bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract 4823: Isoflavones from phytoestrogens and colorectal cancer risk: A nested case-control study within the Korean Multicenter Cancer Cohort.
Authors: Yeo Yohwan , Ko Kwang-Pil , Ma Seung-Hyun , Yang Jae Jeong , Shin Aesun , Park Sue K. , Chang Soung-Hoon , Shin Hai-Rim , Kang Daehee , Yoo Keun-Young 
Published: August 2014

Abstract
Background
The association of soybean products related with colorectal cancer risk is inconsistent. This may be due to information bias from measuring food intake by questionnaires and different degrees of bias according to study design. To assess the association between soybean products and colorectal cancer, we directly measured phytoestrogen biomarkers in a nested case-control study in Korea.
Methods
Study population was composed of 101 cases and 398 matched controls matched for age within 5-year, sex, area and year at recruitment of cases within the Korean Multicenter Cancer Cohort. The concentrations of four biomarkers in the plasma were measured by Liquid Chromatography-Mass Spectrometry. Conditional logistic regression models were used to calculate the odds ratio and 95% confidence intervals (CI).
Results
Median plasma concentrations of genistein, daidzein, glycitein and enterolactone were not statistically significant between cases and controls. However, there was a significant trend of decreasing risk according to an increase of genistein (p=0.03). This protective effect of genistein was more prominent in women. There was no association between other plasma concentrations of isoflavones or lignans and colorectal cancer.
Conclusions
High serum concentrations of isoflavones, i.e, genistein, were associated with a decreased trend of colorectal cancer, especially in women.
Citation Format: Yohwan Yeo, Kwang-Pil Ko, Seung-Hyun Ma, Jae Jeong Yang, Aesun Shin, Sue K. Park, Soung-Hoon Chang, Hai-Rim Shin, Daehee Kang, Keun-Young Yoo. Isoflavones from phytoestrogens and colorectal cancer risk: A nested case-control study within the Korean Multicenter Cancer Cohort. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 4823. doi:10.1158/1538-7445.AM2013-4823
Abstract 4843: Genetic variants in Notch signaling pathway and ovarian cancer.
Authors: Xu Enping , Lu Karen H. , Hildebrandt Michelle AT , Huang Maosheng , Wu Xifeng , Liang Dong 
Published: August 2014

Abstract
The Notch signaling pathway drives proliferation, differentiation, apoptosis, cell fate choices, and has a key role in the regulation of stem cells in a variety of cancers. In this study, we applied a pathway-based approach to evaluate the associations between single nucleotide polymorphisms in Notch signaling pathway and ovarian cancer risk, survival, and response to chemotherapy. Towards this, we systematically genotyped 139 SNPs from 10 genes in the pathway in 339 Caucasian ovarian cancer cases and 349 Caucasian healthy controls. Individually, four SNPs were significantly associated with the ovarian cancer risk. The most significant SNP was NOTCH4: rs397081, with an adjusted odds ratio (OR) of 0.38 (95% CI = 0.22-0.66, P=0.00057). A highly significant gene-dosage effect was observed for these top variants (P for trend &lt; 0.00001) with those carrying ≥ 3 risk genotypes having a nearly 6-fold increase in risk (OR = 5.67, 95% CI = 2.58 - 12.44] . Classification and regression tree (CART) analysis further revealed potential higher order gene-gene interactions between these four SNPs, with the highest risk group having almost 7-fold increased risk. Ten SNPs were significantly associated with overall survival, of which the strongest association was identified for NOTCH4: rs3131290 (OR = 0.48, 95% CI = 0.27-0.84). Cumulative effect analysis showed that multiple adverse genotypes had a significant dose-dependent effect on overall survival. The median survival times for individuals carrying ≤3, 4 to 6, and ≥7 of these adverse genotypes were &gt;186.3, 62.82, and 28.58 months, respectively. Similarly, a significant association was identified between a poor response to platinum-based chemotherapy and the number of unfavorable SNPs (P for trend &lt; 0.0001). Our findings suggest that genetic variants in the Notch signaling pathway are associated with ovarian cancer risk and could serve as potential predictors of clinical outcomes in ovarian cancer patients.
Citation Format: Enping Xu, Karen H. Lu, Michelle AT Hildebrandt, Maosheng Huang, Xifeng Wu, Dong Liang. Genetic variants in Notch signaling pathway and ovarian cancer. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 4843. doi:10.1158/1538-7445.AM2013-4843
Abstract 4852: Comparison of manual and automated scoring of androgen receptor staining in prostate tissue.
Authors: Ondracek Rochelle P. , Mohler James L. , Pilarz Catherine , McEvoy Sarah , Kasza Karin , Morrison Carl , Marshall James 
Published: August 2014

Abstract
Although manual scoring is generally used to evaluate the presence of androgen receptor (AR) protein as detected by immunohistochemistry in tissue, manual evaluation is tedious, inefficient and subjective. Therefore, manual scoring is not feasible for the evaluation of large numbers of patients. In this study, a technician (CP) rated AR staining in tissue sections of 3 tissue microarrays (TMAs) constructed from 3 cores each of benign and malignant tissue from 134 patients who underwent radical prostatectomy between 1993 and 2006 at Roswell Park Cancer Institute. The manual scorer randomly sampled 50 nuclei from each core and scored each nuclei as not stained (score =0), or lightly (score = 1), moderately (score=2) or darkly (score = 3) stained. The average staining intensity was recorded per patient across the benign cores, and across the tumor cores. Automated staining used the Image Pro image processing program, in which the entire core was scanned, all nuclei segmented and average intensity values per between 0 (completely black) and 255 (completely white) were determined for each nucleus. The mean staining score for each core is calculated by taking the average of all the identified nuclei in the core, and an average intensity is calculated per patient across the benign cores, and across the malignant cores.
The Pearson correlation between manual and automated scoring was 0.76. When stratified by benign or malignant tissue, the Pearson correlation between manual and automated scoring was 0.75 (benign) and 0.78 (malignant).
Automated scoring of AR staining is comparable to manual scoring of AR in prostate tissue. In light of the greater efficiency of automated scoring, future evaluations of immunohistochemical staining may be usefully conducted using automated scoring of nuclei.
Citation Format: Rochelle P. Ondracek, James L. Mohler, Catherine Pilarz, Sarah McEvoy, Karin Kasza, Carl Morrison, James Marshall. Comparison of manual and automated scoring of androgen receptor staining in prostate tissue. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 4852. doi:10.1158/1538-7445.AM2013-4852
Abstract 4856: Association between breast cancer and constitutively decreased TGFBR1 signaling.
Authors: Henegan John C. , Moore-Smith Lakisha , Yi Nengjun , Zhang Kui , Ahsan Habibul , Whittemore Alice S. , Pasche Boris ,   BCFR Co-Investigators
Published: August 2014

Abstract
Background: We previously identified a hypomorphic TGF-β type 1 receptor variant (TGFBR1*6A) that is associated with cancer risk, has impaired TGF-β signaling capability and enhances the migration and invasion of breast cancer cells. Two recent large meta-analyses of case control studies have found a significant association between TGFBR1*6A and risk of breast cancer (ORs 1.16,1.01-1.34; 1.15,1.01-1.31). Rs7034462 is a single nucleotide polymorphism (SNP) in a noncoding region more than 9 kilobases upstream of TGFBR1 exon 1, which has been shown to be associated with decreased TGFBR1 expression. In this study we tested the hypothesis that rs7034462 may be associated with breast cancer risk.
Methods: rs7034462 was genotyped in DNA obtained from patients with breast cancer and healthy controls recruited by the Breast Cancer Family Registry. The samples in this multinational cohort were primarily from younger patients (average age 49.4 and 48.1 years for cases and controls, respectively, at time of interview).
Results: Using the Cockerham model, rs7034462 was found to be associated with breast cancer risk under the dominance genetic effect but, unexpectedly, there was a significant decreased association with breast cancer for this SNP under the additive genetic effect for this model.
SNP Cases Controls Cockerham Model Genetic Effect Odds Ratio 95% CI P rs7034462 (n = 2,934) 1509 1425 Additive 0.60 0.38-0.93 0.020 Dominance 2.09 1.29-3.38 0.002
Conclusion: rs7034462 heterozygotes have an increased risk of breast cancer but rare homozygotes have a decreased risk. This is the first evidence in humans that constitutively decreased TGFBR1-mediated TGF-β signaling is associated with breast cancer risk.
Citation Format: John C. Henegan, Lakisha Moore-Smith, Nengjun Yi, Kui Zhang, Habibul Ahsan, Alice S. Whittemore, Boris Pasche, BCFR Co-Investigators. Association between breast cancer and constitutively decreased TGFBR1 signaling. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 4856. doi:10.1158/1538-7445.AM2013-4856
Abstract 4865: Lack of efficacy of aerosolized resveratrol on B[A]P induced pulmonary adenoma formation in A/J mice.
Authors: Seabloom Donna , Gailbraith Art , Antonides Jenny , Wuertz Beverly , Wattenberg Lee , Ondrey Frank G. 
Published: August 2014

Abstract
Natural products constitute an emerging class of compounds for carcinogenesis prevention in a variety of solid tumor malignancies. Resveratrol is a compound that has outstanding efficacy on cancer prevention in in vitro carcinogenesis models but rapid solubility and metabolism limits its efficacy in animal models when delivered in the diet. However, if regional or topical delivery could be achieved effects of first pass metabolism might be avoided. In the present study, we sought to use aerosol resveratrol to examine whether it could inhibit Benzpyrene inducd pulmonary adenoma formation in A/J mice. Eight groups of 24 mice were given Benzpyrene and aerosol resveratrol was started either one week or 8 weeks after the conclusion of the Benzpyrene. Aerosolized resveratrol (1.0, 0.3, and 0.1 mg/kg) was delivered 5x per week Monday through Friday for weeks 2- 15. At the conclusion of the experiment animals were sacrificed and adenomas counted. We found that the animals tolerated the aerosol resveratrol without toxicity and without weight differences between all groups. Animals formed between 9 and 12 adenomas, on average throughout all groups. There were no effects of aerosol resveratrol on either early stage or late stage carcinogenesis, nor were there any trends between the groups. We conclude that the high water solubility of resveratrol likely allowed for its rapid transit and metabolism through the bronchioles and lung parenchyma and that possibly chemical modifications of resveratrol that allow for its deposition in the lung fields in a way to increase its residence time would allow for better efficacy.
Citation Format: Donna Seabloom, Art Gailbraith, Jenny Antonides, Beverly Wuertz, Lee Wattenberg, Frank G. Ondrey. Lack of efficacy of aerosolized resveratrol on B[A]P induced pulmonary adenoma formation in A/J mice. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 4865. doi:10.1158/1538-7445.AM2013-4865
Abstract 4868: Dietary resveratrol promotes breast cancer progression in immunocompromised mice.
Authors: Castillo-Pichardo Linette , Cubano Luis A. , Rodríguez-Orengo José F. , Dharmawardhane Suranganie 
Published: August 2014

Abstract
Resveratrol, a polyphenol from grapes and red wine has been widely studied due to its beneficial effects against cardiovascular diseases and cancer. However, our group and others have provided evidence for a dual cancer promoting or inhibitory role for resveratrol in breast cancer, dependent on the concentration. Moreover, much of the reported inhibitory effects of resveratrol are from studies with high non-physiological concentrations. Herein, we investigated the effects of low (0.5 and 5 mg/kg body weight) and moderate concentrations (50 mg/kg body weight) of resveratrol on mammary tumor growth, using immunocompromised mice. Our findings suggest promotion of mammary tumor growth and metastasis by resveratrol at all concentrations tested in tumors derived from the low metastatic estrogen receptor (ER)α(-), ERβ(+) MDA-MB-231 and the highly metastatic ER(-) MDA-MB-435 cancer cell lines. Additionally, the activity of the migration/invasion regulator Rac, which we have previously shown to be regulated by resveratrol in vitro, was measured in tumors from resveratrol treated mice. Our results show a significant induction of tumoral Rac activity and a trend in increased expression of the Rac downstream effector PAK1, Akt, and jun kinase (JNK) following resveratrol treatment. Taken together, our findings implicate low concentrations of resveratrol in potential promotion of breast cancer. Because of this dual role of resveratrol on cancer progression, measuring circulating plasma levels of resveratrol becomes critical and could be used as a prognostic tool for resveratrol's responsiveness. Since, detection and quantification of low levels of resveratrol is limited by the sensitivity of existing methodologies, we developed a rapid UPLC-tandem MS method to quantify resveratrol from plasma. This method requires minimal sample preparation and allows the quantification of resveratrol in mouse plasma at lower levels and shorter retention times than those previously reported by similar methodologies. This study was supported by DoD/BCRP W81XWH-08-1-0258 to LCP, DoD/BCRP W81XWH-07-1-0330 to SD, the UCC Pilot Project Program, the UCC Postdoctoral Program sponsored by the PR Science, Technology and Research Trust, and the Title V PPOHA grant number PO31M105050 from U.S. Department of Education to UCC.
Citation Format: Linette Castillo-Pichardo, Luis A. Cubano, José F. Rodríguez-Orengo, Suranganie Dharmawardhane. Dietary resveratrol promotes breast cancer progression in immunocompromised mice. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 4868. doi:10.1158/1538-7445.AM2013-4868
Abstract 4872: Gynostemma pentaphyllum saponins alter the gut microflora composition and convert dysbiosis to eubiosis state in xenograft nude mice.
Authors: Chen Lei , Tai William C.S. , Leung Frederick CC , Singh Manreet , Hsiao W.L. Wendy 
Published: August 2014

Abstract
Increasing evidence has shown that the gut microflora may have a crucial role in many diseases, including cancers. In our previous studies, we have demonstrated that treatment with total saponins of Gynostemma pentaphyllum (GpS) exerts anti-cancer effects in cellular and animal models. Our study showed that an unnatural shift in the microflora composition was observed in nude mice with xenografted tumors induced by GFP/Ras cells. To investigate the potential association between the anti-cancer effect of GpS and the gut microflora, we first investigated whether GpS treatment would affect the microflora composition. Enterobacterial Repetitive Intergenic Consensus sequence-based PCR (ERIC-PCR) was used to analyze the bacterial genomic DNA from the fecal samples of the experimental mice. ERIC-PCR analysis revealed that gut microbiota communities were able to restore back to the non-tumor state (day 0)) after treatment with GpS for 10 days. In addition, we found that GpS treatment can increase the levels of certain beneficial bacteria, including Bifidobacterium spp. and Lactobacillus spp. Furthermore, we defined the detailed changes in the gut microbiome by pyrosequencing of the 16S rRNA gene sequences. We found that Bacteroidetes/Firmicutes ratio showed an increased trend upon GpS treatment in xenograft nude mice. Furthermore, GpS altered certain species of bacteria, including the Clostridium cocleatum and Bacteroides acidifaciens, which have well-documented beneficial effects. In conclusion, this study has demonstrated GpS can potentially regulate and balance the gut microbial ecosystem by increasing symbionts. However, further investigation is required on whether this alteration of the gut microflora is the cause or consequence of the drug action. [This study was partially supported by FRG2/11-12/102 to WLWHsiao]
Citation Format: Lei Chen, William C.S. Tai, Frederick CC Leung, Manreet Singh, W.L. Wendy Hsiao. Gynostemma pentaphyllum saponins alter the gut microflora composition and convert dysbiosis to eubiosis state in xenograft nude mice. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 4872. doi:10.1158/1538-7445.AM2013-4872
Abstract 4883: Zinc and prostate cancer: a systematic review.
Authors: Mahmoud Abeer M. , Al-alem Umaima , Shah Ebony , Batai Ken , Dabbous Firas , Ali Mohamed , Kittles Rick 
Published: August 2014

Abstract
Background: Zinc is involved in many essential cellular functions. It has been shown that the prostate contains high concentrations of zinc, but zinc levels decrease in prostate cancer tissues. Although, experimental evidence implicates zinc in the pathogenesis of prostate cancer, epidemiological data are inconsistent. We conducted a systematic review of the literature to summarize the evidence regarding the association between zinc and prostate cancer.
Methods: Relevant studies were identified by searching PubMed and the Cochrane Library databases through November 2012 and reviewing reference lists of retrieved articles. Inclusion criteria were original and peer-reviewed publications reporting the association between zinc intake or status and prostate cancer outcomes (diagnosis, progression). No reviews, editorials, or comments were included. Two investigators abstracted study information and evaluated quality independently using standardized forms.
Results: Sixteen studies met inclusion criteria, including 3 cohorts, 2 nested case-control, 10 case-control, and 1 randomized clinical trial, with a total of 111,288 participants and 11,681 cases of prostate cancer. All studies measured the association between zinc levels and prostate cancer. In most studies, regardless of the study design or source of zinc, the highest dose of zinc was associated with a modest elevation of odds of prostate cancer. Four studies had decreased odds of prostate cancer for the highest dose of zinc but the confidence interval crossed one. There was evidence of a dose-response relationship and subgroup analysis revealed a protective effect of high zinc intake among advanced prostate cancer cases.
Conclusions: Although the level of zinc in prostate cancer tissue is reduced, studies assessing the association of zinc intake and prostate cancer have yielded inconsistent results. We performed a systematic review to assess the role of zinc in prostate cancer. As a result of this systematic review, the evidence is still insufficient to recommend zinc supplementation for cancer patients in clinical practice.
Citation Format: Abeer M. Mahmoud, Umaima Al-alem, Ebony Shah, Ken Batai, Firas Dabbous, Mohamed Ali, Rick Kittles. Zinc and prostate cancer: a systematic review. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 4883. doi:10.1158/1538-7445.AM2013-4883
Abstract 4909: Olig2 phosphorylation by CDK2 implicated in glioma proliferation.
Authors: Fu Jun , Koul Dimpy , Zheng Siyuan , Singh Vivek , Yao Jun , Zheng Yanhua , Lu Zhimin , Sulman Erik P. , Lang Frederick F. , Yung Alfred W.K 
Published: August 2014

Abstract
Oligodendrocyte transcription factor 2 (Olig2) is an important proneural transcription factor that regulates early development of the central nervous system and formation of glioma. Although recent studies established the role of developmentally regulated Olig2 phosphorylation in promoting the proliferation of both normal and malignant neural stem/progenitor cells, the molecular mechanisms by which Olig2 phosphorylation is regulated and functions as a pro-proliferative factor are not completely understood. Here we identified Olig2 as a critical phosphorylation target for cyclin-dependent kinase 2 (CDK2). CDK2 stabilizes and activates Olig2, thereby regulating G1-to-S phase progression by repressing the expression of Cyclin-dependent kinase inhibitor p27kip1. After phosphorylation by CDK2, Olig2 exerts pro-proliferative effects that are reflected in normal neural/glioma stem cells and in murine xenograft models of glioma. Olig2 phosphorylation regulates its binding to E-box sequence in p27 gene promoter and represses p27 expression. We show that constitutive p27 expression antagonizes CDK2-mediated Olig2 phosphorylation and attenuates cell proliferation both in in-vitro and in-vivo glioma models. Expression analysis of TCGA GBM samples also showed that high Olig2 expression is always accompanied with high CDK2 expression in the proneural, classical, and neural subclasses, which could provide a convincing evidence to use a CDK2 inhibitor to treat Olig2-high gliomas. Treatment with CDK2 inhibitor preferentially suppresses proliferation of Olig2-high glioma cells. Thus, we conclude that a CDK2 inhibitor could be of great therapeutic value in patients with Olig2-high glioma and Olig2 might be used as a biological marker for CDK2 inhibitors in the future studies.
Citation Format: Jun Fu, Dimpy Koul, Siyuan Zheng, Vivek Singh, Jun Yao, Yanhua Zheng, Zhimin Lu, Erik P. Sulman, Frederick F. Lang, Alfred W.K Yung. Olig2 phosphorylation by CDK2 implicated in glioma proliferation. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 4909. doi:10.1158/1538-7445.AM2013-4909