bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract 4819: Assessing the environmental factors in two Ontario communities with diverging colorectal cancer incidence rates .
Authors: Sritharan Jeavana , Kamaleswaran Rishikesan , McFarlan Ken , Lemonde Manon , George Clemon , Sanchez Otto 
Published: August 2014

Abstract
Colorectal cancer is the third most diagnosed cancer and second leading cause of cancer related deaths in Canada. As Ontario has the largest population in Canada, it also has great disparities in colorectal cancer incidence. The region of Timiskaming has the highest incidence for colorectal cancer, while the region of Peel has the lowest incidence for colorectal cancer in Ontario. There are no previously published studies regarding cancer or environmental risk factors performed in the Timiskaming region. The purpose of this study was to identify the dominant non-nutritional modifiable environmental risk factors in the region of Timiskaming compared to the reference region of Peel that may be associated with diverging colorectal cancer incidence rates. After reviewing the available published literature, a questionnaire assessment tool regarding environmental exposures was created. This questionnaire tool was created by combining standardized questionnaire tools available in the published literature that assessed environmental exposures. The questionnaire assessment tool was then utilized within a pilot study group followed by the Timiskaming and Peel participant communities. The tool assessed the exposures of tobacco smoking, alcohol use, pesticides/organochlorines, metal toxins, occupational exposures, and medical ionizing radiation. A total of 53 participants completed the questionnaire tool in Timiskaming, and a total of 61 participants completed the questionnaire tool in Peel. Findings indicate that there are dominant non-nutritional modifiable environmental risk factors in the region of Timiskaming that may be associated with colorectal cancer when compared to the region of Peel. The significant dominant environmental factors identified by Timiskaming participants were tobacco smoking, alcohol use, pesticides/organochlorines, and metal toxins. The findings also indicate that the Peel community may have important community health initiatives that can be used in the Timiskaming community to reduce the present colorectal cancer disparities. Following this study, it is imperative that recommendations are directed at a community level and relate to the assessment of potential non-nutritional modifiable environmental risk factors. While colorectal cancer disparities are evident, future research should help to understand the relationship between cancer disparities and environmental risk factors.
Citation Format: Jeavana Sritharan, Rishikesan Kamaleswaran, Ken McFarlan, Manon Lemonde, Clemon George, Otto Sanchez. Assessing the environmental factors in two Ontario communities with diverging colorectal cancer incidence rates . [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 4819. doi:10.1158/1538-7445.AM2013-4819
Abstract 4821: Plasma retinol, but not 25-OH vitamin D or vitamin E, is associated with increased survival in colorectal cancer patients.
Authors: Cooney Robert V. , Chai Weiwen , Franke Adrian A. , Caberto Christian , Wilkens Lynne R. , Kolonel Laurence N. , Custer Laurie , Morrison Cynthia , Le Marchand Loic 
Published: August 2014

Abstract
OBJECTIVE: To determine the association of lipid-soluble vitamin status with survival in colorectal cancer patients.
METHODS: Using stored patient plasma samples from a multiethnic population-based case-control study of colorectal cancer, we determined associations of post-treatment blood levels of retinol, 25 OH-vitamin D, and Vitamin E with survival. Patients (n = 455) were followed (mean of 8 years) after phlebotomy, during which time 20% died of colorectal cancer and 24% from other causes. Hazard ratios (HR) were estimated by Cox proportional hazards regression with adjustment for stage and age at diagnosis, ethnicity, sex, and smoking status.
RESULTS: A strong inverse association with all-cause mortality was observed for plasma retinol (Ptrend &lt;0.0001), with similar significant trends observed for both colorectal cancer-specific deaths and other causes of death (P for heterogeneity = 0.43). The inverse association between retinol and all cause mortality was consistently observed for both sexes, subjects of Caucasian and Japanese ancestry, and for both rectal cancer and colon cancer. Overall no significant associations were observed for plasma 25-OH vitamin D or vitamin E with survival.
CONCLUSIONS: Results are consistent with a direct relationship between low vitamin A status and poor survival among colorectal cancer patients. The absence of a significant association for 25-OH vitamin D levels with survival may be related to the generally higher circulating levels of 25-OH vitamin D in residents of Hawaii where the study was conducted, and results may differ in northern climates and in darker pigmented patients. If verified through larger prospective studies, future complementary intervention trials involving the assessment of vitamin A status and supplementation of individuals with inadequate levels may be warranted.
Citation Format: Robert V. Cooney, Weiwen Chai, Adrian A. Franke, Christian Caberto, Lynne R. Wilkens, Laurence N. Kolonel, Laurie Custer, Cynthia Morrison, Loic Le Marchand. Plasma retinol, but not 25-OH vitamin D or vitamin E, is associated with increased survival in colorectal cancer patients. [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 4821. doi:10.1158/1538-7445.AM2013-4821
Abstract 484: Intratumoral injection of CpG oligonucleotides induces the differentiation and reduces the immunosuppressive activity of myeloid-derived suppressor cells.
Authors: Shirota Hidekazu , Shirota Yuko , Klinman Dennis M. 
Published: August 2014

Abstract
Immunostimulatory CpG oligonucleotides (ODN) activate cells that express TLR9 and have been shown to improve the host's response to tumor Ags. Unfortunately, the immunosuppressive microenvironment that surrounds many cancers inhibits Agspecific cellular responses and thus interferes with CpG-mediated immunotherapy. Myeloid-derived suppressor cells (MDSC) represent an important constituent of this immunosuppressive milieu. Large numbers of MDSC are present in and near tumor sites where they inhibit the activity of Ag-specific T and NK cells. Current studies indicate that the delivery of CpG ODN directly into the tumor bed reduces the immunosuppressive activity of monocytic (CD11b+, Ly6G-, Ly6Chigh) MDSC. Monocytic MDSC express TLR9 and respond to CpG stimulation by 1) losing their ability to suppress T cell function, 2) producing Th1 cytokines, and 3) differentiating into macrophages with tumoricidal capability. These findings provide insight into a novel mechanism by which CpG ODN contribute to tumor regression, and they support intratumoral injection as the optimal route for their delivery.
Citation Format: Hidekazu Shirota, Yuko Shirota, Dennis M. Klinman. Intratumoral injection of CpG oligonucleotides induces the differentiation and reduces the immunosuppressive activity of myeloid-derived suppressor cells. [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 484. doi:10.1158/1538-7445.AM2013-484
Note: This abstract was not presented at the AACR Annual Meeting 2013 because the presenter was unable to attend.
Abstract 4857: Short overall telomere length and chromosome 17p-specific telomere length in peripheral blood leukocytes are associated with increased risk of esophageal adenocarcinoma.
Authors: Chen Meng , Gu Jian , Gong Yilei , Ajani Jaffer A. , Wu Xifeng 
Published: August 2014

Abstract
Esophageal adenocarcinoma (EAC) is a deadly cancer. The incidence of EAC has increased dramatically in the United States in the past three decades. The biological mechanisms of EAC development are not fully understood. Telomeres are specialized chromatin structures essential for the maintenance of chromosomal integrity. Telomere shortening in somatic tissues has been shown as an early event during carcinogenesis. Previous studies also suggested that constitutive short telomeres in peripheral blood leukocytes (PBLs) are associated with increased risks of several cancers, including esophageal cancer. In this study, we measured overall telomere length in PBLs using real-time PCR in a large case control study of 805 EAC cases and 805 age and gender-matched controls. Furthermore, we developed a fluorescence in site hybridization (FISH) based method to evaluate several chromosome-specific telomere length with the risk of EAC in a subset of subjects. The mean overall telomere length in cases was significantly shorter than that in controls (p&lt;0.001). Dichotomized at the median telomere length in controls, individuals with short PBL telomere length was associated with a 1.53-fold (95% CI, 1.26-1.87) increased risk of EAC. There was a significant dose-effect in quartile analysis: Individuals in quartile with the shortest telomeres showed a nearly 2-fold (95%CI: 1.47-2.57) elevated EAC risk compared to the reference group of the longest quartile of telomere length. In chromosome-specific telomere length analysis, we found that short chromosome 17p-specific telomere length (defined as the ratio of chromosome 17p-specific telomere length to overall telomere length), but not 2p- and 7q-specific telomere length, was associated with a significantly increased risk of EAC (OR=2.02, 95% CI, 1.00-4.08). This study validates that short overall telomere length in PBLs predisposes to EAC with a much larger sample size and supports the role of chromosome 17p aberrations in EAC development.
Citation Format: Meng Chen, Jian Gu, Yilei Gong, Jaffer A. Ajani, Xifeng Wu. Short overall telomere length and chromosome 17p-specific telomere length in peripheral blood leukocytes are associated with increased risk of esophageal adenocarcinoma. [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 4857. doi:10.1158/1538-7445.AM2013-4857
Abstract 4858: Mutant p53 depletion: a possible mechanism of inhibition of human prostate cancer by dietary phenethyl isothiocyanate.
Authors: Mi Lixin , Wang Thomas T.Y. , Huang Haiqiu , Fletcher Arnetta , Yu Lu , Wang Xiantao , Chung Fung-Lung 
Published: August 2014

Abstract
Phenethyl isothiocyanate (PEITC) derived from cruciferous vegetables has been shown to inhibit tumor growth by induction of apoptosis. Previously, we demonstrated that PEITC can selectively deplete mutant p53, but not the wild type. However, whether p53, wild type or mutant, plays functional roles in PEITC-induced growth inhibition, remains unsettled. We hypothesize that the direct binding to mutant p53 by PEITC followed by conformational changes, subsequently leading to its depletion or/and restoration to the wild type may constitute a mechanism by which PEITC induces apoptosis. To determine whether PEITC can deplete mutant p53 in vivo and whether its depletion is correlated with tumor inhibition and apoptosis, in this xenograft model study BALB-C Nu/Nu mice carrying prostate tumor cells with either mutant (DU145) or wild type p53 (LNCap) were fed diets with and without PEITC (5 micromol per gram diet) for 8 weeks. Tumors were harvested at the end of bioassay for immunohistochemistry and immunoblot studies. Results showed that the tumor volumes of both LNCap and DU145 were significantly decreased in the PEITC-treated animals, compared with that on a diet without PEITC. The p53 level detected by immunoblot showed a moderate, yet significant, decrease in DU145 tumors, but not in LNCap tumors. Immunohistochemistry assays were carried out to examine the apoptotic markers, such as TUNEL, and anti-proliferation marker Ki67 in tumors from the PEITC-treated vs. untreated mice. This study provides the first in vivo evidence that mutant p53 can be depleted in tumors of mice fed PEITC-containing diet and its depletion seems to correlate with growth inhibition in the mutant p53 tumors. These findings suggest that mutant p53 maybe further investigated as a possible novel target for cancer chemoprevention and therapy by PEITC. (Supported by NCI grant CA100853)
Citation Format: Lixin Mi, Thomas T.Y. Wang, Haiqiu Huang, Arnetta Fletcher, Lu Yu, Xiantao Wang, Fung-Lung Chung. Mutant p53 depletion: a possible mechanism of inhibition of human prostate cancer by dietary phenethyl isothiocyanate. [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 4858. doi:10.1158/1538-7445.AM2013-4858
Abstract 4861: Identification of novel potential targets for selenomethionine-mediated chemoprevention in colorectal carcinoma mouse model via proteomics analysis.
Authors: Rahman Md. Mujibur , Kwon Jee Young , Seo Young Rok 
Published: August 2014

Abstract
Despite some controversy, selenomethionine (SeMet) mediated protection against colorectal carcinoma (CRC) might be a very promising non-cytotoxic option. However, responsive molecular targets and underlying mechanisms of SeMet mediated chemoprevention are still unclear. Our aim was to discover new targets of SeMet mediated chemoprevention in CRC using proteomics analysis. We found dietary SeMet supplementation before carcinoma initiation effectively suppressed polyp incidence and dysplastic lesions without any adverse effects. To determine chemopreventive targets of SeMet, we employed 2-dimensional gel electrophoresis based proteomics analysis in CRC mouse model. Pretreatment with SeMet apparently modulated the expression of 30 proteins with functions in major processes like chronic inflammation, oxidative-stress and apoptosis as discovered through pathway analysis with Pathway studio software.We validated four proteins selected from pathway analysis including prohibitin, purine nucleoside phosphorylase, annexin 2 and c-reactive protein by immuno-histochemistry. 8-hydroxy-2′-deoxyguanosine (8-OHdG), a known oxidative stress marker was decreased by SeMet treatment in CRC mice as seen by immunohistochemistry. Further network analysis was done among these new four validated proteins, 8-OHdG and colorectal cancer. These four proteins found by proteomics analysis might be considered as potential chemopreventive biomarkers of SeMet against colon cancer and can help develop and improve approaches in preventive, therapeutic and prognostic aspects.
Citation Format: Md. Mujibur Rahman, Jee Young Kwon, Young Rok Seo. Identification of novel potential targets for selenomethionine-mediated chemoprevention in colorectal carcinoma mouse model via proteomics analysis. [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 4861. doi:10.1158/1538-7445.AM2013-4861
Abstract 4863: Prostaglandin and associated eicosanoid dose response to omega-3 fatty acid (FA) diet in rat colon.
Authors: Jiang Yan , Djuric Zora , Ren Jianwei , Dmitry Kuklev V. , Curtis Austin , Bentz Gretchen S. , Waters Ian , Sen Ananda , Zhao Lili , Uhlson Charis , Murphy Robert , Smith William L. , Brenner Dean E. 
Published: August 2014

Abstract
Introduction: Prostaglandin (PG) E2 has been linked to higher risk of colorectal carcinogenesis. Our previous in vitro data (Wada et al. J Biol Chem 2007;282;22254) demonstrated reduction of cellular eicosanoids by substituting the n-3 fatty acid EPA for the more common n-6 FA arachidonic acid (AA) as substrate for the cyclooxygenases (Cox). We tested the hypothesis that EPA substitution for n-6 FA in vivo will reduce procarcinogenic eicosanoids in rats.
Methods: F344 male rats were fed EPA: n-6 FA ratio diets of 0, 0.1, 0.2, 0.4, 0.6 for 5 weeks. Eicosanoids (PGs and lipoxins) in proximal, transverse and distal colonic tissue and urinary PG metabolites were assayed on LC-MS-MS. Fatty acids in serum and tissue were measured by GC-MS.
Results: Serum EPA:AA ratio (means(SD)) increased linearly from 0.02(0.004) at baseline (no EPA) to 0.98(0.32) EPA:n-6 ratio of 0.6. Colonic EPA:AA ratios increased from 0.03(0.01) to 0.41(0.15) in distal colon. Representative eicosanoid concentrations (μg/mg protein) in distal colon tissue with associated EPA:n-6 diets in the Table suggest rapid eicosanoid reduction at lower dietary EPA:n-6 ratios and then flattening of the dose response at higher ratios. The distal colon contained the lowest eicosanoid concentrations compared to transverse and proximal colon. Urinary PGE metabolite was reduced from 13.42(1.95) ng/mg creatinine (dietary EPA:n-6 FA=0) to 7.67(0.62) ng/mg creatinine (dietary EPA:n-6 FA=0.6).
Conclusion: Diet induced substitution of omega-3 for omega-6 substrates of Cox and lipoxygenases in F-344 rats causes a rapid, non-linear decline in colonic PGE2 and lipoxin products. PGE3 increases linearly with omega-3 FA dose. These data support the hypothesis that reduction in carcinogenesis stress induced by eicosanoids can be modulated by a dietary intervention in vivo.
Eicosanoids in rat colon EPA: n-6 ratio in diet PGE2 PGE3 5-HETE 12-HETE 0 264.43(77.54) 0.12 (0.14) 2.28 (1.74) 35.67 (26.95) 0.2 116.56 (50.53) 0.89 (0.81) 1.15 (0.99) 11.73 (7.65) 0.4 86.15 (27.28) 1.52 (0.96) 1.80 (2.02) 5.93 (4.01) 0.6 90.89 (20.90) 2.17 (1.36) 1.52 (0.78) 5.68 (2.77)
Citation Format: Yan Jiang, Zora Djuric, Jianwei Ren, Kuklev V. Dmitry, Austin Curtis, Gretchen S. Bentz, Ian Waters, Ananda Sen, Lili Zhao, Charis Uhlson, Robert Murphy, William L. Smith, Dean E. Brenner. Prostaglandin and associated eicosanoid dose response to omega-3 fatty acid (FA) diet in rat colon. [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 4863. doi:10.1158/1538-7445.AM2013-4863
Abstract 4870: High dietary vitamin D prevents dysplastic lesions in an AOM/DSS model of colorectal cancer.
Authors: Hummel Doris M. , Höbaus Julia , Thiem Ursula , Graca Joao , Mesteri Ildiko , Gober Lukas , Obermayer-Pietsch Barbara , Kallay Enikö 
Published: August 2014

Abstract
Diet and lifestyle have an important impact on the etiology of colorectal cancer (CRC), one of the leading causes of cancer morbidity and mortality in Western countries. Epidemiological studies suggest that vitamin D might have chemopreventive effects.
In this study we investigated the effect of increasing dietary vitamin D3 intake on chemically induced colorectal tumor development in mice.
We fed female C57BL/6J mice with a diet containing five different vitamin D3 concentrations ranging from 100 to 5000 IU/kg diet and studied the impact of dietary vitamin D3 on the development of chemically induced colonic dysplasia, a precursor of CRC. To induce dysplasia, we injected mice once with 10 mg/kg azoxymethane (AOM) intraperitoneally, followed by three cycles of dextran sodium sulfate salt (DSS) in the drinking water. Dietary vitamin D3 concentration correlated positively with 25(OH)D3 serum levels (Spearman Correlation Coefficient (SCC) 0.752, p&lt;0.001). Both dietary vitamin D3 concentration and serum 25-hydroxyvitamin D3 levels correlated inversely with the dysplasia score (SCC -0.579, p=0.002; SCC -0.618, p=0.001). Dysplastic regions expressed less vitamin D receptor while the proliferation marker Ki67 was significantly higher expressed in regions with high grade dysplasia compared with the respective normal mucosa of the same colon.
Our data show that high dietary vitamin D3 concentrations reduce the development of chemically induced precursors of colorectal cancer in mice.
Citation Format: Doris M. Hummel, Julia Höbaus, Ursula Thiem, Joao Graca, Ildiko Mesteri, Lukas Gober, Barbara Obermayer-Pietsch, Enikö Kallay. High dietary vitamin D prevents dysplastic lesions in an AOM/DSS model of colorectal 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 4870. doi:10.1158/1538-7445.AM2013-4870
Abstract 4901: BMI1 is not a marker of cancer or stem cells in the prostate.
Authors: Pellakuru Laxmi Gurunatham , Ocal-Gumuskaya Berrak , Zheng Qizhi , Hicks Jessica , De Marzo Angelo 
Published: August 2014

Abstract
The polycomb gene, BMI1, has been reported to be critical in regulating self-renewal and proliferation of a number of tissue-specific normal as well as cancer stem cells, and it has been shown to be overexpressed in several tumor types. BMI1 has been reported to be highly expressed in the prostate basal cell compartment (Lukacs et al 2010, Cell Stem Cell 7: 682-693), which houses prostate stem cells (Robinson et al 1998, Prostate 37: 149-160), as well as being upregulated in prostate cancer (Lukacs et al 2010, van Leenders et al 2007, Eur Urol 52: 455-463). However, other studies have not found BMI1 levels to correlate with prostate cancer (Wolters et al 2010, BJU Int 106: 280-286). We used immunohistochemical staining as well as chromogenic in situ hybridization to characterize the pattern of BMI1 expression in normal prostate as well as primary and metastatic adenocarcinoma specimens using both standard glass slides and tissue microarrays. For our IHC staining, we used the antibody from Cell Signaling, and we validated that on human prostate tissue, a single band is obtained by western immunoblot. Using this antibody, we were unable to show any consistent difference in BMI1 protein between prostate basal and luminal cells, with generally abundant staining in both compartments. Similar findings were seen with in situ hybridization for BMI1 mRNA. We also found that BMI1 is not consistently upregulated in primary or metastatic human prostate cancers, albeit most tumor cells in most cases showed robust nuclear staining. The findings that BMI1 is not enriched in the stem cell compartment, does not label only a subset of prostate cancer cells, and is not generally upregulated in prostate cancer to any significant degree supports the concept that BMI1 would not be considered a marker of stem cells, cancer stem cells or a cancer biomarker in the prostate.
Citation Format: Laxmi Gurunatham Pellakuru, Berrak Ocal-Gumuskaya, Qizhi Zheng, Jessica Hicks, Angelo De Marzo. BMI1 is not a marker of cancer or stem cells in the prostate. [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 4901. doi:10.1158/1538-7445.AM2013-4901