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Special Issue "Diet and Cancer Prevention"

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A special issue of Nutrients (ISSN 2072-6643).

Deadline for manuscript submissions: closed (31 July 2011)

Special Issue Editor

Guest Editor
Dr. Cindy D. Davis

Director of Grants and Extramural Activities, Office of Dietary Supplements, National Institutes of Health, 6100 Executive Blvd., Room 3B01, MSC 7517, Bethesda, MD 20892-7517, USA
Website | E-Mail
Phone: 301-496-0168
Fax: +301 4801845
Interests: diet and cancer prevention; selenium; vitamin D

Special Issue Information

Dear Colleagues,

Malignant cells are characterized by numerous alterations in multiple signaling pathways that promote proliferation, inhibit apoptosis, promote angiogenesis in the case of solid tumors, and enable cancer cells to invade and migrate through tissues. Bioactive dietary components have been shown to modify all of the major signaling pathways which are deregulated in cancer. Estimates suggest that 30-70% of all cancer cases might be preventable by diet, depending on the dietary components and the specific type of cancer. A better understanding of the bioactive components present in food, the mechanism(s) of action of these dietary components towards cancer prevention, the critical intake of dietary components, duration and when they should be provided to optimize the desired physiological response is needed. The purpose of this special issue is to focus on the role of bioactive food components in cancer prevention.

Dr. Cindy D. Davis
Guest Editor

Keywords

  • diet
  • cancer prevention
  • nutrigenomics
  • molecular targets
  • cell proliferation
  • apoptosis
  • angiogenesis
  • metastasis
  • inflammation

Published Papers (6 papers)

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Research

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Open AccessArticle Caffeinated Coffee, Decaffeinated Coffee and Endometrial Cancer Risk: A Prospective Cohort Study among US Postmenopausal Women
Nutrients 2011, 3(11), 937-950; doi:10.3390/nu3110937
Received: 3 August 2011 / Revised: 19 October 2011 / Accepted: 21 October 2011 / Published: 2 November 2011
Cited by 19 | PDF Full-text (194 KB) | HTML Full-text | XML Full-text
Abstract
There is plausible biological evidence as well as epidemiologic evidence to suggest coffee consumption may lower endometrial cancer risk. We evaluated the associations between self-reported total coffee, caffeinated coffee and decaffeinated coffee, and endometrial cancer risk using the Women’s Health Initiative Observational Study
[...] Read more.
There is plausible biological evidence as well as epidemiologic evidence to suggest coffee consumption may lower endometrial cancer risk. We evaluated the associations between self-reported total coffee, caffeinated coffee and decaffeinated coffee, and endometrial cancer risk using the Women’s Health Initiative Observational Study Research Materials obtained from the National Heart, Lung, and Blood Institute Biological Specimen and Data Repository Coordinating Center. Our primary analyses included 45,696 women and 427 incident endometrial cancer cases, diagnosed over a total of 342,927 person-years of follow-up. We used Cox-proportional hazard models to evaluate coffee consumption and endometrial cancer risk. Overall, we did not find an association between coffee consumption and endometrial cancer risk. Compared to non-daily drinkers (none or < 1 cup/day), the multivariable adjusted hazard ratios for women who drank ≥4 cups/day were 0.86 (95% confidence interval (CI) 0.63, 1.18) for total coffee, 0.89 (95% CI 0.63, 1.27) for caffeinated coffee, and 0.51 (95% CI 0.25, 1.03) for decaf coffee. In subgroup analyses by body mass index (BMI) there were no associations among normal-weight and overweight women for total coffee and caffeinated coffee. However among obese women, compared to the referent group (none or < 1 cup/day), the hazard ratios for women who drank ≥2 cups/day were: 0.72 (95% CI 0.50, 1.04) for total coffee and 0.66 (95% CI 0.45, 0.97) for caffeinated coffee. Hazard ratios for women who drank ≥2 cups/day for decaffeinated coffee drinkers were 0.67 (0.43–1.06), 0.93 (0.55–1.58) and 0.80 (0.49–1.30) for normal, overweight and obese women, respectively. Our study suggests that caffeinated coffee consumption may be associated with lower endometrial cancer risk among obese postmenopausal women, but the association with decaffeinated coffee remains unclear. Full article
(This article belongs to the Special Issue Diet and Cancer Prevention)
Open AccessArticle Differential Mammary Gland Development in FVB and C57Bl/6 Mice: Implications for Breast Cancer Research
Nutrients 2011, 3(11), 929-936; doi:10.3390/nu3110929
Received: 3 August 2011 / Revised: 5 October 2011 / Accepted: 11 October 2011 / Published: 25 October 2011
Cited by 7 | PDF Full-text (421 KB) | HTML Full-text | XML Full-text
Abstract
A growing body of research suggests a linkage between pubertal mammary gland development and environmental factors such as diet as modifiers of long term breast cancer risk. Much of this research is dependent upon mouse models, which may vary between studies. However, effects
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A growing body of research suggests a linkage between pubertal mammary gland development and environmental factors such as diet as modifiers of long term breast cancer risk. Much of this research is dependent upon mouse models, which may vary between studies. However, effects may be strain dependent and further modified by diet, which has not been previously examined. Therefore, the objective of the present study was to determine whether mammary gland development differs between FVB and C57Bl/6 strains on diets containing either n-6 or n-3 polyunsaturated fats. Developmental measures related to onset of puberty and mammary gland development differed between strains. Mice fed the n-3 polyunsaturated fatty acids (PUFA) diet were shown to have lower numbers of terminal end buds, a marker of mammary gland development. This study helps to further clarify differences in development and dietary response between FVB and C57Bl/6 mice in order to more appropriately relate mammary gland research to human populations. Full article
(This article belongs to the Special Issue Diet and Cancer Prevention)
Open AccessArticle Hydroxytyrosol Protects against Oxidative DNA Damage in Human Breast Cells
Nutrients 2011, 3(10), 839-857; doi:10.3390/nu3100839
Received: 27 July 2011 / Revised: 8 September 2011 / Accepted: 14 September 2011 / Published: 13 October 2011
Cited by 40 | PDF Full-text (1172 KB) | HTML Full-text | XML Full-text
Abstract
Over recent years, several studies have related olive oil ingestion to a low incidence of several diseases, including breast cancer. Hydroxytyrosol and tyrosol are two of the major phenols present in virgin olive oils. Despite the fact that they have been linked to
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Over recent years, several studies have related olive oil ingestion to a low incidence of several diseases, including breast cancer. Hydroxytyrosol and tyrosol are two of the major phenols present in virgin olive oils. Despite the fact that they have been linked to cancer prevention, there is no evidence that clarifies their effect in human breast tumor and non-tumor cells. In the present work, we present hydroxytyrosol and tyrosol’s effects in human breast cell lines. Our results show that hydroxytyrosol acts as a more efficient free radical scavenger than tyrosol, but both fail to affect cell proliferation rates, cell cycle profile or cell apoptosis in human mammary epithelial cells (MCF10A) or breast cancer cells (MDA-MB-231 and MCF7). We found that hydroxytyrosol decreases the intracellular reactive oxygen species (ROS) level in MCF10A cells but not in MCF7 or MDA-MB-231 cells while very high amounts of tyrosol is needed to decrease the ROS level in MCF10A cells. Interestingly, hydroxytyrosol prevents oxidative DNA damage in the three breast cell lines. Therefore, our data suggest that simple phenol hydroxytyrosol could contribute to a lower incidence of breast cancer in populations that consume virgin olive oil due to its antioxidant activity and its protection against oxidative DNA damage in mammary cells. Full article
(This article belongs to the Special Issue Diet and Cancer Prevention)
Open AccessArticle Deficiency in the 15 kDa Selenoprotein Inhibits Human Colon Cancer Cell Growth
Nutrients 2011, 3(9), 805-817; doi:10.3390/nu3090805
Received: 1 August 2011 / Revised: 15 August 2011 / Accepted: 29 August 2011 / Published: 5 September 2011
Cited by 13 | PDF Full-text (572 KB) | HTML Full-text | XML Full-text
Abstract
Selenium is an essential micronutrient for humans and animals, and is thought to provide protection against some forms of cancer. These protective effects appear to be mediated, at least in part, through selenium-containing proteins (selenoproteins). Recent studies in a mouse colon cancer cell
[...] Read more.
Selenium is an essential micronutrient for humans and animals, and is thought to provide protection against some forms of cancer. These protective effects appear to be mediated, at least in part, through selenium-containing proteins (selenoproteins). Recent studies in a mouse colon cancer cell line have shown that the 15 kDa selenoprotein (Sep15) may also play a role in promoting colon cancer. The current study investigated whether the effects of reversing the cancer phenotype observed when Sep15 was removed in mouse colon cancer cells, were recapitulated in HCT116 and HT29 human colorectal carcinoma cells. Targeted down-regulation of Sep15 using RNAi technology in these human colon cancer cell lines resulted in similarly decreased growth under anchorage-dependent and anchorage-independent conditions. However, the magnitude of reduction in cell growth was much less than in the mouse colon cancer cell line investigated previously. Furthermore, changes in cell cycle distribution were observed, indicating a delayed release of Sep15 deficient cells from the G0/G1 phase after synchronization. The potential mechanism by which human colon cancer cells lacking Sep15 revert their cancer phenotype will need to be explored further. Full article
(This article belongs to the Special Issue Diet and Cancer Prevention)

Review

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Open AccessReview Chemopreventive Activity of Vitamin E in Breast Cancer: A Focus on γ- and δ-Tocopherol
Nutrients 2011, 3(11), 962-986; doi:10.3390/nu3110962
Received: 29 September 2011 / Revised: 20 October 2011 / Accepted: 3 November 2011 / Published: 14 November 2011
Cited by 28 | PDF Full-text (288 KB) | HTML Full-text | XML Full-text
Abstract
Vitamin E consists of eight different variants: α-, β-, γ-, and δ-tocopherols (saturated phytyl tail) and α-, β-, γ-, and δ-tocotrienols (unsaturated phytyl tail). Cancer prevention studies with vitamin E have primarily utilized the variant α-tocopherol. To no avail, a majority of these
[...] Read more.
Vitamin E consists of eight different variants: α-, β-, γ-, and δ-tocopherols (saturated phytyl tail) and α-, β-, γ-, and δ-tocotrienols (unsaturated phytyl tail). Cancer prevention studies with vitamin E have primarily utilized the variant α-tocopherol. To no avail, a majority of these studies focused on variant α-tocopherol with inconsistent results. However, γ-tocopherol, and more recently δ-tocopherol, have shown greater ability to reduce inflammation, cell proliferation, and tumor burden. Recent results have shown that γ-enriched mixed tocopherols inhibit the development of mammary hyperplasia and tumorigenesis in animal models. In this review, we discuss the possible differences between the variant forms, molecular targets, and cancer-preventive effects of tocopherols. We recommend that a γ-enriched mixture, γ- and δ-tocopherol, but not α-tocopherol, are promising agents for breast cancer prevention and warrant further investigation. Full article
(This article belongs to the Special Issue Diet and Cancer Prevention)
Open AccessReview Induction of Cancer Cell Death by Isoflavone: The Role of Multiple Signaling Pathways
Nutrients 2011, 3(10), 877-896; doi:10.3390/nu3100877
Received: 1 August 2011 / Revised: 29 September 2011 / Accepted: 9 October 2011 / Published: 17 October 2011
Cited by 24 | PDF Full-text (1166 KB) | HTML Full-text | XML Full-text
Abstract
Soy isoflavones have been documented as dietary nutrients broadly classified as “natural agents” which plays important roles in reducing the incidence of hormone-related cancers in Asian countries, and have shown inhibitory effects on cancer development and progression in vitro and in vivo,
[...] Read more.
Soy isoflavones have been documented as dietary nutrients broadly classified as “natural agents” which plays important roles in reducing the incidence of hormone-related cancers in Asian countries, and have shown inhibitory effects on cancer development and progression in vitro and in vivo, suggesting the cancer preventive or therapeutic activity of soy isoflavones against cancers. Emerging experimental evidence shows that isoflavones could induce cancer cell death by regulating multiple cellular signaling pathways including Akt, NF-κB, MAPK, Wnt, androgen receptor (AR), p53 and Notch signaling, all of which have been found to be deregulated in cancer cells. Therefore, homeostatic regulation of these important cellular signaling pathways by isoflavones could be useful for the activation of cell death signaling, which could result in the induction of apoptosis of both pre-cancerous and/or cancerous cells without affecting normal cells. In this article, we have attempted to summarize the current state-of-our-knowledge regarding the induction of cancer cell death pathways by isoflavones, which is believed to be mediated through the regulation of multiple cellular signaling pathways. The knowledge gained from this article will provide a comprehensive view on the molecular mechanism(s) by which soy isoflavones may exert their effects on the prevention of tumor progression and/or treatment of human malignancies, which would also aid in stimulating further in-depth mechanistic research and foster the initiation of novel clinical trials. Full article
(This article belongs to the Special Issue Diet and Cancer Prevention)
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