bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract PO-126: PVT1 exon 9 transcript regulates claudin 4 expression and migration in triple negative breast cancer
Authors: Levine Fayola , Ogunwobi Olorunseun 
Published: December 2020

Abstract
Breast cancer (BC) is a heterogeneous disease that is classically driven by the estrogen receptor (ER), progesterone receptor (PR) and human epithelial growth factor receptor 2 (EGFR2/HER2) signaling pathways. Triple negative breast cancer (TNBC), is a lethal subtype of invasive BC tumors that are ER-, PR- and HER2-. A subtype of TNBC is claudin low (CL). Dysregulation of claudin proteins disrupts tight junctions, consequently inducing the epithelial-to-mesenchymal transition (EMT) in cancers. This leads to enhanced motility and metastasis. Patients with CL TNBC have worse prognosis than patients with other BC subtypes. PVT1 is a long noncoding RNA (lncRNA) transcribed from the 8q24 genomic locus that has been implicated in multiple cancers including BC. Amplification of the 8q24 gene locus is a common event in many malignant diseases and is associated with poor clinical outcomes.
Although previous research has implicated PVT1 as an important player in BC, the underlying molecular mechanisms of PVT1 in CL TNBC was previously unknown. We assessed PVT1 expression in BC, and we observed that PVT1 exons 4A, 4B, and 9 are significantly upregulated in MDA MB 231 cells (claudin low) and significantly downregulated in MDA MB 468 cells (claudin high), in comparison to T47D (ER+). We have confirmed that claudin expression, specifically claudins 1, 3, 4 and 7, are significantly higher in MDA MB 468 cells and significantly lower in MDA MB 231 cells. Knockdown of PVT1 exon 9 expression in the MDA MB 231 cell line, led to a significant reduction in migration when compared to cells transfected with a control scramble siRNA, indicating that PVT1 exon 9 regulates migration in CL TNBC. Interestingly, we observed that claudin 4 expression, and not claudins 1, 3 and 7, was increased in cells where PVT1 exon 9 was knocked down when compared to the control cells. This indicates that PVT1 exon 9 regulates claudin 4 protein stability in CL TNBC. We also assessed the expression of EMT markers (vimentin, fibronectin, and E-cadherin) in MDA MB 231 cells. We observed no changes in EMT markers when PVT1 exon 9 is knocked down; however, our data suggests that EMT markers are more highly expressed in MDA MB 231 cells in comparison to MDA MB 468 cells. Taken together, our data indicate that PVT1 exon 9 regulates claudin expression and migration in CL TNBC, and may have implications for clinical outcomes in TNBC.
Citation Format: Fayola Levine, Olorunseun Ogunwobi. PVT1 exon 9 transcript regulates claudin 4 expression and migration in triple negative breast cancer [abstract]. In: Proceedings of the AACR Virtual Conference: Thirteenth AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2020 Oct 2-4. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2020;29(12 Suppl):Abstract nr PO-126.
Abstract PO-142: Development of Empirical Dietary Inflammatory Pattern (EDIP) scores with different food groups and biomarkers
Authors: Guyonnet Emma , Amankwah Millicent , Chen Yalei , Martini Rachel , Davis Melissa , Newman Lisa 
Published: December 2020

Abstract
Background: The empirical dietary inflammatory pattern (EDIP) is a hypothesis- driven dietary pattern used to assess the inflammatory potential of diet in the US population. It is usually composed of food groups obtained from a food-frequency questionnaire. Methods: EDIP scores were calculated for 4 models from 24hr recalls reported by 67 women noncancer controls that had signed an informed consent prior to participation. The Luminex Human Chemokine Multiplex Assay was used to measure 11 chemokines and cytokines. As seen in previous studies, we first derived a model, EDIP-Limited (EDIP-L), by entering 18 food groups in reduced rank regression models followed by a multivariable regression analysis to identify a dietary pattern that predicts concentrations of two inflammatory biomarkers: IL-6 and TNF-a. We derived another EDIP score using a new model, EDIP-All Inclusive (EDIP-AI), which included the same 18 food groups to predict all 11 biomarkers. Lastly, we developed two other EDIP models. EDIP-Limited New (EDIP-LN) used 14 new food groups derived from the same 24hr recalls, only predicting IL-6 and TNF-a. EDIP-All New (EDIP-AN) used those 14 food groups with all 11 biomarkers. Results: In this study, we optimize models for EDIP and report the differences in EDIP scores based on the inflammatory biomarkers and food groups used in analysis. Briefly, the components of EDIP-L were not significant. After including all the biomarkers, the components of EDIP-AI were: “fruit juice” (p = 0.0009), “snacks” (p = 0.0008), “leafy green vegetables” (p = 0.0074), “low-energy beverages” (p = 0.0098), “red meat” (p = 0.0038), “fruit” (p = 0.0002) and “whole wheat grains” (p = 0.0138). Similarly, after reorganizing our food items into 14 food groups, the components of EDIP-LN were not significant. However, components of EDIP-AN were: “fruit juice” (p = 0.0107), “snacks” (p = 0.0116) and “fruit” (p = 0.0026). Conclusions: Findings demonstrate the EDIP scores differ based on the inflammatory biomarkers and food groups used in the analysis on the same noncancer controls. Depending on the methods used, an individual’s diet may be considered more pro- or anti-inflammatory. This study provides insight into the inflammatory potential of an individual’s diet and the factors that may affect how we calculate this potential.
Citation Format: Emma Guyonnet, Millicent Amankwah, Yalei Chen, Rachel Martini, Melissa Davis, Lisa Newman. Development of Empirical Dietary Inflammatory Pattern (EDIP) scores with different food groups and biomarkers [abstract]. In: Proceedings of the AACR Virtual Conference: Thirteenth AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2020 Oct 2-4. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2020;29(12 Suppl):Abstract nr PO-142.
Abstract PO-175: National trends in younger onset obesity-related cancer incidence
Authors: Begi Talia , Tripathi Osika , Offor Paris , Thompson Caroline A. 
Published: December 2020

Abstract
Obesity is a risk factor for many cancers, and obesity-related cancer incidence in the United States (U.S.) has been rising over the years. In the recent decades, the younger population of the United States has experienced an increase in obesity.
These increases have been the highest among ethnic minorities, and in the Southeast, while they have been less evident in the Northeast. The impact of rising rates of obesity among younger individuals on younger onset cancer incidence is less well understood. We estimated 15-year trends in incidence for 11 obesity-related cancers among adults under the age of 50 stratified by race/ethnicity and geographic region of the United States. Age adjusted incidence rates for cancers of the female breast, colorectal, endometrial, esophageal, hepatocellular carcinoma, kidney, multiple myeloma, non-cardia gastric, ovarian, pancreatic, and thyroid cancers were calculated from 2001-2016 using data obtained from Surveillance, epidemiology, and End Results (SEER-18). Data were stratified by age +/- 50 years old, four racial/ethnic groups: non-Hispanic white (NHW), non-Hispanic black (NHB), Asian American or Pacific Islander (AAPI), and Hispanic, and four geographical regions: West, Midwest, Northeast, and Southeast, and by sex. We used SEER*Stat and JoinPoint software for analysis. We observed statistically significant increasing 15-year trends among younger adults for colorectal cancer in NHWs, NHBs, and Hispanics, kidney cancer in all race groups, multiple myeloma among NHBs, non-cardia gastric cancer in Hispanic males and thyroid cancer in NHW and AAPI males. Stratification by geography revealed increasing trends of younger onset female breast cancer in the Midwest and that increasing trends for younger onset myeloma, non-cardia gastric, and thyroid cancers are steepest in the Northeastern U.S. and steepest for younger onset colorectal cancer in the Southeast U.S. We observed increasing trends in younger onset cancers of the kidney, colorectal, multiple myeloma, non-cardia gastric, thyroid, and female breast. Preventing obesity in ways such as education, better food produce availability and programs, and lower healthcare costs may reduce the impact of these cancers. Reduced age for screening for colorectal cancer may improve opportunity for earlier detection and improved prognoses in younger adults.
Citation Format: Talia Begi, Osika Tripathi, Paris Offor, Caroline A. Thompson. National trends in younger onset obesity-related cancer incidence [abstract]. In: Proceedings of the AACR Virtual Conference: Thirteenth AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2020 Oct 2-4. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2020;29(12 Suppl):Abstract nr PO-175.
Abstract PO-184: Air pollution in relation to risk of pancreatic cancer in the Multiethnic Cohort Study
Authors: Bogumil David , Wu Anna H. , Stram Daniel , Tseng Chiu-Chen , Cheng Iona , Setiawan Veronica Wendy 
Published: December 2020

Abstract
Background: There are limited studies that have investigated the association between ambient gaseous and particulate matter (PM) air pollutants and risk of pancreatic cancer. Results from published studies are inconsistent, the strongest evidence was a significant, 16% increase in risk of pancreatic cancer mortality per 10 µg/m3 increase in PM &lt;2.5 µm (PM2.5) in China. We used data from the Multiethnic Cohort Study to examine prospectively associations between ambient air pollutants and incident pancreatic cancer, while adjusting for a comprehensive list of confounding factors. Methods: Kriging Interpolation was used to estimate individual, time varying, monthly, air pollutant exposure levels of nitrogen oxides (NOX, NO2) and PM (PM2.5, PM10) pollutants for 100,527 men and women, who resided largely in Los Angeles County at the time of enrollment (1993-1996) through 2014. We observed 844 incident cases of pancreatic cancer among cohort members during the 18-years of follow up. Cox proportional hazard models were used to estimate the association between each air pollutant and risk of pancreatic cancer. All models adjusted for age, sex, race/ethnicity, neighborhood socioeconomic status, body mass index, diabetes mellitus, and smoking history. Results: PM2.5 was non-significantly positively associated with risk of pancreatic cancer (hazard ratio [HR]=1.33; 95% CI: 0.91, 1.95 per 10 µg/m3). No associations were observed with other pollutants (PM10 [HR=0.99; 95% CI=0.96, 1.07 per 10 ppb], NO2 [HR=0.99, 95% CI 0.93; 1.17], NOx [HR=1.01 95% CI=0.96, 1.07]). In stratified analyses, we did not observe heterogeneity by race/ethnicity (PM2.5 p=0.17, PM10 p=0.16, NO2 p=0.30, NOx p=0.27) or smoking status (PM2.5 p=0.72, PM10 p=0.85, NO2 p=0.53, NOx p=0.28). Conclusions: In this prospective cohort study of air pollution and risk of pancreatic cancer, we did not observe an increase in risk associated with PM2.5, PM10, NO2, or NOx. These results add to the scarce data on the association between air pollution and pancreatic cancer risk.
Citation Format: David Bogumil, Anna H. Wu, Daniel Stram, Chiu-Chen Tseng, Iona Cheng, Veronica Wendy Setiawan. Air pollution in relation to risk of pancreatic cancer in the Multiethnic Cohort Study [abstract]. In: Proceedings of the AACR Virtual Conference: Thirteenth AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2020 Oct 2-4. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2020;29(12 Suppl):Abstract nr PO-184.
Abstract PO-192: Exploring the contribution of introgressed ancient DNA to prostate cancer racial disparity
Authors: Useh Evi O. , Venugopal Suresh , Molokwu Chidi N. 
Published: December 2020

Abstract
Introduction Prostate cancer is the most common cancer in men and there is racial disparity in prostate cancer incidence and mortality globally, with greater disease burden in men of African ancestry, followed by European ancestry and least in men of Asian ancestry. The etiology of prostate cancer is not fully understood but includes genetic and environmental factors. Present day non-Africans are reported to have introgressed DNA from Neanderthal and Denisovan ancestors. Over 170 prostate cancer associated single nucleotide polymorphisms (SNPs) have been identified from several genome-wide association studies (GWAS), with SNPS on chromosomes 2, 8 and 22 reported as showing variation between African and non-African men with prostate cancer. We performed analysis of prostate cancer associated SNPs on chromosomes 2, 8 and 22 to determine if DNA introgression could explain the racial variation. Methods We obtained data on prostate cancer associated SNPs from the GWAS catalog (https://www.ebi.ac.uk/gwas) and from reports that were not included in the catalog. Using an Ancient Genome Browser provided by the Max Plank Institute (https://www.eva.mpg.de/genetics/genome-projects/neandertal/index.html), we determined whether SNPs on chromosomes 2, 8 and 22 were present in African, Neanderthal or Denisovan genomes. Based on the results, we inferred that SNPs were introgressed if they were present in Neanderthal or Denisovan genomes but absent from African genomes. Results 49, 59 and 17 prostate cancer SNPs were reported in chromosomes 2, 8 and 22 respectively. 23/49 in ch2, 25/59 in c 8 and 9/17 in ch22 were present in in Neanderthal and or Denisovan genomes. SNPs in ch2 (rs13403657, rs12621278) and ch8 (rs7825414) were present in Neanderthal or Denisovan genomes but absent in African genomes. These SNPs lie in regions that have previously been reported to harbour introgressd DNA. Conclusion Our analyses identified prostate cancer associated SNPs that are likely to have been introgressed into present day non-Africans by extinct Neanderthal and Denisovan ancestors. Phenotypic changes caused by introgressed DNA could be contributing to racial disparities in prostate cancer in present day humans.
Citation Format: Evi O. Useh, Suresh Venugopal, Chidi N. Molokwu. Exploring the contribution of introgressed ancient DNA to prostate cancer racial disparity [abstract]. In: Proceedings of the AACR Virtual Conference: Thirteenth AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2020 Oct 2-4. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2020;29(12 Suppl):Abstract nr PO-192.
Abstract PO-193: Gender, women, and lung cancer: Times are changing
Authors: Tandon Radhika , Stanifer B. Payne , D'Ovidio Frank , Saqi Anjali , Sonett Joshua 
Published: December 2020

Abstract
Objective Recent literature has indicated a shift in the pattern of incidence rates of lung cancer among men than among women in non-Hispanic whites and Hispanics born since the mid-1960’s. These changes are not fully explained by differences in smoking behaviors. The goal of our study is to determine the role, if any, of race on lung cancer in never-smokers in patients undergoing lung cancer surgery. Methods Our institutional database (Columbia University Medical Center) was queried from 2006 to 2018 for all patients undergoing lung cancer surgery. A total of 1631 cases of NSCLC were reported. We analyzed the cohort for differences in basic demographics, including sex, race, and smoking status. Results In Hispanic, Asian, and Black, but not White populations undergoing lung cancer surgery, non-smokers were significantly more likely to be women (p=0.01, 0.00001, 0.03). The proportion of never-smoking patients in men and women is dependent on race in Asian, Black, Hispanic, Non- Hispanic White, and all White populations (p=0.09). Conclusions The varying epidemiology of male and female lung cancer patients shows significant differences, by smoking status and race. This emphasizes the necessity for further research into the pathogenesis of nonsmoking related lung cancer. Our further research will utilize genomic analysis and multi-institutional statistical analyses to further investigate these differences.
Citation Format: Radhika Tandon, B. Payne Stanifer, Frank D'Ovidio, Anjali Saqi, Joshua Sonett. Gender, women, and lung cancer: Times are changing [abstract]. In: Proceedings of the AACR Virtual Conference: Thirteenth AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2020 Oct 2-4. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2020;29(12 Suppl):Abstract nr PO-193.
Abstract PO-209: Breast cancer survival disparities by insurance status or racial/ethnic in specific patient populations
Authors: Wang Kaicheng , Hu Jennifer J. , Reis Isildinha M. , Zhao Wei , Yang George R. , Herna Stuart 
Published: December 2020

Abstract
Introduction: Health insurance status reflects patients’ socioeconomic status, which determines healthcare access and is associated with prognosis and survival. Limited research has reported the association between insurance status and breast cancer survival, potentially mediated through healthcare access. Method: Tumor registry data from University of Miami Health System and Jackson Memorial Hospital between 2008 to 2018 were used to estimate the association between race/ethnicity, insurance status and tumor stage at diagnosis; effect of insurance status on the likelihood of receiving specific breast cancer treatment; and overall survival by race/ethnicity and insurance status. Overall, 4392 breast cancer patients were included in the study. Odds ratios (ORs) and 95% confidence intervals (CIs) for the likelihood of being diagnosed with advanced stage breast cancer by race/ethnicity and insurance status, and likelihood of receiving specific treatments by insurance status and race/ethnicity were evaluated. Five-year overall survival probabilities and hazard ratios (HRs) by race/ethnicity and insurance status were also examined. Results: African-American patients and patients who had Medicaid or were uninsured were more likely to be diagnosed with advanced stage breast cancer. Under-coverage patients were less likely to receive cancer-specific treatment. Five- year survival rate was significantly lower in African-Americans compared to non- Hispanic whites (74.2% and 85.7%; p&lt;.001). Overall survival was also significantly worse in African-Americans compared to non-Hispanic Whites (HR, 1.40; 95%CI, 1.12-1.76). Patients who had Medicare (&lt;65 years of age) (HR, 1.84; 95%CI, 1.19- 2.86) or Medicaid (HR, 1.23; 95%CI, 1.00-1.51) had significantly worse survival compared to patients with private insurance. Among HER2 positive patients, those who were covered by Medicare (≥65 years) (HR, 3.02; 95%CI, 1.04-8.80), Medicaid (HR, 2.31; 95%CI, 1.14-4.69), or no insurance (HR, 3.02; 95%CI, 1.44-6.32) had significantly higher hazards of death than privately insured patients. Conclusions: This study identified Medicare, Medicaid, and uninsured patients as having higher hazards of death compared to privately insured patients, which can inform health professionals and policy makers to advocate for equal health outcomes regardless of insurance.
Citation Format: Kaicheng Wang, Jennifer J. Hu, Isildinha M. Reis, Wei Zhao, George R. Yang, Stuart Herna. Breast cancer survival disparities by insurance status or racial/ethnic in specific patient populations [abstract]. In: Proceedings of the AACR Virtual Conference: Thirteenth AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2020 Oct 2-4. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2020;29(12 Suppl):Abstract nr PO-209.
Abstract PO-222: Co-morbid risk factors and NSAID use among white and black Americans that predicts overall survival from diagnosed colon cancer
Authors: Koi Minoru , Okita Yoshiki , Koeppe Erika , Stoffel Elena M. , Galanko Joseph A. , McCoy Nikki , Keku Temitope , Carethers John M. 
Published: December 2020

Abstract
Black Americans (BA) have higher incidence and higher mortality rates for colorectal cancers (CRC) as compared to White Americans (WA). While there are several identified risk factors associated with the development of CRC and evidence that high levels of adequate screening can reduce differences in incidence for CRC between BA and WA, there remains little data regarding patient co-morbid contributions towards survival once an individual has CRC. Here we set out to identify patient risk factors that influenced overall survival in a cohort of 293 BA and 348 WA with colon cancer, ages 40 to 84 years old, with at least 10 years of follow- up. We utilized the logistic regression test for statistical associations, the Kaplan- Meier method with log rank test for survival analyses, and Cox Proportional Hazards Models for covariate independence. Amid our cohort, we found that patients’ age, tobacco usage, and pre-diagnosed medical conditions such as hypertension and diabetes were associated with shorter overall survival (OS) from colon cancer. We identified pre-diagnosed hypertension (19.6% contribution) and diabetes (12% contribution) among BA were together responsible for nearly one-third of the colon cancer mortality disparity compared with WA. We also identified long-term regular use (&gt;5 years aggregated years of drug use) of non-steroidal anti-inflammatory drugs (NSAIDs), including aspirin, was associated with shorter OS from colon cancer among WA &gt;65 years of age (Hazard Ratio 1.76, 95% confidence interval 1.12-2.77), but not younger WA patients or any aged BA patients. Our results raise the importance of not only treating the colon cancer itself, but also taking into consideration co-morbid medical conditions and NSAID usage to enhance patient OS. Further evaluation regarding adequate treatment of co-morbidities and timing of NSAID continuance after cancer therapy will need to be studied.
Citation Format: Minoru Koi, Yoshiki Okita, Erika Koeppe, Elena M. Stoffel, Joseph A. Galanko, Nikki McCoy, Temitope Keku, John M. Carethers. Co-morbid risk factors and NSAID use among white and black Americans that predicts overall survival from diagnosed colon cancer [abstract]. In: Proceedings of the AACR Virtual Conference: Thirteenth AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2020 Oct 2-4. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2020;29(12 Suppl):Abstract nr PO-222.