bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract B35: Molecular characterization of colorectal tumors from Puerto Rican Hispanic patients
Authors: Díaz-Algorri Yaritza , Pérez-Mayoral Julyann , González-Pons Maria , Rodríguez Natalia , Suárez Belisa , Colón Giancarlo , Sevilla Javier , Jorge Daphne L. , Llor Xavier , Xicola Rosa , Tous Luis , Reyes José S. , Torres Marla , Goel Ajay , Rodriguez Segundo , Cruz-Correa Marcia 
Published: May 2016

Abstract
Background and Objectives: Accumulating evidence supports that colorectal cancer (CRC) is comprised of different genetic diseases affecting the same organ. The molecular classification of CRC is evolving as we gain a comprehensive knowledge about the mechanisms and processes resulting in colorectal carcinogenesis. Tumors display distinct characteristics depending on the molecular subtype, which may affect response to treatment, prognosis, and survival. CRC is the leading cause of cancer deaths among Puerto Rican Hispanics (PRH). The aim of this study was to characterize colorectal tumors at a molecular level in a cohort of PRH in order to determine the prevalence of molecular markers.
Methods: The molecular markers evaluated were microsatellite instability (MSI), CpG island methylation phenotype (CIMP), and mutations in KRAS and BRAF oncogenes. In addition, HPV infection status was assessed, as it has been associated with CRC. Sociodemographic and clinicopathological characteristics were evaluated according to MSI, CIMP, KRAS/BRAF mutation and HPV-status using Pearson's Chi-Square and Mann-Whitney U-test.
Results: A total of 201 CRC tumors were included in our study. Of the evaluated tumors 2.6% (n=3) showed MSI and 1.8% of the studied tumors had CIMP high phenotype (n=2). The incidence of KRAS and BRAF mutations for our study was 30.6% (n= 38) and 9.2% (n=11), respectively. Furthermore, KRAS positive individuals were more likely to have private or Medicare insurance (p=0.017). In addition, BRAF mutation-positive tumor were more likely to be poorly differentiated when compared to BRAF mutation-negative tumors (p=0.009). HPV infection was not associated with any molecular characteristics examined.
Conclusions: We present for the first time the molecular characterization of CRC tumors in PRH. The observation of a different molecular signature for the CRC tumors (low MSI, CIMP Zero and mainly wild-type for KRAS and BRAF) suggests that CRC in this population might be driven by additional genetic, epigenetic and environmental factors than other racial/ethnic groups.
Citation Format: Yaritza Díaz-Algorri, Julyann Pérez-Mayoral, Maria González-Pons, Natalia Rodríguez, Belisa Suárez, Giancarlo Colón, Javier Sevilla, Daphne L. Jorge, Xavier Llor, Rosa Xicola, Luis Tous, José S. Reyes, Marla Torres, Ajay Goel, Segundo Rodriguez, Marcia Cruz-Correa. Molecular characterization of colorectal tumors from Puerto Rican Hispanic patients. [abstract]. In: Proceedings of the Eighth AACR Conference on The Science of Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; Nov 13-16, 2015; Atlanta, GA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2016;25(3 Suppl):Abstract nr B35.
Abstract C06: Examining reasons for breast cancer disparities in African American women in Duval County, FL
Authors: Osian Sarah , Albertie Monica , Monticalvo David , Ames Steven , Samiian Laila , Colon-Otero Gerardo 
Published: May 2016

Abstract
Background/Purpose: Cancer registry data suggests that Duval County (greater Jacksonville, FL) has the highest breast cancer mortality rate for African American (AA) women in the southeastern US. Recent research revealed that race, residence, and insurance were associated with significantly poorer breast cancer outcomes in this area. Therefore we conducted a series of focus groups with AA breast cancer survivors from the urban core of Jacksonville, FL to directly address the disparities observed in our quantitative data.
Methods: A series of focus groups were conducted to obtain qualitative data topics that included: breast cancer beliefs; delays to diagnosis and treatment; disparities; and health behaviors.
Results: A total of 56 AA breast cancer survivors living in the urban core, with either Medicaid or who were uninsured, participated in the focus groups. Mean age was 62 years, with an average of 3.4 years since diagnosis. Only 21% of women were employed. Participants reported their mean time to see a doctor initially for their breast cancer was 39 days, and mean time to first treatment was 178 days. Participants responded that fear, financial limitations, and personal beliefs played the biggest roles in delays to diagnosis and treatment. Participants responded that poor health behaviors, genetics, lack of education, and personal beliefs accounted for both causing breast cancer, and the disparities observed in breast cancer mortality, and felt that environmental factors from living in the urban core also contribute.
Conclusions: Our findings highlight several areas for potential intervention to reduce disparities in breast cancer.
Citation Format: Sarah Osian, Monica Albertie, David Monticalvo, Steven Ames, Laila Samiian, Gerardo Colon-Otero. Examining reasons for breast cancer disparities in African American women in Duval County, FL. [abstract]. In: Proceedings of the Eighth AACR Conference on The Science of Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; Nov 13-16, 2015; Atlanta, GA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2016;25(3 Suppl):Abstract nr C06.
Abstract C26: Epigenetics and pancreatic cancer: The role of nutrigenomics in cancer health disparities
Authors: Lyn-Cook Beverly , Word Beverly , Joseph Stancy , Hammons Goorge 
Published: May 2016

Abstract
In vivo, in vitro and epidemiological studies have shown that an individual's diet may contribute to their susceptibility to develop cancer. Pancreatic cancer remains a very complex and challenging disease that is increasing in African Americans. This cancer carries one of the worst prognosis of any major malignancy, mainly due to its lack of early detection and lack of effective therapeutic agents. Although improvements in imaging technology has aided in diagnosis and identification of patients with the disease, these new technologies have not greatly improved the mortality rate of pancreatic cancer. Evidence has shown that epigenetic mechanisms play an important role early in this cancer and furthermore, epigenetic modifications can be altered by external or internal environmental factors, such as components found in diets, and have the potential to also be reversed. We and others have shown that dietary agents found in cruciferous vegetables, such as indole-3-carbinol, have tremendous anti-cancer effects and can modulate key signals in pancreatic cancer through various mechanisms, such as inactivation of STAT3, reactivation of p16, the ability to up-regulate critical drug transporters such as hENT, to increase drug efficacy and recently modulate Wnt signaling pathways. All of these targets are potentially significant in developing chemopreventive strategies for reducing cancer health disparities among higher risk populations. Results will be shown where indole-3-carbinol has demonstrated effects on all of these targets in pancreatic cancer. Educational strategies are needed to increase knowledge of the importance of proper diet to vulnerable populations.
Citation Format: Beverly Lyn-Cook, Beverly Word, Stancy Joseph, Goorge Hammons. Epigenetics and pancreatic cancer: The role of nutrigenomics in cancer health disparities. [abstract]. In: Proceedings of the Eighth AACR Conference on The Science of Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; Nov 13-16, 2015; Atlanta, GA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2016;25(3 Suppl):Abstract nr C26.
Abstract C50: Sensitivity of triple-negative breast cancer cell lines to cytotoxic and targeted agents as a function of molecular subtype
Authors: Colley Heather , Saxena Roopali , Ogden Angela , Cantuaria Guilherme , Reid Michelle D. , Li Xiaoxian (Bill) , Krishnamurthy Uma , Rida Padmashree CG , Aneja Ritu 
Published: May 2016

Abstract
Triple-negative breast cancer is a heterogeneous disease with no approved targeted therapies. The disease course is very aggressive, characterized by relapse within 3 years of treatment and metastases to the viscera, including the brain. The prognosis in the setting of distant metastases is grim, as median survival is less than one year. Recently, insight into the molecular complexity of TNBC was provided by gene expression analysis, which identified six unique subtypes with distinct gene ontologies that differ with respect to drug sensitivity. These subtypes, each enriched in unique molecular components and pathways, suggest target-based strategies for treatment. A multiplicity of targeted drugs has entered clinical trials for the potential treatment of TNBC, but no uncontested victor has emerged that can appreciably extend overall survival. For instance, one of the most promising experimental drugs is iniparib, which significantly improved outcomes in a Phase II clinical trial of metastatic TNBC when combined with carboplatin/gemcitabine; however, overall survival was still unacceptably short at ~1 year. Therefore, there remains a dire need to identify novel therapeutic modalities for TNBC. A promising research strategy towards this goal is to determine the differential sensitivities of the TNBC molecular subtypes to combinations of cytotoxic and targeted drugs. We are determining the responses of a panel of TNBC cell lines representing different molecular subtypes, including the basal-like 1 (HCC1143 and MDA-MB-468), basal-like 2 (HCC1806 and HCC70), immunomodulatory (HCC1187), mesenchymal stem-like (MDA-MB-436, MDA-MB-231, and MDA-MB-157), and luminal androgen receptor (MFM-223) subtypes, to variable doses of carboplatin, capecitabine, cyclophosphamide, docetaxel, and everolimus, used alone and in combination. These drugs were chosen because they target molecular regulators of prominent signaling pathways specific to certain TNBC molecular subtypes, so we expect to find that sensitivity to these drugs is a function of subtype. The results of this study will enable characterization of TNBC subtypes in finer detail and provide a preclinical framework for the development of subtype-dependent regimens for TNBC treatment.
Citation Format: Heather Colley, Roopali Saxena, Angela Ogden, Guilherme Cantuaria, Michelle D. Reid, Xiaoxian (Bill) Li, Uma Krishnamurthy, Padmashree CG Rida, Ritu Aneja. Sensitivity of triple-negative breast cancer cell lines to cytotoxic and targeted agents as a function of molecular subtype. [abstract]. In: Proceedings of the Eighth AACR Conference on The Science of Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; Nov 13-16, 2015; Atlanta, GA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2016;25(3 Suppl):Abstract nr C50.
Abstract C52: Targeting the obesity/leptin link to TNBC: A breast cancer disparity problem
Authors: Dill Courtney D. , Harbuzariu Adriana , Harmon Tia L. , Lipsey Crystal C. , Loye Ayobami , Gonzalez-Perez Ruben Rene 
Published: May 2016

Abstract
Triple Negative Breast Cancer (TNBC) is an aggressive cancer associated with poor prognosis and is difficult to treat. Standard therapy for TNBC includes a combination of chemotherapeutic drugs: doxorubicin (DOX), paclitaxel (TAX), and cyclophosphamide (CTX). Current epidemiological data show that obesity increases TNBC incidence, which is more relevant for African American women. Recent findings suggest that leptin (an adipokine increased in obesity) is involved in TNBC acquired drug resistance via induction of breast cancer stem cells (BCSCs). Understanding the role of obesity in TNBC is vital to the development of new and effective therapies. Chemotherapeutic drugs exhibit shortcomings that may be due to increased drug resistance, survival, proliferation, and angiogenic signal redundancy induced by leptin. Our lab has developed and tested a novel, specific inhibitor of leptin signaling, LPrA2. A pegylated derivative of LPrA2 (PEG-LPrA2) has previously shown to enhance, 68 fold, LPrA2's bioavailability in mouse breast cancer models. The objective of this study was to determine the adjuvant effects of PEG-LPrA2 on TNBC in vitro. We hypothesized that PEG-LPrA2 can serve as an adjuvant for standard TNBC chemotherapeutics. This adjuvant would allow for the reduction of chemoresistance and TNBC recurrence. It could also reduce chemotherapeutic dose and undesirable side effects associated with standard therapy for the disease. Two human TNBC cell lines were cultured: MDA-MB-231 (highly metastatic) and MDA-MB-468 (minimally invasive). Cellometer imaging technologies were used to determine S-phase progression in cells treated with PEG-LPrA2 and leptin. Flow cytometry technologies were used to determine the effects of leptin on BCSC surface markers. Additionally, in vitro toxicity of PEG-LPrA2 was tested in non-malignant mammary cells (MCF-10A) via MTT assay. Our data shows that leptin (1.2 nM, equivalent to serum levels of overweight individuals) induced S-phase progression and increased BCSC markers and the formation of TNBC tumorspheres. Remarkably, PEG-LPrA2 (1.2 nM) abrogated leptin induction of S-phase, BCSC markers, and tumorspheres. It also showed no toxicity in non-malignant cells. These results suggest leptin-signaling inhibition could be used as an adjuvant strategy for chemotherapy of TNBC. These results are most relevant for obese African American women suffering from TNBC.
Citation Format: Courtney D. Dill, Adriana Harbuzariu, Tia L. Harmon, Crystal C. Lipsey, Ayobami Loye, Ruben Rene Gonzalez-Perez. Targeting the obesity/leptin link to TNBC: A breast cancer disparity problem. [abstract]. In: Proceedings of the Eighth AACR Conference on The Science of Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; Nov 13-16, 2015; Atlanta, GA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2016;25(3 Suppl):Abstract nr C52.
Abstract C73: A relationship between mast cells and the racial disparity of prostate cancer
Authors: Hempel Heidi A. , Kulac Ibrahim , Cuka Nathan S. , Cornish Toby C. , Marzo Angelo M. De , Sfanos Karen S. 
Published: May 2016

Abstract
Prostate cancer afflicts African American men to a greater degree than European American men, with a 60% greater incidence and 2-3 times greater mortality. In addition, studies have shown that the incidence rate of distant metastasis is 4 times greater in African American men than in European American men, consistent with the notion that prostate cancer is more aggressive in African Americans. Of interest, African American men are also significantly more likely to present with inflammation in benign prostate biopsies, and studies have shown higher expression of a number of inflammatory markers in prostate cancer tissue from African Americans compared to European Americans. One immune cell type of particular interest in the context of prostate cancer are mast cells, which have the potential to play a number of roles in cancer, and have also been shown to increase in number in prostate cancer versus benign regions of the prostate. In the present study, immunohistochemistry (IHC) was used to directly visualize and localize mast cells in the prostate microenvironment of African American and European American men in a tissue microarray (TMA) containing tumor and benign tissues from 75 African American and 75 European American prostate cancer patients matched on tumor grade and stage. Automated counting of mast cell numbers as well as the calculation of mast cell-to-epithelial ratio (MC/Ep) and mast cell numbers per total tissue area (density) was aided by novel digital image analysis using a software framework integrating whole slide imaging, virtual microscopy, and ImageJ based analysis algorithms. Key results to date include the finding that mast cell density in prostate tumor tissues of African American men is significantly lower than that of Caucasian Americans (p &lt; 0.0001). This same trend was observed for total mast cell numbers and MC/Ep (p=0.001). These results suggest the intriguing possibility that a decrease in tumor-infiltrating mast cells may contribute to the racial disparity observed in association with prostate cancer and additional studies are underway to determine the biological function of mast cells in the prostate tumor microenvironment.
Citation Format: Heidi A. Hempel, Ibrahim Kulac, Nathan S. Cuka, Toby C. Cornish, Angelo M. De Marzo, Karen S. Sfanos. A relationship between mast cells and the racial disparity of prostate cancer. [abstract]. In: Proceedings of the Eighth AACR Conference on The Science of Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; Nov 13-16, 2015; Atlanta, GA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2016;25(3 Suppl):Abstract nr C73.
Abstract C78: NILCO: A marker for obesity-related endometrial cancer in African American women
Authors: Daley-Brown Danielle , Oprea-Ilies Gabriela , Lee Regina , Vann Kiara T. , Lanier Viola , Quarshie Alexander , Lillard James , Pattillo Roland , Gonzalez-Perez Ruben Rene 
Published: May 2016

Abstract
Obesity is a pandemic in Western countries and has a significant impact on endometrial cancer (EmCa) incidence and prognosis. Although EmCa is more common in Caucasian women, higher mortality is found in African Americans who also show higher incidence of obesity. The reasons for this cancer health disparity are not completely understood. Obesity is characterized by high levels of leptin. Leptin signaling may play a key role in the progression of the more aggressive form of EmCa, Type II, which is independent from hormonal cues. We have shown that leptin induces a signaling crosstalk in breast cancer with oncogenic and angiogenic factors (NILCO: Notch, IL-1 and Leptin Crosstalk Outcome). Hence, we hypothesize that NILCO could play an important role in Type II Emca developed by obese African American women. However, no data on NILCO signaling in EmCa is currently available. Real-Time PCR, Immunohistochemistry and Western Blot analyses were used to determine whether NILCO components are differentially expressed in EmCa biopsies (Type I vs Type II EnCa) obtained from obese African American women. All tissue samples had a paired control sample from adjacent non-tumor endometrial tissue determined by pathologists. The tissue samples (n=29) were obtained from Grady Memorial Hospital, Atlanta, GA. Patient's written informed consent was obtained for all samples collected as well as IRB approval from Morehouse School of Medicine, Atlanta, GA. In addition, commercially available EmCa tissue arrays from Chinese patients were co-examined for the expression of NILCO. Biopsy features included age, grading, and TNM staging. However, no body weight or body mass index information was available. Each array contained 150 cores, including 75 cases in duplicate. Overall, NILCO molecules were expressed higher in Type II EmCa regardless of obesity status. Notably, Type II EmCa from obese African American women showed the highest expression of NILCO. Present data suggest for the first time that NILCO could be instrumental for the development of EmCa; more specifically for obesity-related Type II EmCa, and may play a role as potential biomarkers for the disease.
Citation Format: Danielle Daley-Brown, Gabriela Oprea-Ilies, Regina Lee, Kiara T. Vann, Viola Lanier, Alexander Quarshie, James Lillard, Roland Pattillo, Ruben Rene Gonzalez-Perez. NILCO: A marker for obesity-related endometrial cancer in African American women. [abstract]. In: Proceedings of the Eighth AACR Conference on The Science of Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; Nov 13-16, 2015; Atlanta, GA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2016;25(3 Suppl):Abstract nr C78.
Abstract IA11: Understanding and overcoming cancer disparities in the U.S. and abroad
Authors: Lowy Douglas R. 
Published: May 2016

Abstract
In the United States, although differences in cancer-associated mortality rates between various minority groups have decreased somewhat, substantial disparities remain for several cancer types. Groups with these disparities are, therefore, high-risk populations whose risk factors need to be understood and overcome when feasible. Several factors – including biology, lifestyle, and health care access/utilization – contribute to these differences. For a given cancer type, research can, in principle, determine the relative importance of each factor, the mechanisms, and the potential for short-term and long-term intervention to mitigate them. The National Cancer Institute is committed to supporting research with the potential to make substantial advances in this important field.
In low- and middle-income countries (LMICs), cancer incidence and mortality rates are projected to increase for the foreseeable future. Many factors contribute to these increases. They include success against acute infectious diseases, increased life expectancy, increased tobacco consumption, limited resources, and inadequate infrastructure. There are many opportunities for research to advance understanding and mitigation of cancer in LMICs. Here, I highlight how technological advances and ongoing research – with HPV vaccination and cervical cancer screening – can lead to the cost-effective ability in LMICs to drastically reduce the incidence and mortality from cervical cancer, which remains the third most common cancer of women worldwide and is the most common female cancer in many LMICs.
Citation Format: Douglas R. Lowy. Understanding and overcoming cancer disparities in the U.S. and abroad. [abstract]. In: Proceedings of the Eighth AACR Conference on The Science of Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; Nov 13-16, 2015; Atlanta, GA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2016;25(3 Suppl):Abstract nr IA11.
Abstract IA25: Immunotherapy: Is it within everyone's reach?
Authors: Salazar Lupe G. 
Published: May 2016

Abstract
Cancer immunotherapy is an exciting and active area of cancer research; and several new immunotherapies have been approved for treatment of melanoma and lung cancer. Moreover, in melanoma, treatment with these immunotherapeutic agents has shown to nearly double the survival rate of patients with metastatic disease. Additionally, in on-going clinical trials, immunotherapy is also showing promise in regards to both safety and effectiveness in other types of cancer including breast and ovarian. However, access to these new immunotherapies is not the same for all cancer patients. Within medically underserved populations there are various factors that prohibit cancer patients from receiving these new and promising therapies. This presentation will review current cancer immunotherapeutic agents, their effectiveness and cost, as well as the challenges around ensuring that all patients who would benefit from these agents have access to them.
Citation Format: Lupe G. Salazar. Immunotherapy: Is it within everyone's reach? [abstract]. In: Proceedings of the Eighth AACR Conference on The Science of Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; Nov 13-16, 2015; Atlanta, GA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2016;25(3 Suppl):Abstract nr IA25.