bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract B23: Curcumin suppresses the growth and metastasis of prostate cancer cells by downregulation of SKP2.
Authors: Gong Yuanying , Lu Wenfu , Xie Yingqiu , Yang Qing , Matusik Robert J. , Chen Zhenbang 
Published: August 2014

Abstract
Purpose: Prostate Cancer (PCa) is the second leading cause of cancer-related deaths in American men. The morbidity and mortality to PCa are 2.39-fold higher in African American men as compared to Caucasian males. Aberrant overexpression of SKP2 is frequently found in human cancers including prostate cancer, but little is known about pharmacological compounds targeting Skp2 activity. This study investigated inhibitory effects of curcumin (diferuloylmethane) on malignant features of prostate cancer cells in vitro and xenograft mouse models in vivo, and mechanistically on Skp2 level.
Design Methods: Prostate cancer cells (PC3) and mouse prostate cancers cells (MPC3) in culture were treated with curcumin solution for indicated periods of time in vitro. Quantitative real-time reverse-transcription polymerase chain reaction (qRT-PCR) and Western blot analyses were used to determine mRNA and protein expression of Skp2 in cancer cells. Cell proliferation, colony formation, and invasion assay were compared between curcumin-treated and control cells. Mouse prostate cancer cells were injected into immunodeficient mice followed with curcumin administration (200mg/kg/day). Tumorigenesis was analyzed in curcumin-treated and control mice after 20 days.
Results: Curcumin treatment of PC3 cells resulted in a significant reduction of cell proliferation, soft agar transformation and invasion as compared to controls. Curcumin treatment led to a decrease of Skp2 level through a reduction of Skp2 mRNA and a shortened half-life of Skp2 protein. As expected, p27 protein, a major downstream target of Skp2, was increased upon curcumin treatment, whereas c-Myc protein level was not affected by curcumin treatment in prostate cancer cells. MPC3 cells, administered into immunodeficient mice via tail vein or orthotopic implantation, developed lung metastasis or enlarged prostate tumors, respectively. Importantly, cancer progression was significantly suppressed by curcumin treatment. A reduced level of Skp2 protein and induction of cell senescence were detected in tumors of curcumin-treated mice, but not in tumors of control mice.
Conclusion: Our results indicated that curcumin suppresses both the tumor growth in mouse prostates and distant metastasis of prostate cancer cells in lung by inhibiting Skp2 level.
Citation Format: Yuanying Gong, Wenfu Lu, Yingqiu Xie, Qing Yang, Robert J. Matusik, Zhenbang Chen. Curcumin suppresses the growth and metastasis of prostate cancer cells by downregulation of SKP2. [abstract]. In: Proceedings of the Fifth AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2012 Oct 27-30; San Diego, CA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2012;21(10 Suppl):Abstract nr B23.
Abstract B46: Isolation, identification, and sensitivity pattern on fatty acid composition of edible oil in Bangladesh: From preclinical studies to international clinical trials.
Authors: Mollik Md. Ariful Haque 
Published: August 2014

Abstract
Bangladesh is a potential market for essential commodities, including edible oils, because of insufficient local production, a steadily growing population that now exceeds 150 million, and its improving economy. Edible oil is an energy-dense food nutrient providing 9.0 kcal/g. Oil rich in long chain monounsaturated fatty acids and polyunsaturated fatty acids, especially essential fatty acids (linoleic, and linolenic), is of primary importance for its digestion and absorption. Butter oil, corn oil, mustard oil, olive oil, palm oil, and soybean oil are the six major edible oils consumed in Bangladesh. Soybean oil is the highest consumed edible oil, catering to 59% of the demand. Find out a suitable variety of locally available edible oil for general mass to combat malnutrition and to control cardiovascular diseases and gastrointestinal disorders. Fatty acid analysis of six varieties included butter oil, corn oil, mustard oil, olive oil, palm oil, and soybean oil of locally consumed edible oils was carried out on a gas chromatograph equipped with a flame ionization detector and stainless steel-packed column. Nitrogen was used as a carrier gas. Corn oil contained the highest percentage of long chain monounsaturated fatty acids and polyunsaturated fatty acids (93.10±3.59%) compared to mustard oil (79.25±5.99%), soybean oil (75.88±2.93), palm oil (51.48±0.75%), olive oil (24.18±.96%), and butter oil (8.29±1.33%). Corn oil with the highest percentage of monounsaturated fatty acids and polyunsaturated fatty acids appears to be the most suitable edible oil for consumption, especially from the standpoint of cardiovascular disease, gastrointestinal disorders, and nutritional rehabilitation of post-diarrheal patients.
Note: This abstract was not presented at the conference.
Citation Format: Md. Ariful Haque Mollik. Isolation, identification, and sensitivity pattern on fatty acid composition of edible oil in Bangladesh: From preclinical studies to international clinical trials. [abstract]. In: Proceedings of the Fifth AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2012 Oct 27-30; San Diego, CA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2012;21(10 Suppl):Abstract nr B46.
Abstract B65: Profiling and characterization of ethnicity-associated metabolic pathways in breast cancer.
Authors: Terunuma Atsushi , Putluri Nagireddy , Samanta Susmita , Mishra Prachi , Mathe Ewy , Dorsey Tiffany H. , Kittles Rick , Ambs Stefan 
Published: August 2014

Abstract
Large variations in breast cancer incidence and survival among the various population groups in the United States continue to exist and differences in the clinical presentation of the disease between African American (AA) and European-American women have been recognized. Specifically, AA develop breast cancer at a relatively younger age, have a two-fold increased risk of developing triple-negative (TN) tumors and present more commonly with the stage IV disease, when compared with EA women. While the precise reasons for this disparity are still debated, genetic, environmental, and health care access/utilization factors may all contribute to the excessive burden of breast cancer among the AA patients. We therefore asked the question whether metabolomic differences in either breast tissue or body fluids may exist between AA and EA women that could help explain the substantial inequality in TN breast cancer-related outcomes.
Metabolomics describes the science of quantifying the levels of metabolites (e.g., small molecules &lt;1kDa) that are the byproducts of cellular metabolism. Metabolomic analysis is less complex than genomic, transcriptomic and proteomic studies (i.e., ~3,000 metabolites vs. 40,000 genes, 150,000 transcripts and 1x106 proteins) and may accentuate subtle upstream gene/protein level alterations. To date, a systematic breast cancer metabolomic analysis focusing on the distinction between AA and EA women has not been reported. Furthermore, a metabolomically derived prognostic model for TN in each of these ethnic groups has not yet been defined. The presentation will discuss our results on profiling and validating the levels of 120 metabolites in both TN breast tumors from AA and EA women and in cell lines representing the two patient groups. A subset of the functional pathways has been characterized for their activity using BIOLOG-based flux assays to identify their role in TN breast cancer. The information gleaned from this study could reveal the biochemical underpinnings of TN breast cancer health disparity
Citation Format: Atsushi Terunuma, Nagireddy Putluri, Susmita Samanta, Prachi Mishra, Ewy Mathe, Tiffany H. Dorsey, Rick Kittles, Stefan Ambs. Profiling and characterization of ethnicity-associated metabolic pathways in breast cancer. [abstract]. In: Proceedings of the Fifth AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2012 Oct 27-30; San Diego, CA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2012;21(10 Suppl):Abstract nr B65.
Abstract B79: Assessing colorectal cancer screening behaviors and knowledge among at-risk Hispanics in southern New Mexico.
Authors: Sanchez Janet , Martinez Vanessa , Thompson Beti , O'Connell Mary 
Published: August 2014

Abstract
Introduction: Colorectal cancer (CRC) mortality rates in New Mexico have not decreased as much as the US national rates, and mortality rates among Hispanics in the state are higher than among this ethnic group in the US.
Methods: A Colorectal Cancer Knowledge Assessment Survey (KAS) was administered in either English or Spanish to 247 individuals attending community events and health fairs throughout southern New Mexico. A subset of these individuals completed an electronic CRC risk assessment managed by National Institutes of Health (NIH) National Cancer Institute (NCI). Data analysis was performed using SPSS (Statistical Package for the Social Sciences) to test for significant differences in knowledge, and/or screening rates based on ethnicity.
Results: There were significant differences among participants &gt; 50 years old based on ethnicity for knowledge about CRC, physician discussions and recommendations, and screening rates. In all cases, with the exception of knowledge of CRC risk, Hispanics of CRC screening age, were less likely to be recommended for screening by their physician, less likely to discuss CRC screening, knew less about CRC and about the different types of screening modalities, and reported CRC screening in the past at about half the rate of their non-Hispanic white counterparts.
Conclusions: The increased mortality rates for New Mexican Hispanics with colorectal cancer are likely due to the very low screening rates, which in turn are related to the lack of knowledge about this condition. Expanded education and outreach efforts for minority populations to increase knowledge and awareness of prevention and screening behaviors is critical.
This work was supported in part by the NM AES and by grants NIH NCI 5 U54CA132383 (O'Connell) and NIH NCI 5 U54CA132381 (Thompson).
Citation Format: Janet Sanchez, Vanessa Martinez, Beti Thompson, Mary O'Connell. Assessing colorectal cancer screening behaviors and knowledge among at-risk Hispanics in southern New Mexico. [abstract]. In: Proceedings of the Fifth AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2012 Oct 27-30; San Diego, CA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2012;21(10 Suppl):Abstract nr B79.
Abstract ED01-04: Advancing the science of recruitment and retention of ethnically diverse populations.
Authors: Nápoles Anna M. 
Published: August 2014

Abstract
We highlight two critical challenges that must be addressed to accelerate the advancement of the science of recruitment and retention of ethnically diverse populations into clinical research. First, we present evidence of the relative lack of attention by researchers to recruitment and retention of ethnically diverse populations. Then, we present data on the inadequacy of dedicated funding to advance systematically this field. To begin to address these challenges, we describe strategies used by the National Institute on Aging (NIA)-funded Resource Centers on Minority Aging Research and other NIA-funded programs to advance the science of recruitment and retention. Finally, we propose broad recommendations for generating a body of evidence on successful methods of recruitment and retention of ethnically diverse populations in clinical research. To eliminate cancer health disparities in ethnically diverse populations, much more research is needed on effective strategies for increasing minority enrollment in cancer research. Experimental studies in the recruitment literature that rigorously test recruitment or retention methods are an exception despite the valuable evidence they contribute. Comparative effectiveness research on recruitment and retention methods designed to address mechanisms of underrepresentation in clinical research will require dedicated funding and concerted efforts by investigators.
Citation Format: Anna M. Nápoles. Advancing the science of recruitment and retention of ethnically diverse populations. [abstract]. In: Proceedings of the Fifth AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2012 Oct 27-30; San Diego, CA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2012;21(10 Suppl):Abstract nr ED01-04.
Abstract ED02-03: Gaining epidemiologic insights from ancestry associations with cancer risk factors.
Authors: Signorello Lisa B. 
Published: August 2014

Abstract
The ability to estimate ancestry using genetic markers brings the potential for deeper understandings of the biological basis for cancer health disparities but also presents challenges regarding how best to incorporate this information into epidemiologic studies. New insights can be gained by evaluating the association between ancestry and established cancer risk factors. Using an example of African ancestry, strong associations between the level of African ancestry and various cancer-related biomarkers may provide compelling new information that leads to a better understanding of genetic underpinnings of excess cancer burden in the African American population. African ancestry also has the potential, however, to be correlated with sociodemographic, geographic, and/or behavioral factors. Investigators should be cognizant of these potential correlations to avoid misinterpretation of ancestry-related findings.
Citation Format: Lisa B. Signorello. Gaining epidemiologic insights from ancestry associations with cancer risk factors. [abstract]. In: Proceedings of the Fifth AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2012 Oct 27-30; San Diego, CA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2012;21(10 Suppl):Abstract nr ED02-03.
Abstract PL05-02: Global perspective on the prevention of HPV-related cancers in men: From epidemiology to intervention.
Authors: Giuliano Anna R. 
Published: August 2014

Abstract
HPV causes multiple cancers in both men and women; HPV 16 is a cause of vulvar, vaginal and anal cancers in women, as well as anal, penile, and oropharyngeal cancers in men. While cervical cancer incidence is declining, the incidence of anal cancers and HPV related oropharyngeal cancers is rising. In some regions of the world penile cancer incidence is also increasing. This increase in cancer incidence is occurring for cancers for which there is no routine method for screening and early detection, as there is for cervical cancer. In this presentation the epidemiology of HPV infection in men, and HPV vaccine efficacy in men by race/ethnicity and world region will be presented.
Citation Format: Anna R. Giuliano. Global perspective on the prevention of HPV-related cancers in men: From epidemiology to intervention. [abstract]. In: Proceedings of the Fifth AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2012 Oct 27-30; San Diego, CA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2012;21(10 Suppl):Abstract nr PL05-02.
Abstract PL05-05: Molecular profiling of stage II and III breast cancer in Latin American women receiving standard-of-care treatment.
Authors: Gomez Jorge 
Published: August 2014

Abstract
The United States-Latin America Cancer Research Network (US-LA CRN) launched its first breast cancer pilot study in 2010 in 29 hospitals and research facilities in Argentina, Brazil, Chile, Mexico, and Uruguay. The primary goal is to characterize molecular profile distribution (luminal A, luminal B, HER2-like, and basal) in Latin American women with non-metastatic stage II or III breast cancer. Molecular profiles are correlated with epidemiological, histological, and clinical data, including pathologic response to standard neoadjuvant chemotherapy. This prospective cohort study (1) will not dispense investigational drugs, (2) will characterize molecular profiles of breast cancer in Latin America and (3) will examine associations between response to neoadjuvant therapy and molecular profiles. Tissue samples for gene expression profiling will be collected during routine core biopsies or surgery. Core biopsies and surgical resection specimens will undergo histopathologic evaluation and tumor ER, PgR, HER2, and Ki67 status assessment. Next, patients will be sorted by hormone receptor and HER2 status and receive standard neoadjuvant chemotherapy. Tissue samples will be re-assessed for residual cancer burden for pathologic response to neoadjuvant treatment and gene expression. Five-year patient follow-up will determine associations between molecular profiles and disease evolution after standard treatment. Besides providing data on the effectiveness of standard chemotherapy in Latin American women, the study will establish biobanks in participating countries to conduct new clinical trials on complex genomic and pathologic biomarkers and investigational therapies. Studying the molecular profile of breast cancer in Latin America will improve diagnosis and treatment, correlate molecular subtypes with long-term survival and response to therapy, and identify indolent-disease subpopulations of cancer patients, perhaps enabling future personalized cancer management. Dr. Gomez will provide outcomes of the study to date and reflect on the implications of creating international biobanking repositories and gene studies in Latin America.
Citation Format: Jorge Gomez. Molecular profiling of stage II and III breast cancer in Latin American women receiving standard-of-care treatment. [abstract]. In: Proceedings of the Fifth AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2012 Oct 27-30; San Diego, CA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2012;21(10 Suppl):Abstract nr PL05-05.
Abstract PL06-03: Inflammation and cancer: Interweaving microRNA, free radical, innate immune, and p53 networks.
Authors: Harris Curtis C. 
Published: August 2014

Abstract
Infection and chronic inflammation contribute to the etiology and pathogenesis of about 1 in 4 of all cancer cases. Mediators of the inflammatory response, e.g., cytokines, free radicals, prostaglandins, non-coding RNAs, and growth factors, can induce genetic and epigenetic changes including point mutations in tumor suppressor genes, DNA methylation and post-translation modifications, causing alterations in critical pathways responsible for maintaining the normal cellular homeostasis and leading to the development and progression of cancer IL-6 and IL-8 cooperate with microRNA in the induction of cellular senescence in benign tumors and as autocrine growth factors in carcinoma.
Cellular senescence is also a tumor suppressor mechanism of p53. We are studying the molecular mechanisms of cellular senescence in normal and malignant human cells and the role of the telomeric multiprotein complex, shelterin, that includes TRF2 and POT1. Our ongoing studies have revealed that p53 and its endogenous isoforms regulate both specific microRNAs and TRF2 expression as mechanisms of replicative senescence. In addition, POT1 isoforms are functionally diverse in both maintaining telomeric integrity and preventing p53-dependent senescence induced by telomeric shortening. A switch in the expression patterns of p53 isoforms Δ133Np53 and p53beta can cause cellular senescence in vitro and is also associated with the transition of benign to malignant human colon tumors in vivo. A positive feedback between p53 and TRF2 during telomere-damage signaling and cellular senescence has been discovered.
Expression of microRNAs and inflammatory genes are biomarkers of cancer risk, diagnosis, prognosis, and therapeutic outcome. We are especially interested in the interaction of the innate immune pathway with environmental tobacco smoking in lung cancer risk and the interaction of inflammatory cytokines, p53 isoforms, and microRNAs as prognostic classifiers of early stage lung, esophageal, and colon cancer and their functional role in the development of micrometastases.
Citation Format: Curtis C. Harris. Inflammation and cancer: Interweaving microRNA, free radical, innate immune, and p53 networks. [abstract]. In: Proceedings of the Fifth AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2012 Oct 27-30; San Diego, CA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2012;21(10 Suppl):Abstract nr PL06-03.
Abstract A05: Ubiquilin1 represses migration and epithelial to mesenchymal transition of human non-small cell lung cancer cells.
Authors: Shah Parag P. , Lockwood William W. , Saurabh Kumar , Kurlawala Zimple , Waigel Sabine , Zacharias Wolfgang , Beverly Levi J. 
Published: August 2014

Abstract
Ubiquilin1 (UBQLN1) is a ubiquitin-like domain and a ubiquitin-associated domain containing protein that has been reported to be involved in shuttling proteins to the proteasome, especially during endoplasmic reticulum-associated protein degradation (ERAD). Thus, UBQLN1 function has been shown to be critical for combating a number of neurological disorders caused by protein aggregation, such as Amyotrophic lateral sclerosis (ALS), Alzheimer's disease and Huntington's disease. A role for UBQLN1 in regulating processes involved in tumorigenesis has not been demonstrated. Herein, we show that loss of UBQLN1 causes increased cell migration and invasion, actin cytoskeleton reorganization and induction of epithelial mesenchymal transition (EMT). Loss of UBQLN1 results in a significant decrease in the expression of epithelial markers including E-cadherin and claudin1, whereas expression of mesenchymal markers including Vimentin, Snail and ZEB1 are significantly elevated. Interestingly, we found that ZEB1 is required for induction of mesenchymal-like properties following loss of UBQLN1 and ZEB1 is capable of repressing expression of UBQLN1, suggesting a physiological, reciprocal regulation of EMT by UBQLN1 and ZEB1. Furthermore, we observed that loss of UBQLN1 sensitizes lung cancer cells to treatment with cytotoxic drugs. These observations have potential clinical relevance because the UBQLN1 gene is lost and under-expressed in a large percentage of human cancer cell lines and primary human lung cancer samples. Taken together, our results suggest for the first time a role of UBQLN1 in the regulation of EMT and a potential role in cancer biology and in predictive cancer therapeutics.
Citation Format: Parag P. Shah, William W. Lockwood, Kumar Saurabh, Zimple Kurlawala, Sabine Waigel, Wolfgang Zacharias, Levi J. Beverly. Ubiquilin1 represses migration and epithelial to mesenchymal transition of human non-small cell lung cancer cells. [abstract]. In: Proceedings of the AACR-IASLC Joint Conference on Molecular Origins of Lung Cancer; 2014 Jan 6-9; San Diego, CA. Philadelphia (PA): AACR; Clin Cancer Res 2014;20(2Suppl):Abstract nr A05.