bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract 1880: Sun exposure and the risk of prostate cancer in an Asian population: The Singapore Prostate Study
Authors: Chia Sin-Eng , Wong Kin Yoke , Lau Weber , Cheng Christopher 
Published: August 2014

Abstract
INTRODUCTION: Recent epidemiological studies have reported an inverse association between sun exposure and prostate cancer which may be related to vitamin D or other factors, but these studies have been conducted almost exclusively in the Western countries, and in temperate locations. The objective of this paper is to study the association of sun exposure and risk of prostate cancer (PC). METHODS: The Singapore Prostate Cancer study is a hospital-based, case-control study conducted in Singapore between April 2007 and May 2009. Singapore residents (ethnic Chinese/Malays/Indians) aged 50 and above formed the study population. Detailed information on outdoor activities under sun (for recreational or occupational purposes) during childhood and in adulthood, skin color and sun sensitivity, and other information on other possible risk factors were collected in personal interviews. A total of 240 incident prostate cancer cases and 268 controls were recruited. Odds ratios (OR) and 95% confidence intervals (CI) were calculated using unconditional logistic regression analysis, adjusted for age, ethnicity, education, family history of any cancers, BMI and skin color. RESULTS: Subjects with black/dark brown eye compared with light brown pigmentation have an adjusted OR of 5.88 (3.17-10.92) of getting PC. The adjusted ORs for skin color “Light Tan” and “Tan/Dark brown/black” subjects when compared with of “very white/white” subjects were 4.43 (2.26-8.69) and 7.62 (3.41-17.03); respectively. Sunburn frequency is associated with increase risk of PC. The adjusted ORs with “Never” sunburn as referent were 1.30 (0.71-2.39) for “Seldom”; 2.27 (0.96-5.35) for “Occasionally”; 4.30 (1.66-11.16) for “Frequently”. This trend was significant (p=0.001). Sun exposure in adulthood (hrs/week) is also associated with increase risk of PC. The adjusted ORs with “0 hrs” sunburn as referent were 1.71 (0.90-3.25) for “0.1-10hrs” and 2.03 (1.09-3.81) for “&gt;10 hrs”. This trend was significant (p=0.017). CONCLUSION: Pigment characteristics (eye and skin color) and sun exposure and possible sensitivity showed association with risk of PC, after adjusting for likely confounders. We observed an overall risk of PC among subjects who reported spending time outdoors regularly.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 1880. doi:10.1158/1538-7445.AM2011-1880
Abstract 1922: Ethnic and racial differences in colorectal cancer
Authors: Simon Michael S. , Thomson Cynthia A. , Pettijohn Erin , Kato Ikuko , Rodabough Rebecca , Lane Dorothy , Hubbell F Allan , O'Sullivan Mary Jo , Adams-Campbell Lucille L. , Mouton Charles P. , Abrams Judith , Chlebowski Rowan T. 
Published: August 2014

Abstract
Introduction: The Women's Health Initiative (WHI) provides a robust database to determine whether differences in known colorectal cancer (CRC) risk factors influence ethnic and racial differences in incidence and mortality. Methods: The WHI is a multi-center longitudinal study of postmenopausal women age 50-79 years recruited from 40 centers across the US. Baseline self-administered questionnaires were used to collect self-identified ethnicity or race, other demographics and health status. Cancer screening information was collected annually and cancer diagnoses were centrally adjudicated. Cox proportional hazards regression was used to compute hazard ratios (HRs) and 95% confidence intervals (CIs) for invasive CRC by ethnicity/race. Results: The ethnic and racial composition of the sample is 131,481 (84%) White, 14,323 (9%) African American (AA), 6,362 (4%) Hispanic, 694 (&lt;1%) Native American and 4,148 (3%) Asian/Pacific Islander (API). After a mean follow-up of 10.8 years (SD 2.9), CRC incidence was highest among AA (annualized percent 0.14%), followed by Whites and Native Americans (0.12% each), API (0.10%) and Hispanics (0.08%). After adjustment for age and cohort assignment, Hispanics had a lower risk of CRC compared to Whites, HR 0.73 (95% CI: 0.54-0.97) (p=0.03), and AA had a marginally greater risk, HR 1.16 (95% CI: 0.99-1.34), p=0.06. Adjustment for other covariates, eliminated the difference in incidence between AA and Whites (HR 0.99, 95% CI: 0.82-1.20), however the difference in incidence between Hispanics and Whites increased (HR 0.68, 95% CI: 0.48-0.97), p = 0.03. Conclusions: Differences in CRC risk between Hispanics and Whites are not explained by sociodemographic or behavioral factors in the WHI cohort.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 1922. doi:10.1158/1538-7445.AM2011-1922
Abstract 1927: Race, health conditions, and endometrial cancer survival
Authors: Olson Sara H. , Atoria Coral L. , Cote Michele L. , Cook Linda S. , Rastogi Radhai M. , Soslow Robert , Brown Carol L. , Elkin Elena 
Published: August 2014

Abstract
Background: Endometrial cancer shows the largest disparity in outcomes between black and white cases of any cancer in the US. Black women have higher prevalence of diabetes and hypertension, conditions that might be associated with poorer survival. Our objectives were to determine whether the presence of diabetes or hypertension was related to disease-specific survival and to investigate whether accounting for these conditions influenced the survival difference for the two racial groups. Methods: Using Surveillance, Epidemiology and End Results cancer registry data linked with Medicare claims, we identified women with diabetes (as defined by Hebert et al, Univ of Minn Rural Health Research Center Working Paper 22, March 1998) and hypertension (defined as 2 claims at least 30 days apart for ICD9 codes 401-404) and investigated the influence of these conditions on survival in black and white women age &gt;=66 diagnosed with endometrial cancer between 2000 and 2005. We used Cox proportional hazards models, adjusted for demographics, tumor characteristics, and treatment, to evaluate whether presence of diabetes or hypertension influenced disease-specific survival and whether adjustment for these factors influenced the difference in outcome between blacks and whites. Results: 22% of whites and 41% of blacks with endometrial cancer met the criteria for diabetes and 52% and 73%, respectively, met the criteria for hypertension. Having diabetes was associated with poorer endometrial cancer specific survival in whites (HR=1.19, 95% CI 1.06-1.35) but not in blacks (HR=0.97, 95% CI 0.73-1.30), after adjustment for variables related to demographics, tumor characteristics, and treatment. Presence of hypertension did not significantly influence survival in either group. As expected, both overall survival and endometrial cancer specific survival were poorer in black women compared to whites, with adjusted hazard ratios for blacks of 1.19 (95% CI 1.08-1.31) for overall survival and 1.30 (95% CI 1.11-1.52) for disease-specific survival. Very little influence was found for diabetes or hypertension for either overall or disease specific survival: after adjustment for these variables the hazard ratios were 1.16 (95% CI 1.05-1.28) for overall survival and 1.27 (95% CI 1.08-1.49) for disease-specific survival. Conclusions: Diabetes influences disease-specific survival only in white women, while hypertension is not associated with disease-specific survival. The racial disparity in survival after a diagnosis of endometrial cancer is not explained by the presence of diabetes or hypertension.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 1927. doi:10.1158/1538-7445.AM2011-1927
Abstract 1928: Travel distance and pattern of care for laryngeal cancer in Kentucky
Authors: Huang Bin , Gal Thomas J. , Han Daikwon , Shelton Brent J. , Tucker Thomas C. , Dignan Mark 
Published: August 2014

Abstract
Introduction: Previous studies have found that access to medical care was associated with stage at cancer diagnosis and receipt of treatment. For laryngeal cancer, radiation related treatments are a preferred option in the majority of cases. Travel distance to the radiation facilities may impact patient access to radiation treatment, especially in a rural mountainous state such as Kentucky. The aim of the study is to assess the influence of travel distance to the nearest radiation center and other factors on inclusion of radiation in the first course treatment for laryngeal cancer.
Study Population and Methods: 1995-2006 Kentucky Cancer Registry data were used for this study. A total of 2099 patients age 20 and older at diagnosis with no previous history of cancer and with known TNM stage laryngeal cancer (C32.0-C32.2) were included for the analysis. The road travel distance from their home address to the nearest radiation center was calculated based on road network in GIS. Poverty rate and high school education rate at census tract level were linked with the case data. The SAS procedure GLIMMIX was used to fit random intercept logistic models to predict the association between treatment and other demographic and clinic factors.
Results: About 78% of patients received treatment that included radiation as part of first course treatment. The rate of radiation related treatment increased from 68% to 79% in the study period. The average travel distance was 13.5 miles for the group receiving radiation treatment vs. 13.9 miles for the group not receiving radiation treatment. The multivariate logistic model indicated that the travel distance was not associated with radiation treatment. In addition, patients diagnosed recently (per year) were more likely to have radiation related treatment (OR=1.05, p=0.001), and patients treated in large hospitals were positively associated with radiation treatment (OR=2.72, p=0.002) than patients in small hospitals.
Conclusions: Although longer travel distance has been found as a barrier for cancer patients living in this rural state, we did not find a similar association for laryngeal cancer. The increasing use of radiation related treatment is encouraging and may be associated with increasing availability of radiation centers in this region. Under utilization of radiation treatment for patients treated in smaller hospitals is a serious concern. Further research is needed to investigate the cause of this under utilization.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 1928. doi:10.1158/1538-7445.AM2011-1928
Abstract 1935: EBP50 inhibits breast cancer cell proliferation by blocking EGFR phosphorylation
Authors: Zheng Junfang , Yao Wenfang , Feng Duiping , Bian Weihua , Xiong Ying , Yang Xiaomei , Yang Longyan , Zhou Yunying , Zhai Renyou , He Junqi 
Published: August 2014

Abstract
EBP50 (Ezrin-radixin-moesin-binding phosphoprotein-50, also known as NHERF, NHERF1) has been reported to interact with epidermal growth factor receptor (EGFR) and enhance EGFR activity and its downstream ERK signaling in a cervical cancer cell line HeLa. However, our previous results demonstrated that EBP50 could suppress breast cancer cell proliferation, suggesting its inhibitory effect on EGFR signaling in breast cancer cell. So we detected the effect of EBP50 expression on EGF-induced cell proliferation and the activation of EGFR signaling in breast cancer cell lines, MDA-MB-231 and MCF-7. In MDA-MB-231 cells which expressed low level of EBP50, EBP50 over-expression inhibited EGF-induced cell proliferation. In MCF-7 cells which expressed high level of EBP50, EBP50 knockdown promoted EGF-induced cell proliferation. EBP50 was reported to interact with EGFR via its carboxyl terminal regulatory domain, which is adjacent to the autophosphorylation domain of the receptor, so it is possible that the association of EBP50 and EGFR mask the phosphorylation site of EGFR so as to prevent EGFR activation. To test this hypothesis, we detected the phosphorylation status of EGFR in the presence or absence of the EBP50 expression. Over-expression of EBP50 in MDA-MB-231 inhibits EGF-stimulated EGFR phosphorylation, and knockdown of EBP50 in MCF-7 cells led to the enhanced EGF-stimulated EGFR phosphorylation. Meanwhile, the total expression levels of EGFR were not affected by the different expression level of EBP50 during EGF stimulation. In the case of EBP50 expression on the EGFR downstream signaling, EBP50 over-expression inhibited EGF-stimulated ERK activity in MDA-MB-231 cells, and EBP50 knockdown resulted in the enhanced EGF-stimulated ERK activity in MCF-7 cells. These data are consistent with results of MDA-MB-231 and MCF-7 cell lines pretreated with EGFR tyrosine kinase inhibitor-AG1478, that EGF-stimulated ERK activity was inhibited when EGFR phosphorylation was blocked. Taken together, our results demonstrated that EBP50 can suppress EGF-induced proliferation of breast cancer cells by retarding EGFR phosphorylation and blocking EGFR downstream signaling in breast cancer cells. These results provide further insights into the molecular mechanism by which EBP50 regulates the development and progression of breast cancer.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 1935. doi:10.1158/1538-7445.AM2011-1935
Abstract 1936: Notch signaling is switched off and displays properties of a tumor suppressor in Ewing's sarcoma
Authors: Bennani-Baiti Idriss M. , Aryee Dave N.T. , Ban Jozef , Kauer Maximilain , Mühlbacher Karin , Machado Isidro , Amann Gabriele , Llombart-Bosch Antonio , Kovar Heinrich 
Published: August 2014

Abstract
Notch can act as an oncogene or as a tumor suppressor and thus can either promote or inhibit tumor cell growth. To establish Notch status in Ewing's sarcoma family of tumors (ESFT), we investigated the Notch pathway by gene expression profiling meta-analysis or immunohistochemistry in samples obtained from 96 and 24 ESFT patients, respectively. We find that although Notch receptors were highly expressed, Notch did not appear to be active as evidenced by the absence of Notch receptors in cell nuclei. High expression of the Notch effector HES1 transcription factor, usually used as a surrogate marker for active Notch, was also restricted to outside of the nucleus in the majority of tumors, and analysis of HES1 gene targets indicated HES1 to be transcriptionally inactive. Neither forced activation nor pharmacological or genetic blocking of Notch affected HES1 expression in ESFT cells, indicating HES1 expression to be uncoupled from the Notch pathway. Additional functional studies in ESFT cell lines confirmed Notch to be switched off. Finally, unlike experiments in which HES1 expression was modulated, experimental activation of Notch in ESFT cell lines via several means blocked cell proliferation. These indicate that HES1 is uncoupled from Notch in ESFT, that EWS-FLI1-mediated inhibition of Notch contributes to ESFT aggressive cell growth, and supports a role for Notch in ESFT tumor suppression, at least partly through the Notch effector HEY1.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 1936. doi:10.1158/1538-7445.AM2011-1936
Abstract 1937: Nemo-like kinase expression is altered during prostate cancer progression
Authors: Brown Lisha G. , Pitts Tiffany EM , Zhang Xiaotun , Vessella Robert L. , Corey Eva 
Published: August 2014

Abstract
MAPKs have been implicated in cancer progression. We have previously shown that Nemo-like kinase (NLK) inhibits androgen receptor signaling and induces apoptosis in prostate cancer cell in vitro. The objective of this study was to investigate NLK expression in clinical samples of primary prostate cancer and in prostate cancer xenografts using immunohistochemistry. TMAs containing primary prostate cancer samples and prostate cancer xenograft tissues were used. Our data show that NLK immunoreactivity is 0.34 higher in primary prostate cancer vs. normal prostate epithelium (p=0.01) but our analysis did not reveal any significant correlations of NLK immunoreactivity with PSA, Gleason score or recurrence of the disease. When we examined NLK immunoreactivity in prostate cancer xenografts our results show that there are signficant differences in cellular localization of NLK between xenografts that respond well to castration vs. those that do not. Xenografts that respond well to castration exhibit lower levels of NLK in nucleoplasm and higher leves of NLK in nucleoli vs. xenografts that do not respons well to castration (t=−4.211, p&lt;.0001, and z=3.994, p&lt;.0001 respectively). Our in vitro studies show that DHT increases localization of NLK in nucleoli of LNCaP. NLK levels in nucleoli negatively correlate with levels of nucleophosmin, a protein involved in regulation of proliferation, in the xenografts and in LNCaP cells in vitro. Interestingly we have also shown that in vitro NLK stimulates wnt signaling in LNCaP cells and this effecst in dependent on expresison of androgen receptor. In summary our data show that NLK expression is altered during prostate cancer progression and that NLK alters androgen receptor and wnt signaling pathways. Further studies to investigate mechanisms of NLK effects and NLK involvement in response to androgen ablation in prostate cancer are ongoing.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 1937. doi:10.1158/1538-7445.AM2011-1937
Abstract 1940: Reg4 induces the expression of D-type cyclins and associated kinases to induce mitotic division of human colorectal cancer cells
Authors: Bishnupuri Kumar S. , Sainathan Satheesh K. , Luo Qizhi , Dieckgraefe Brian K. 
Published: August 2014

Abstract
Background: Cyclins and cyclin-dependent kinases (CDK) are important component of the cell cycle machinery. D-type cyclins are positive regulators of cell cycle and a known target of Wnt/β-Catenin signaling. Cyclin D1 and cyclin D3 play a prominent role in differentiation and proliferation and is highly upregulated in many cancers. Recent studies also showed frequent upregulation of regenerating (Reg) gene 4 expression in many human gastrointestinal (GI) malignancies including colorectal cancer (CRC). We further observed a Reg4-mediated increase in β-Catenin expression and its subsequent nuclear translocation. Therefore, we tested the hypothesis that Reg4 induces the expression of D-type cyclins and associated kinases to induce the mitotic division of human CRC cells.
Methods: Real time RT-PCR and western blot analyses were performed to determine the effects of Reg4 treatments on the expression of D-type cyclins and associated kinases. Mitotic and MTT assays were performed to determine its association with regulation of mitotic division and proliferation of human CRC cells.
Results: Following real-time RT-PCR and western blot analyses we observed a time-dependent increase in cyclin D1 and D3 expression following the addition of recombinant human Reg4 (rhR4) to the cultures of HCT116 and HT29 human CRC cells. Furthermore, addition of rhR4 to the cell cultures also led to an increased expression of CDK4 and CDK6, the known kinase partners of cyclin D. We previously observed the involvement of Akt kinase, GSK-3β, and β-Catenin activities in mediating Reg4-signaling. Therefore, in the present study we utilized a specific Akt inhibitor as an antagonist and SB216763, an inhibitor of GSK-3β as an agonist of Reg4-signaling and examined their effects on expression of D-type cyclins and mitotic index of human CRC cells. Treatments of specific Akt inhibitor (10 μM) to the human CRC cells significantly inhibited the expression of cyclin D1 and D3, and subsequently inhibited their mitotic index. Furthermore, an addition of rhR4 (200 nM) to the cultures of human CRC cells pretreated with specific Akt inhibitor (10 μM) did not increase the expression of these cyclins, hence the mitotic index of human CRC cells. In addition, the treatments of SB216763 (10 μM) positively modulated the Reg4-signaling and led to significant increases in the expression of D-type cyclins, hence mitotic index of human CRC cells.
Conclusions: These results suggest that Reg4 is a potent regulator of mitotic division of human CRC cells and involves Akt kinase and GSK-3β as important mediators to induce the expression of D-type cyclins.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 1940. doi:10.1158/1538-7445.AM2011-1940
Abstract 1943: Anticarcinogenic effect of curcumin by insulin-like growth factor-1 signaling inhibition
Authors: Kim Hyoseon , Kim Eunjung 
Published: August 2014

Abstract
Curcumin (diferuloylmethane) is an active polyphenol natural product isolated from turmeric (the rhizome of the plant Curcuma longa Linn) and is traditionally used as a coloring agent and spice in food. Curcumin has also been shown to a powerful therapeutic agent against many human diseases including cancer. Insulin-like growth factor-1(IGF-1) signaling plays a critical role in regulation of cell survival, proliferation and growth. In this study, we investigated IGF-1 signaling inhibitory activity of curcumin and its mechanism in in vitro cell culture studies and in vivo tumor studies using BK5. IGF-1 transgenic mice.
Serum starved HeLa cells were treated with curcumin of various concentrations and times and then stimulated with IGF-1(20 ng/ml) for 30 min. Akt(S473) and S6K(T389) phosphorylation was inhibited by 1 hr treatment of 40 and 30 μM curcumin, respectively. Moreover, curcumin treatment inhibited S6K phosphorylation even after 10 min treatment. Akt was not affected at this dosage and time of curcumin treatment. Curcumin also inhibited amino acids stimulated S6K phosphorylation whereas it activated Akt phosphorylation by negative feedback inhibition. This S6K phospholylation inhibitory activity of curcumin was comparable to that of rapamycin(20 nM) but the effect of curcumin appears to be transient.
In our in vivo tumor study, supplementaion of curcumin to AIN-93G diet(0.02 % curcumin wt/wt) decreased mouse skin tumor multiplicity by 50 % as well as tumor size in BK5. IGF-1 transgenic mice. Curcumin supplementation also inhibited skin epithelial cell proliferation in 5-bromo-2-deoxyuridine(BrdU) incorporation experiment.
Taken together, these data suggest that curcumin may exert its anticarcinogenic effect by directly inhibit IGF-1 stimulated mammalian target of rapamycin(mTOR) signaling.
[This research was supported by Basic Science Research Program(C00308) and by SRC program(Center for Food & Nutritional Genomics:2010-0001886) through the National Research Foundation of Korea(NRF) funded by the Ministry of Education, Science and Technology.]
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 1943. doi:10.1158/1538-7445.AM2011-1943