Vegetables, but not pickled vegetables, are negatively associated with the risk of breast cancer.

Yu, Hyejin,Hwang, Ji-Yun,Ro, Jungsil,Kim, Jeongseon,Chang, Namsoo Lawrence Erlbaum Associates, Publishers [etc.] 2010 Nutrition and cancer Vol.62 No.4

<P>This study investigated the association between pickled vegetable consumption and the risk of breast cancer using a validated food frequency questionnaire. A total of 358 patients with breast cancer who were matched to 360 healthy controls by age (using a 5-yr age distribution) were recruited from the National Cancer Center in South Korea. After adjusting for nondietary risk factors, total vegetable intake was inversely associated with risk of breast cancer. However, unlike nonpickled vegetables, pickled vegetable intake and its proportion relative to total vegetables were positively associated with the risk of breast cancer, and this association was more profound and consistent when pickled vegetable intake was considered as a proportion relative to total vegetables (odds ratio [OR] = 6.24, 95% confidence interval [CI] = 3.55-10.97; P for trend <0.001 for highest vs. lowest quartiles of intake) than as the absolute consumed amount (OR = 2.47, 95% CI = 1.45-4.21; P for trend = 0.015 for highest vs. lowest quartiles of intake). These results suggest that not only the amount of total vegetable intake but also the amounts of different types of vegetable (i.e., pickled or nonpickled) and their proportions relative to total vegetables are significantly associated with the risk of breast cancer.</P>

Dietary Factors Affecting Thyroid Cancer Risk: A Meta-Analysis.

Cho, Young Ae,Kim, Jeongseon Lawrence Erlbaum Associates, Publishers [etc.] 2015 Nutrition and cancer Vol.67 No.5

<P>Some dietary factors are proposed to affect thyroid carcinogenesis, but previous studies have reported inconsistent findings. Therefore, we performed a meta-analysis, including 18 eligible studies, to clarify the role of dietary factors in the risk of thyroid cancer. The relative risks (RRs) with 95% confidence intervals (95% CIs) were estimated to assess the association and heterogeneity tests and subgroup and sensitivity analyses, and bias assessments were performed. When the results from all studies were combined, dietary iodine, fish, and cruciferous vegetable intake were not associated with thyroid cancer. However, when the data were divided by geographic location based on iodine availability, a slight increase in the risk of thyroid cancer was observed among those consuming a high total amount of fish in iodine nondeficient areas (RR: 1.18; 95% CI: 1.03-1.35; P for heterogeneity = 0.282). When excluding the studies examining a single food item and hospital-based controls, a high intake of cruciferous vegetables was associated with an increased risk of thyroid cancer in iodine-deficient areas (RR: 1.43; 95% CI: 1.18-1.74; P for heterogeneity = 0.426). This meta-analysis implies that the role of dietary factors, such as fish and cruciferous vegetables, in thyroid cancer risk can differ based on iodine availability.</P>

Magnolol suppresses vascular endothelial growth factor-induced angiogenesis by inhibiting Ras-dependent mitogen-activated protein kinase and phosphatidylinositol 3-kinase/Akt signaling pathways.

Kim, Ki Mo,Kim, No Soo,Kim, Jinhee,Park, Jong-Shik,Yi, Jin Mu,Lee, Jun,Bang, Ok-Sun Lawrence Erlbaum Associates, Publishers [etc.] 2013 Nutrition and cancer Vol.65 No.8

<P>Magnolol, a hydroxylated biphenyl compound isolated from Magnolia officinalis, has been reported to possess anticancer activity. Recent studies have also demonstrated that magnolol inhibits cell growth and induces the apoptosis of cancer cells. However, the effects of magnolol on vascular endothelial growth factor (VEGF)-induced angiogenesis in endothelial cells have not been studied. In the present study, we have used human umbilical vein endothelial cells (HUVECs) to investigate the antiangiogenic effect and molecular mechanism of magnolol. Magnolol inhibited the VEGF-induced proliferation, chemotactic motility and tube formation of HUVECs in vitro as well as the vessel sprouting of the aorta ex vivo. Furthermore, magnolol inhibited VEGF-induced Ras activation and subsequently suppressed extracellular signal-regulated kinase (ERK), phosphatidylinositol-3-kinase (PI3K)/Akt and p38, but not Src and focal adhesion kinase (FAK). Interestingly, the knockdown of Ras by short interfering RNA produced inhibitory effects that were similar to the effects of magnolol on VEGF-induced angiogenic signaling events, such as ERK and Akt/eNOS activation, and resulted in the inhibition of proliferation, migration, and vessel sprouting in HUVECs. In combination, these results demonstrate that magnolol is an inhibitor of angiogenesis and suggest that this compound could be a potential candidate in the treatment of angiogenesis-related diseases.</P>

Fisetin inhibits matrix metalloproteinases and reduces tumor cell invasiveness and endothelial cell tube formation.

Park, Jun Hyoung,Jang, Yoon-Jung,Choi, Yu Jung,Jang, Jin Wook,Kim, Joo-Hyon,Rho, Yang-Kook,Kim, In Ja,Kim, Hwa-Jung,Leem, Moon Jeong,Lee, Seung-Taek Lawrence Erlbaum Associates, Publishers [etc.] 2013 Nutrition and cancer Vol.65 No.8

<P>Matrix metalloproteinases (MMPs) play an important role in tissue remodeling during normal physiological situations and pathological implications such as tumor invasion and metastasis. MMP inhibitors were screened from extracts of medicinal herbs by an enzymatic assay using the MMP-14 catalytic domain. Among samples tested, a methanol extract of the root of Dalbergia odorifera T. CHEN (Leguminosae) showed the strongest inhibitory activity. The inhibitory component was purified through fractionation methods and identified as fisetin, abundant in many fruits and vegetables. In addition to inhibition of MMP-14, fisetin inhibits MMP-1, MMP-3, MMP-7, and MMP-9, more efficiently than a naturally occurring MMP inhibitor tetracycline. Fisetin dose-dependently inhibits proliferation of fibrosarcoma HT-1080 cells and human umbilical vascular endothelial cells (HUVECs), MMP-14-mediated activation of proMMP-2 in HT-1080 cells, invasiveness of HT-1080 cells, and in vitro tube formation of HUVECs. Therefore, fisetin could be valuable as a chemopreventive agent against cancer and a lead compound for development of therapeutic MMP inhibitors.</P>

Piceatannol Inhibits Phorbol Ester-Induced NF-kappa B Activation and COX-2 Expression in Cultured Human Mammary Epithelial Cells.

Liu, Dan,Kim, Do-Hee,Park, Jong-Min,Na, Hye-Kyung,Surh, Young-Joon Lawrence Erlbaum Associates, Publishers [etc.] 2009 Nutrition and cancer Vol.61 No.6

<P>There are multiple lines of evidence supporting that inflammation is causally linked to carcinogenesis. Abnormal upregulation of cyclooxygenase-2 (COX-2), a rate-limiting enzyme in the prostaglandin biosynthesis, has been implicated in carcinogenesis. Trans-3,4,3',5'-tetrahydroxystilbene (piceatannol), a naturally occurring hydroxylated stilbene with potent anti-inflammatory and antioxidative activities, has been shown to inhibit the proliferation of several cancer cells by inducing apoptosis or blocking cell cycle progression. In this study, we examined the effect of piceatannol on activation of the nuclear transcription factor NF-kappa B, one of the major transcription factors that regulate proinflammatory COX-2 gene transcription, in human mammary epithelial (MCF-10A) cells treated with the tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA). When pretreated to MCF-10A cells, piceatannol markedly inhibited TPA-induced NF-kappa B DNA binding to a greater extent than resveratrol and oxyresveratrol, stilbene analogs structurally related to piceatannol. Piceatannol also inhibited TPA-induced phosphorylation and degradation of Ikappa Balpha as well as nuclear translocation of the phosphorylated form of p65, the functionally active subunit of NF-kappa B. Likewise, TPA-induced expression of COX-2 was abrogated by piceatannol pretreatment. The thiol reducing agent dithiothreitol abolished the inhibitory effects of piceatannol on NF-kappa B DNA binding activity, suggesting that piceatannol may directly modify NF-kappa B or its regulator through reaction with the cysteine thiol(s).</P>

Lunasin is prevalent in barley and is bioavailable and bioactive in in vivo and in vitro studies.

Jeong, Hyung Jin,Jeong, Jin Boo,Hsieh, Chia Chien,Hernandez-Ledesma, Blanca,de Lumen, Ben O Lawrence Erlbaum Associates, Publishers [etc.] 2010 Nutrition and cancer Vol.62 No.8

<P>Lunasin, a unique 43-amino acid peptide found in a number of seeds, has been shown to be chemopreventive in mammalian cells and in a skin cancer mouse model. To elucidate the role of cereals in cancer prevention, we report here the prevalence, bioavailability, and bioactivity of lunasin from barley. Lunasin is present in all cultivars of barley analyzed. The liver and kidney of rats fed with lunasin-enriched barley (LEB) show the presence of lunasin in Western blot. Lunasin extracted from the kidney and liver inhibits the activities of HATs (histone acetyl transferases), yGCN5 by 20% and 18% at 100 nM, and PCAF activity by 25% and 24% at 100 nM, confirming that the peptide is intact and bioactive. Purified barley lunasin localizes in the nuclei of NIH 3T3 cells. Barley lunasin added to NIH 3T3 cells in the presence of the chemical carcinogen MCA activates the expression of tumor suppressors p21 and p15 by 45% and 47%, decreases cyclin D1 by 98%, and inhibits Rb hyperphosphorylation by 45% compared with the MCA treatment alone. We conclude that lunasin is prevalent in barley, bioavailable, and bioactive and that consumption of barley could play an important role of cancer prevention in barley-consuming populations.</P>

2,4-bis (p-hydroxyphenyl)-2-butenal (HPB242) induces apoptosis via modulating E7 expression and inhibition of PI3K/Akt pathway in SiHa human cervical cancer cells.

Kim, Man Sub,Kim, Jung Hee,Bak, Yesol,Park, Yun Sun,Lee, Dong Hun,Kang, Jeong Woo,Shim, Jung-Hyun,Jeong, Heon Sang,Hong, Jin Tae,Yoon, Do Young Lawrence Erlbaum Associates, Publishers [etc.] 2012 Nutrition and cancer Vol.64 No.8

<P>The Maillard reaction is a chemical reaction occurring between an amino acid and a reducing sugar, usually requiring thermal processing. Maillard reaction products (MRPs) have antioxidant, antimutagenic, and antibacterial effects, and although 2,4-bis (p-hydroxyphenyl)-2-butenal (HPB242), a fructose-tyrosine MRP, appears to inhibit proliferation of cancer cells, its mechanism of action has not been studied in detail. We found that HPB242 treatment modulated expression of cyclins and tumor suppressor genes in SiHa human cervical cancer cell lines: cyclins and phospho-pRB were downregulated, whereas the expression of CDK inhibitors and p53 was enhanced. HPB242 induced apoptosis dose-dependently by suppressing E7 expression and leading to sub-G1 cell-cycle arrest in SiHa cell lines; treatment also led to the proteolytic cleavage of caspase-3, -9, and poly (ADP-ribose) polymerase. Moreover, HPB242 upregulated Fas expression, altered expressions of pro- and antiapoptotic factors, and also inhibited nuclear translocation of nuclear factor κB and phosphorylation of IκB. HPB242 treatment decreased phosphatidyl inositol-3 kinase and p-Akt expression levels, demonstrating that this survival pathway may also be inhibited by HPB242. Cumulatively, HPB242 promotes apoptosis by influencing E7 expression, inducing cell-cycle arrest at sub-G1 phase, and promoting both intrinsic (mitochondrial) and extrinsic (Fas-dependent) apoptosis in SiHa human cervical cancer cells.</P>

Children’s interpretation of ambiguous focus in sentence with “only”

패터슨,K. B. Lawrence Erlbaum Associates, Inc. 2006 Language acquisition Vol.13 No.3

Endometrial cancer in relation to coffee, tea, and caffeine consumption: a prospective cohort study among middle-aged women in Sweden.

Weiderpass, Elisabete,Sandin, Sven,Lof, Marie,Oh, Jin-Kyoung,Inoue, Manami,Shimazu, Taichi,Tsugane, Shoichiro,Adami, Hans-Olov Lawrence Erlbaum Associates, Publishers [etc.] 2014 Nutrition and cancer Vol.66 No.7

<P>This study aimed to add to prospective data on the possible inverse association between coffee consumption and endometrial cancer risk, already supported by several case-control studies. Coffee and tea consumption and possible confounding factors were assessed among 42,270 women aged 30-49 years at enrollment in 1991-1992 in the Swedish Women's Lifestyle and Health cohort study, with complete follow-up through 2009. We calculated caffeine intake per day; Cox proportional hazard models were used to estimate multivariable relative risks (mRR) for endometrial cancer with 95% confidence intervals (CIs). One hundred forty-four endometrial cancers were diagnosed during follow-up. Women with and without endometrial cancer had a similar mean daily coffee consumption (549 vs. 547 g), tea consumption (104 vs. 115 g), and caffeine intake (405 vs. 406 mg). Compared to those consuming <2 cups of coffee per day, women consuming >3 cups had a mRR of 1.56 (95% CI: 0.94-2.59; P for trend = 0.17). Compared with the lowest tertile of caffeine intake, the highest tertile had a mRR of 1.32 (95% CI: 0.87-1.99; P for trend = 0.27). Our study provides no convincing evidence of an association between coffee consumption, tea consumption, or caffeine intake and endometrial cancer risk among middle-aged women.</P>

Nobiletin induces apoptosis and potentiates the effects of the anticancer drug 5-fluorouracil in p53-mutated SNU-16 human gastric cancer cells.

Moon, Jeong Yong,Cho, Moonjae,Ahn, Kwang Seok,Cho, Somi Kim Lawrence Erlbaum Associates, Publishers [etc.] 2013 Nutrition and cancer Vol.65 No.2

<P>Nobiletin is a typical polymethoxyl flavone from citrus fruits that has anticancer properties, but the molecular mechanism of its inhibitory effects on the growth of p53-mutated SNU-16 human gastric cancer cells has not been explored. In this study, nobiletin was found to be effective at inhibiting the proliferation of SNU-16 cells than other flavonoids. Nobiletin induced the death of SNU-16 cells through apoptosis, as evidenced by the increased cell population in the sub-G1 phase, the appearance of fragmented nuclei, an increase in the Bax/Bcl-2 ratio, the proteolytic activation of caspase-9, an increase in caspase-3 activity, and the degradation of poly(ADP-ribose) polymerase (PARP) protein. We found that the combination of nobiletin plus the anticancer drug 5-fluorouracil (5-FU) reduced the viability of SNU-16 cells in a concentration-dependent manner and exhibited a synergistic anticancer effect (combination index = 0.38) when 5-FU was used at relatively low concentrations. The expression of p53 protein increased after treatment with 5-FU, but not nobiletin, whereas the expression of p21 (WAF1/CIP1) protein increased after treatment with nobiletin, but not 5-FU. The cellular responses to nobiletin and 5-FU occurred through different pathways. The results of this study suggest the potential application of nobiletin to the enhancement of 5-FU efficiency in p53 mutant tumors.</P>