bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract 594: Effect of caloric restriction and high fat diet on azoxymethane-induced carcinogenesis in LETO and OLETF rats
Authors: Takasu Chie , Takahashi Tetsuyuki , Izumi Keisuke 
Published: August 2012

Abstract
We showed recently that diabetic and mildly obese Otsuka Long-Evans Tokushima Fatty (OLETF) rats are more susceptible to azoxymethane (AOM)-induced Zymbal gland and intestinal carcinogenesis than control Long-Evans Tokushima Otsuka (LETO) rats. In the present study, we examined the effect of caloric restriction (CR) and high-fat diet (HFD) on AOM-induced carcinogenesis in these strains. Experiment 1: Six-week-old male LETO and OLETF rats (n=21) were given s.c. injections of 15 mg/kg AOM once weekly for 3 weeks, then fed, Group 1) control diet, Group 2) 20% CR diet, or Group 3) HFD (control diet with 10% safflower oil), and killed at 36 weeks of age. In LETO rats, the incidences of colon tumors (adenoma plus adenocarcinoma) in Groups 1-3 were 45%, 33% and 55%, respectively. Average number of tumors/rat in CR group was fewer than that in HFD group (P&lt;0.05). In OLETF rats, the incidences of colon tumors in Groups 1-3 were 76%, 48% and 62%, respectively. Zymbal gland tumors in CR group developed later than those in control and HFD groups in OLETF rats. Experiment 2: Male LETO and OLETF rats (n=5) were fed control diet, 20% CR diet or HFD for 5 weeks, and killed at 24 weeks of age. In LETO rats, serum triglyceride, total cholesterol, insulin and leptin levels decreased by 20% CR, and increased by HFD compared to the control group. In OLETF rats, those levels decreased by 20% CR, and increased by HFD except leptin. Expression of hepatic IGF-1 and Sirt-1 mRNA elevated by 20% CR in both strains. The liver of OLETF rat HFD group showed severe fatty change histologically. In conclusion, 20% CR inhibited, and HFD promoted colon carcinogenesis in LETO rats. In OLETF rats, 20% CR inhibited, but HFD did not promote colon carcinogenesis because of early development of Zymbal gland tumors. Hyperinsulinemia and/or hyperlipidemia may exert the promoting effect in rat carcinogenesis.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 594. doi:1538-7445.AM2012-594
Abstract 6: Investigating the functional significance of FGFR2 SNP status in breast cancer
Authors: Robbez-Masson Luisa , Grose Richard 
Published: August 2012

Abstract
Familial Breast cancer is now seen as a polygenic disease. Although several major susceptibility genes, including BRCA1 and BRCA2, have been identified in several cases, breast cancer susceptibility seems to arise from a large number of genetic loci, each conferring a minor influence on overall risk. Recent genome-wide association studies (GWAS), have identified several SNPs that associate with increased risk of breast cancer. Some of the most significant are located in the second intron of the fibroblast growth factor receptor 2 (FGFR2) gene, indicating that the association with breast cancer is mediated through regulation of FGFR2. Functional SNPs within this region map to binding sites for the transcription factors Oct-1, Runx2 and C/EBPβ. Preliminary studies have shown that the Runx2 site is functional only in the minor, disease associated allele, resulting in increased expression of FGFR2 in cancer from patients homozygous for that allele. Moreover, the increased risk conferred by the minor FGFR2 allele is associated most strongly with ER+ breast tumours, suggesting a potential interaction between the two pathways. Our approach is to study the functional role of this new risk locus on the biology of cancer at the regulatory level. To study allele-specific gene expression (ASGE), we are using two surrogate SNP markers in the coding region of FGFR2, rs755793 and rs1047100. Taqman analysis of cDNA and genomic DNA from a panel of breast cancer samples allow us to evaluate the degree of SNP-dependent differential expression in a high throughput manner. Thus our study ultimately will allow us to test the hypothesis that the disease-associated allele of rs2981578 increases FGFR2 expression. Additionally, a genome editing approach using Zinc Finger Nucleases (ZFN) allows us to target the putative ‘regulatory’ SNP in breast cancer cell lines. A change, as small as a single nucleotide, can be made on MFC7 cell line to create new in vitro models that only differ in SNP status. These cell based models will be crucial in the study of the influence of FGFR2 SNPs in tumour initiation and progression. Thus our study will allow for the first time, investigation of the true physiological function of SNP status on breast cancer cell line behaviour.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 6. doi:1538-7445.AM2012-6
Abstract 604: The ginger compound, 6-shogaol, inhibits prostate cancer cell growth through reduced activation of signal transducer and activator of transcription 3 (Stat3)
Authors: Saha Achinto , Silver Eric S. , Sessler Jonathan L. , DiGiovanni John 
Published: August 2012

Abstract
Prostate cancer is the most common non-skin neoplasm and second leading cause of death in men in the USA with an estimated 240,890 new cases and 33,720 deaths from this disease in 2011. The risk for developing prostate cancer increases with age and overall 1 in 6 men will be diagnosed with this disease. Despite much recent progress, prostate cancer continues to represent a major cause of cancer-related mortality and morbidity in men. Ginger (Zingiber officinale) has been widely used as a spice, and as a medicinal herb in traditional herbal medicine. It is a natural dietary ingredient with antioxidant, anti-inflammatory, and anticarcinogenic properties. Ginger contains several pungent constituents such as gingerols, shogaols, paradols, and gingerdiols. The shogaols are predominant constituents in the dried ginger. Several studies reported that 6-shogaol has anticancer and anti-inflammatory activity. However the mechanism(s) involved in anticancer effect of 6-shogaol has not been clearly elucidated. In the current study, we found that 6-shogaol inhibited the proliferation of human prostate cancer cells including LNCap, DU145 and PC-3 in a concentration dependent manner. In order to find the mechanism associated with the antiproliferative effect of 6-Shogaol, we performed Western blotting and found that this compound inhibited the constitutive (DU145) and IL-6 (LNCap and DU145) induced phosphorylation of Stat3(Tyr705). 6-shogaol also inhibited constitutive and IL-6 induced phosphorylation of Stat3(Ser727) in both cell lines. It also decreased the level of several Stat3 regulated molecules such as cyclin D1 and survivin. Next we measured the apoptosis inducing activity of 6-shogaol and found that this compound induced apoptosis in LNCap and DU145 cells also in a concentration dependent manner. In order to confirm the mechanism involved in apoptosis induction, we measured the level of various apoptosis markers and found that 6-shogaol induced cleavage of PARP and caspase7 in both LNCap and DU145 cell lines. Quantitative real time PCR data showed that 6-shogaol decreased the mRNA level of Bcl2, CCL5, IL-6, IL-7 and increased the expression of Bax, p21, IRF1 and SOCS1. Collectively, the current data lead us to suggest that 6-shogaol may possess properties for further consideration as a therapeutic and/or chemopreventive agent for human prostate cancer.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 604. doi:1538-7445.AM2012-604
Abstract 606: Inhibitory effects of piceatannol on tumor angiogenesis and lung metastasis in the 4T1 mammary cancer model
Authors: Song Hyerim , Kim Eun Ji , Park Jung Han Yoon 
Published: August 2012

Abstract
Piceatannol (trans-3,4,3′,5′-tetrahydroxystilbene) is a polyphenol found in Rheum undulatum, grapes, red wine, and berries and has been shown to exert anticarcinogenic effects. In the present study, we determined whether oral administration of piceatannol inhibits solid tumor growth, angiogenesis, and lung metastasis of mammary cancer cells. 4T1 cells (5 x 104 cells) were injected into the mammary fat pad of syngeneic, 6-week old, female BALB/c mice. One day after, the mice were subjected to gavage for 30 days with piceatannol (0, 10, or 20 mg/kg body weight/day). Oral piceatannol treatment induced a significant reduction in the growth of solid tumors. Immunohistochemical staining of tumor tissues revealed that the expression of Ki67 (prototypic cell cycle related nuclear antigen), cyclin D1, cyclin A, cyclin-dependent kinase (CDK)4, CDK2, hypoxia-inducible factor 1, vascular endothelial growth factor, CD31 (platelet endothelial cell adhesion molecule-1) and LYVE-1 (lymphatic vessel endothelial receptor 1) was significantly decreased in the mice received 20 mg/kg piceatannol as compared to mice received vehicle. Piceatannol significantly increased the numbers of TUNEL-positive, apoptotic cells in tumor tissues, which was accompanied by increased Bax and cleaved caspase-3 expression and reduced Bcl-2 expression. Additionally, piceatannol feeding reduced the number and volume of pulmonary tumor nodules, which was accompanied by reduced expression of matrix metalloproteinase-9 in lung tissues. Piceatannol induced a significant reduction in the blood levels of chemokine ligand (CXCL) 16, CXCL13 (BCA-1), interleukin-16, macrophage colony-stimulating factor, monocyte chemoattractant protein-1, triggering receptor expressed on myeloid cells-1, stromal cell-derived factor-1, and plasminogen activator inhibitor-1 compared to the vehicle-fed mice. The present results indicate that piceatannol has an ability to inhibit breast cancer development and metastasis and this effect is attributable to its ability to inhibit tumor angiogenesis, lymphangiogenesis and reduce the blood levels of a broad variety of cytokines and chemokines.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 606. doi:1538-7445.AM2012-606
Abstract 610: The role of oxidative stress in the growth inhibitory and proapoptotic effects of brown button mushrooms (Agaricus bisporus) in human prostate cancer cells
Authors: Xu Tongtong , Beelman Robert , Lambert Joshua 
Published: August 2012

Abstract
An increasing body of clinical and in vivo/in vitro studies suggests that some chemical components in specialty mushrooms like maitake (Grifola frondosa) may exert cancer preventive effects. Edible mushrooms, which have a similar content of polysaccharides, proteoglycans, steroids, etc., have been less well-studied for their anticancer and cancer preventive activity. For example, only one publication has reported the inhibition of human breast cancer cell growth by brown button mushrooms (Agaricus bisporus). The objectives of our research were to evaluate the anti-prostate cancer activity and mechanism(s) of action of brown button mushroom extracts. A hot water extract was prepared from freeze-dried brown button mushroom powder and fractioned with hexane and ethyl acetate. The IC50 of ethyl acetate fraction from brown button mushrooms (BBEA) was ∼0.1mg/ml. The inhibitory potency against LNCaP human prostate cancer cells correlated with the total phenol content, suggesting that these may be the active anticancer components. To further investigate the mechanisms of BBEA's anticancer effects, we examined the production of H2O2 by the extract using FOX assay and examined oxidative stress, proapoptotic, and cell cycle arrest markers by western blot. BBEA (0.1mg/ml) produced ∼50µM H2O2 under cell culture conditions after 6h. The expression of the oxidative stress marker, αH2A.X, in LNCaP cells was enhanced by BBEA after 12 and 24h, suggesting that pro-oxidative effects may be a possible anticancer mechanism. BBEA also increased caspase-3 and PARP cleavage and reduced the expression of Cyclin D1 and Cyclin E2, suggesting induction of apoptosis and cell cycle arrest by BBEA. In summary, this is the first report of the anticancer effects of phenolic compounds in brown button mushrooms and these results demonstrate that further study of BBEA is warranted. Microarray studies are currently under way to better characterize the anticancer activity of BBEA against human prostate cancer cells.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 610. doi:1538-7445.AM2012-610
Abstract 614: Increased oxidative DNA damage in human prostate cancer and its relationship to GSTP1 expression
Authors: Kanwal Rajnee , Fu Pingfu , Gupta Sanjay 
Published: August 2012

Abstract
The pi-class glutathione S-transferase (GSTP1) has been described as a ‘caretaker’ gene, as it actively protects the cell from oxidative genome damage mediated by carcinogens and electrophilic compounds. Loss of GSTP1 expression via promoter hypermethylation is one of the most common epigenetic alterations observed in human prostate cancer. Silencing of GSTP1 can increase prostate epithelial cells more vulnerable to both oxidant and electrophile carcinogens and causes genetic aberrations leading to increased risk of tumor progression. Observations suggest that increased reactive oxygen species (ROS) causes DNA damage in cells, as measured by 8-hydroxy-2′-deoxyguanosine (8-OHdG), contribute to increased incidence of prostate cancer. However there are no studies which demonstrate correlation between GSTP1 protein/activity and DNA damage in prostate cancer. We took a panel of 24 human prostate specimens obtained after surgery which comprised of matched primary tumor and adjacent nontumorous (benign) prostate tissues. Oxidative DNA damage, GSTP1 protein expression and its activity, and GSTP1 promoter methylation was assessed. The 8-OHdG levels in DNA of prostate cancer tissues ranged from 0.307 to 0.609ng/μg DNA, whereas the levels in benign tissue range from 0.156 to 0.322ng/μg DNA, respectively. 8-OHdG and GSTP1 promoter methylation levels were higher in adenocarcinoma compared to their benign counterparts, which positively correlated with the loss of GSTP1 activity. The GSTP1 protein activity of prostate cancer tissues ranged from 738.2 to 1754.4ng/mg protein, whereas the levels in benign tissue range from 1728.6 to 2580.4ng/mg protein. The loss of GSTP1 expression in cells might increase their vulnerability to cytotoxicity and reactive oxygen species (ROS)-mediated DNA damage. In further experiments, human prostate carcinoma LNCaP cells, which contains a silenced GSTP1 gene, was genetically modified to constitutively express high levels of GSTP1. Introduction of GSTP1 lowered endogenous ROS levels in LNCaP cells; treatment with H2O2 significantly reduced ROS and 8-OHdG in LNCaP-GSTP1 cells, compared to parental cell line. Furthermore, treatment with green tea polyphenols to LNCaP cells caused re-expression of GSTP1 which protected the cells from H2O2-mediated DNA damage compared to pretreated cells. These results suggest that oxidative stress-induced DNA damage may be an important measure for primary prevention of prostate cancer.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 614. doi:1538-7445.AM2012-614
Abstract 620: Chemoprevention of hydroxybutyl(butyl)nitrosamine (OH-BBN)-induced mouse urinary bladder cancer by the kava chalcone flavokawain A
Authors: Xu Xia , Liu Zhongbo , Liu Shuman , Li Xuesen , Zi Xiaolin 
Published: August 2012

Abstract
About 75% of human bladder cancers are associated with cigarette smoking or exposure to industrial carcinogens. Kava roots have been traditionally used to prepare beverage and herb medicine in the South Pacific Island nations (Fiji, Vanutu, Samoa, etc.) for thousands of years. Recently, an epidemiological study has linked high kava consumption to lower incidences of cancers, including lung and bladder cancers, despite the presence of many smokers in the populations of the South Pacific Islands. We therefore examined the potential of flavokawain A, a predominant chalcone isolated from the kava plant for prevention of mouse urinary bladder cancer induced by the organ-specific and tobacco-smoking related nitrosamine OH-BBN. B6D2F1 mice at 8 weeks of age were gavaged 7.5 mg OH-BBN once per week for 12 weeks. In the standard prevention protocol, 0.1% FKA or vehicle food was administered as a dietary supplement to each group of mice beginning 1 week before the first OH-BBN administration and ending 32 weeks after the initial OH-BBN treatment. Dietary feeding of OH-BBN treated mice with 0.1% flavokawain A in the mouse diet decreased bladder wet weight by about 57% (Bladder weights for control versus flavokawain A were 74.18 ± 16.7 versus 32 ± 1.5 mg; P&lt;0.01). In the standard promotion protocol, 0.1% FKA or vehicle food was given 1 week after the final OH-BBN administration for 19 weeks. Flavokawain A also significant reduced the bladder wet weight by about 27% (Bladder weights for control versus flavokawain A were 89.4 ± 23.4 versus 65.5 ± 10.6 mg; p&lt;0.05). To increase the incidence of palpable OH-BBN induced bladder tumors, we extended 7.5mg OH-BBN treatment once per week for one more week up to a total of 13 weeks. In this modified promotion protocol, the percentage of palpable tumors in control group has reached to about 53%, which is similar to that reported by published literatures. Dietary feeding of 0.6% flavokawain A significantly decrease bladder wet weight by 73% (Bladder weights for control versus flavokawain A were 314.9 ± 106.7 versus 87.3 ± 15.2 mg, p=0.0265). In addition, we showed that flavokawain A induced activities of phase II enzyme (i.e. glutathione S-transferase and quinone reductase) in different organs (bladder, liver, prostate, etc.) of mice. Taken together, these results suggest that flavokawain A deserves further investigation for bladder cancer chemoprevention by targeting smoking or carcinogens exposed populations.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 620. doi:1538-7445.AM2012-620
Abstract 621: The importance of antioxidant, antiangiogenesis and immune stimulation in cancer
Authors: Thornthwaite Jerry T. , Respess Henry , Shah Hare , Peeples William , Thornthwaite Kyle , Thornthwaite Bonita , Kent Patrick , Allen Mark 
Published: August 2012

Abstract
In our quest over the last nine years to find comprehensive over-the- counter supplements, designed to facilitate current classical treatments in fighting diseases, include antiangiogenic, immune and antioxidant defense systems. These supplements include, in part, Acetyl L-Carnitine (ALC), Alpha Lipoic Acid (ALA), Coenzyme Q10 (CoQ10), Curcumin with Piperine, Genistein, Lentinan, N-AcetylCysteine (NAC), Resveratrol, selenium, Vitamin B Complex, Vitamin C, Vitamin E and zinc. These ingredients have been demonstrated, either individually or collectively, to have antioxidant, anti-angiogenesis, and immune stimulation and antioxidant properties. Furthermore, the scientific literature supports direct cancer cell cytotoxicity for Curcumin, Geinstein and NAC. The dietary supplement activities are supported by over 50,000 references in the scientific literature (PubMed.com) and over 150 clinical trials (clinicaltrials.gov), not including the human-cancer publications (23,000) and clinical trials (2,100) with zinc and the vitamins. From the literature there is evidence that some of the antiangiogenesis components that affect the majority if not all pathways of angiogenesis, such as Curcumin, Genistein and NAC, actually stimulate the in vivo production of natural antiangiogenic compounds that include Angiostatin, Endostatin and Thrombospotin 1. All of the components play a role in serving as either water or lipid soluble (able to cross the blood-brain barrier) antioxidants. Curcumin, Genistein, Resveratrol, Lentinen, NAC, zinc, selenium and the B and C vitamins all stimulate the immune system. Except for ALC and CoQ10, the other components show anti-inflammatory activity. ALC, Resveratrol along with the B and C vitamins are helpful in treating fatigue. The components that help protect the brain and promote nerve regeneration include ALA, CoQ10, Resveratrol, NAC, selenium, zinc and the B/C vitamins. In conclusion, effective prevention and treatment from and for diseases such as cancer, heart disease and immune deficiency will require multiple compounds.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 621. doi:1538-7445.AM2012-621
Abstract 646: Soy food intake and risk of lung cancer: Evidence from the Shanghai Women's Health Study and a meta-analysis
Authors: Yang Gong , Shu Xiao-Ou , Chow Wong-Ho , Zhang Xianglan , Li Hong-Lan , Ji Bu-Tian , Cai Hui , Wu Sheng-Hui , Gao Yu-Tang , Zheng Wei 
Published: August 2012

Abstract
Background: Recent large-scale clinical trials raised concerns regarding increased risk of aggressive lung cancer and lung cancer mortality among users of postmenopausal estrogen therapy. Soy and its phytoestrogens have been shown to act as a natural estrogen antagonist and have cancer-inhibitory activities in experimental studies. Objective: We prospectively evaluated the association of soy food intake with lung cancer risk, overall and by tumor aggressiveness, and perform a meta-analysis of published data. Methods: Included in this analysis were 71,550 women recruited in the Shanghai Women's Health Study, a population-based cohort study. Usual soy food intake was assessed at baseline and re-assessed during follow-up through in-person interviews. Previous studies were identified through a MEDLINE search. Results: During a mean follow-up of 9.1 years, 370 incident lung cancer cases were identified; 340 were lifetime never smokers. After adjustment for potential confounders, soy food intake was inversely associated with subsequent risk of lung cancer; the hazard ratio (HR) for the highest compared with lowest quintile of intake was 0.63 (95% CI: 0.44 - 0.90; P trend = 0.004). This inverse association appeared predominately among women with a later age at menopause (P interaction = 0.01) and varied by tumor aggressiveness as defined by length of survival (&lt;12 versus β12 months), with corresponding HR of 0.49 for more aggressive lung cancer versus 0.76 for less aggressive lung cancer (P heterogeneity = 0.057). Similar inverse associations were observed for isoflavone intake. A meta-analysis of seven studies conducted among never smokers found a summary odds ratio of 0.59 (95% CI: 0.49 - 0.71) for the highest versus lowest categories of soy or isoflavone intake. Conclusion: This study suggests that soy food consumption may reduce lung cancer risk in nonsmoking women, particularly for aggressive lung cancer, and its effect may be modified by endogenous estrogens.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 646. doi:1538-7445.AM2012-646