, we found that monocillin II could inhibit activation ...

Mots clés : Sein; Prévention (Chimioprévention)

Menée à partir d'entretiens auprès de 902 femmes atteintes d'un carcinome épithélial de l'ovaire et de 1 802 témoins, cette étude évalue l'association entre l'utilisation d'aspirine, d'anti-inflammatoires non stéroïdiens ou de paracétamol et le risque de cancer de l'ovaire

Aspirin, Nonaspirin Nonsteroidal Anti-inflammatory Drugs, or Acetaminophen and Risk of Ovarian Cancer
• Epidemiology, sous presse, 2012 (résumé)

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Menée à partir d'entretiens auprès de 902 femmes atteintes d'un carcinome épithélial de l'ovaire et de 1 802 témoins, cette étude évalue l'association entre l'utilisation d'aspirine, d'anti-inflammatoires non stéroïdiens ou de paracétamol et le risque de cancer de l'ovaire

“Aspirin, Nonaspirin Nonsteroidal Anti-inflammatory Drugs, or Acetaminophen and Risk of Ovarian Cancer”

• Lo-Ciganic, Wei-Hsuan;Zgibor, Janice C.;Bunker, Clareann H.;Moysich, Kirsten B.;Edwards, Robert P.;Ness, Roberta B.

Background: Aspirin, nonaspirin nonsteroidal anti-inflammatory drugs (NA-NSAIDs) and acetaminophen all have biologic effects that might reduce the risk of ovarian cancer. However, epidemiologic data on this question are mixed. Methods: A population-based, case-control study in western Pennsylvania, eastern Ohio, and western New York State included 902 women with incident epithelial ovarian cancer who were diagnosed between February 2003 and November 2008 as well as 1802 matched controls. Regular use (at least 2 tablets per week for 6 months or more) of aspirin, NA-NSAIDs, and acetaminophen before the reference date (9 months before interview date) was assessed by in-person interview. We used logistic regression to calculate adjusted odds ratios (ORs) and 95% confidence intervals (CIs). Results: The OR for aspirin use was 0.81 (95% CI = 0.63-1.03). Decreased risks were found among women who used aspirin continuously (0.71 [0.54-0.94]) or at a low-standardized daily dose (0.72 ...

Mots clés : Ovaire; Prévention (Chimioprévention)

Menée sur un modèle murin, cette étude montre qu'une supplémentation en acide folique peut prévenir un cancer de l'estomac lié à la bactérie Helicobacter pylori en augmentant le niveau global de méthylation de l'ADN et en réduisant l'inflammation gastrique

Folic Acid Increases Global DNA Methylation and Reduces Inflammation to Prevent Helicobacter-Associated Gastric Cancer in Mice
• Gastroenterology, sous presse, 2012 (résumé)

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Menée sur un modèle murin, cette étude montre qu'une supplémentation en acide folique peut prévenir un cancer de l'estomac lié à la bactérie Helicobacter pylori en augmentant le niveau global de méthylation de l'ADN et en réduisant l'inflammation gastrique

“Folic Acid Increases Global DNA Methylation and Reduces Inflammation to Prevent Helicobacter-Associated Gastric Cancer in Mice”

• Gonda, Tamas A.;Kim, Young-In;Salas, Martha C.;Gamble, Mary V.;Shibata, Wataru;Muthupalani, Sureshkumar;Sohn, Kyoung-Jin;Abrams, Julian;Fox, James G.;Wang, Timothy C.;Tycko, Benjamin

Previous studies have suggested that dietary folic acid (FA) can protect against certain types of cancers. However the findings have varied and the mechanisms by which FA exerts chemopreventive effects remain to be clarified. We examined the effects of FA supplementation on DNA methylation, gene expression and gastric dysplasia in a transgenic mouse model that is etiologically and histologically well matched with human gastric cancers. Hypergastrinemic mice (INS-GAS) infected with Helicobacter felis were studied at multiple stages of gastric dysplasia and early cancer with FA supplementation initiated both at weaning and later in life. Global DNA methylation was assessed by a methylation sensitive cytosine incorporation assay, bisulfite pyrosequencing of B1 repetitive elements and immunohistochemistry (IHC) with anti-5-methylcytosine. We also profiled gene expression in the same tissues. We found a decrease in global DNA methylation and tissue folate and an increase in serum ...

Mots clés : Estomac; Prévention (Chimioprévention)

Menée sur des lignées cellulaires humaines de cancer du côlon, cette étude montre que le resvératrol, un polyphénol présent dans le raisin, peut inhiber l'activation du facteur de transcription NF-κB par les lipopolysaccharides et réduire l'inflammation

Anti-inflammatory effects of resveratrol occur via inhibition of lipopolysaccharide-induced NF-κB activation in Caco-2 and SW480 human colon cancer cells
• British Journal of Nutrition, pp. 1-10, 2012 (résumé)

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Menée sur des lignées cellulaires humaines de cancer du côlon, cette étude montre que le resvératrol, un polyphénol présent dans le raisin, peut inhiber l'activation du facteur de transcription NF-κB par les lipopolysaccharides et réduire l'inflammation

“Anti-inflammatory effects of resveratrol occur via inhibition of lipopolysaccharide-induced NF-κB activation in Caco-2 and SW480 human colon cancer cells”

• Panaro,Maria Antonietta;Carofiglio,Vito;Acquafredda,Angela;Cavallo,Pasqua;Cianciulli,Antonia

Resveratrol, a polyphenol abundantly found in grapes and red wine, exhibits beneficial health effects due to its anti-inflammatory properties. In the present study, we evaluated the effect of resveratrol on inflammatory responses induced by lipopolysaccharide (LPS) treatment of human intestinal Caco-2 and SW480 cell lines. In the LPS-treated intestinal cells, resveratrol dose-dependently inhibited the expression of inducible NO synthase (iNOS) mRNA as well as protein expression, resulting in a decreased production of NO. In addition, Toll-like receptor-4 expression was significantly diminished in LPS-stimulated cells after resveratrol pre-treatment. To investigate the mechanisms by which resveratrol reduces NO production and iNOS expression, we examined the activation of inhibitor of κB (IκB) in LPS-stimulated intestinal cells. Results demonstrated that resveratrol inhibited the phosphorylation, as well as the degradation, of the IκB complex. Overall, these results show that ...

Mots clés : Colon-rectum; Prévention (Chimioprévention)

Cette étude montre que la metformine, un antidiabétique oral, peut réduire la production d'espèces réactives oxygénées d'origine endogène et responsables d'altérations de l'ADN

Metformin reduces endogenous reactive oxygen species and associated DNA damage
• Cancer Prevention Research, sous presse, 2012 (résumé)

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Cette étude montre que la metformine, un antidiabétique oral, peut réduire la production d'espèces réactives oxygénées d'origine endogène et responsables d'altérations de l'ADN

“Metformin reduces endogenous reactive oxygen species and associated DNA damage”

• Algire, Carolyn;Moiseeva, Olga;Deschenes-Simard, Xavier;Amrein, Lilian;Petruccelli, Luca A;Birman, Elena;Viollet, Benoit;Ferbeyre, Gerardo;Pollak, Michael N

Pharmacoepidemiological studies provide evidence that use of metformin, a drug commonly prescribed for type II diabetes, is associated with a substantial reduction in cancer risk. Experimental models show that metformin inhibits the growth of certain neoplasms by cell autonomous mechanisms such as activation of AMP kinase with secondary inhibition of protein synthesis, or by an indirect mechanism involving reduction in gluconeogenesis leading to a decline in insulin levels and reduced proliferation of insulin-responsive cancers. Here we show that metformin attenuates paraquat-induced elevations in reactive oxygen species (ROS), and related DNA damage and mutations, but has no effect on similar changes induced by H202, indicating a reduction in endogenous ROS production. Importantly, metformin also inhibited Ras-induced ROS production and DNA damage. Our results reveal previously unrecognized inhibitory effects of metformin on ROS production and somatic cell mutation, providing a novel ...