bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract B062: Prevalence of pathogenic BRCA1/2 variants among Latinas in the All of Us Cohort
Authors: Samayoa Cathy , Olivares Erick , Gavile Catherine , Visbal Adriana 
Published: December 2023

Abstract
Latinas in the United States are disproportionately affected by breast cancer, but little is known about genetic risk factors for breast cancer in this population. Genetic variants in BReast CAncer genes 1 and 2 (BRCA1/2) are known to be associated with heritable cancer risk, yet the prevalence of BRCA1/2 pathogenic variants in the Latina population is not well characterized. This study aims to examine the prevalence of pathogenic BRCA1/2 variants among Latinas in the NIH All of Us research program, which includes a large number of individuals representative of the diversity of the United States population. Using data from the All of Us research program, we will analyze the prevalence of these variants among Latinas, in addition to all other racial and ethnic groups. To date, the All of Us cohort contains 245,400 genomes, and of those 41,940 (17%) are from self-identified Hispanic/Latino/or Spanish participants. We will compare the prevalence of pathogenic, or likely pathogenic, variants across self-reported race/ethnicity and continental genetic ancestry categories. Our study will leverage the diversity of All of Us and enable us to compare our data with those from more Eurocentric databases. With these data, we can potentially 1) identify novel variants that could predispose to increased cancer risk; and 2) clarify the previous designations of variants characterized to have undetermined/unknown significance due to the limitations of using a single Eurocentric reference genome. Identifying the actual prevalence of pathogenic BRCA1/2 variants among Latinas is important for improving breast cancer prevention, detection, and treatment in this population. The findings of this study have the potential to inform genetic counseling and testing recommendations for Latina patients at high risk of developing breast cancer, as well as others. This will also enable healthcare providers to better understand the unique genetic factors contributing to breast cancer risk among this population. Ultimately, this knowledge can improve the care of Latina patients and contribute to the broader effort to advance health equity and reduce disparities in breast cancer outcomes among Latinas.
Citation Format: Cathy Samayoa, Erick Olivares, Catherine Gavile, Adriana Visbal. Prevalence of pathogenic BRCA1/2 variants among Latinas in the All of Us Cohort [abstract]. In: Proceedings of the 16th AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2023 Sep 29-Oct 2;Orlando, FL. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2023;32(12 Suppl):Abstract nr B062.
Abstract B069: Lung cancer risk in women and racial minorities and genetic variants of UGT genes
Authors: Gallagher James W. , Vicks Talayshia , Gallagher Carla J. 
Published: December 2023

Abstract
The major research focus of this project is the identification of genetic variants involved in disparities in carcinogen metabolism and risk for cancer. Specifically, this research focuses on the identification of genetic variants in carcinogen metabolism genes, that increase lung cancer risk, particularity when the risk differs between men and women or by racial groups. Although cigarette smoking causes the vast majority of lung cancers, most lifetime smokers do not develop this disease. Many studies suggest that women have greater susceptibility than men for lung cancer, and that risk varies by racial groups. Genetic variation in tobacco carcinogen-metabolizing enzymes could give details as to why only some smokers develop lung cancer and why women or certain racial groups may be at a greater risk. Genetic changes have been shown to vary significantly between individuals of different races, which could contribute to racial disparities in cancer risk. Uridine glucuronosyltransferase (UGT) genes detoxify many carcinogens found in tobacco, so variants in UGT genes could explain differences in lung cancer risk among smokers. Many genetic association studies of UGT genes and lung cancer risk have been performed to identify alleles (SNPs and Copy Number Variants) in UGT genes that increase risk for lung cancer, and to determine if some variants display a gender or racial-specific association with this cancer. cBioPortal provides gene-based visualizations and analyses, so that users can find altered genes and/or networks within a study of interest or across all cancer studies. cBioPortal is a web application platform that facilitates data exploration and analysis through the use of a variety of visualization and analytical tools using populations of cancer cases and controls. cBioPortal has been utilized in this study to visualize variations in UGT genes across many lung cancer data sets. A copy number variant that deletes the entire UGT2B17 gene (which metabolizes the lung cancer carcinogen, NNAL) is a particular focus in this study using data from cBioPortal, as well as common copy number alterations (amplifications) in UGT3A1 and UGT3A2.
Citation Format: James W. Gallagher, Talayshia Vicks, Carla J. Gallagher. Lung cancer risk in women and racial minorities and genetic variants of UGT genes [abstract]. In: Proceedings of the 16th AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2023 Sep 29-Oct 2;Orlando, FL. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2023;32(12 Suppl):Abstract nr B069.
Abstract B096: Cigarette smoking and prostate cancer aggressiveness among African and European American men
Authors: Ellis Edgar T. , Fairman Brian J. , Stahr Shelbie D. , Su L. Joseph , Hsu Ping-Ching 
Published: December 2023

Abstract
Background: Smoking is a modifiable lifestyle factor linked to prostate cancer (PCa) risk, but its association with PCa aggressiveness is unclear. Further, African-American men are likelier to smoke and be at risk for PCa. Therefore, we examined racial disparities in the association between cigarette smoking and PCa aggressiveness. Methods: Data for this study came from the North Carolina-Louisiana Prostate Cancer Project, a registry-based cohort study of incident PCa cases from 2004-2009 (n = 1,457). We defined PCa aggressiveness as high (Gleason score ≥ 8, Gleason score = 7 and TNM T3-T4, or prostate-specific antigen (PSA) score &gt; 20 ng/mL) or low (Gleason score &lt; 7, TNM T1-T2, and PSA &lt; 10 ng/mL). We classified cigarette smoking as current, former, or never. Our analyses used multivariable logistic regression to estimate adjusted odds ratios (OR) and 95% confidence intervals (CI). Results: One-third (35%) of PCa cases were high-aggressive. Half (48%) of the study sample was African-American. Current smoking, but not former smoking, was associated with high-aggressive PCa compared to never (OR = 2.2; 95% CI [1.5, 3.3]). African-Americans who currently smoked had higher odds of high-aggressive PCa than those who never smoked (OR = 3.2; 95% CI [1.9, 5.4]), as did those who formerly smoked (OR = 1.8; 95% CI [1.2, 2.3]). However, smoking did not significantly predict PCa aggressiveness in European-Americans. Conclusion: Cigarette smoking is associated with PCa aggressiveness, an association moderated by race. Future research should investigate the biological and social effects of smoking and PCa aggressiveness between racial groups.
Citation Format: Edgar T. Ellis, Brian J. Fairman, Shelbie D. Stahr, L. Joseph Su, Ping-Ching Hsu. Cigarette smoking and prostate cancer aggressiveness among African and European American men [abstract]. In: Proceedings of the 16th AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2023 Sep 29-Oct 2;Orlando, FL. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2023;32(12 Suppl):Abstract nr B096.
Abstract B109: Guidelines from the PRIMED Consortium on the use of population descriptors in polygenic risk model development and application
Authors: Kraft Peter , Konigsberg Iain , Gogarten Stephanie 
Published: December 2023

Abstract
Whether and how to use descriptors such as race, ethnicity, and ancestry in genomic research and clinical risk models is an ongoing and evolving topic of debate, because how we refer to populations and individuals can have known and unforeseen consequences, including detrimental scientific, clinical, social, and ethical impacts. Clinical risk models incorporating polygenic risk scores (PRS) may perform differently for individuals from populations different from those used in training and validation; in particular, the correlation between polygenic predictions and predicted traits often decrease as a function of genetic distance between training and target samples. Thus, describing the populations used to develop risk models and the populations where they will be applied is essential to evaluate clinical validity and utility. Previous work has often used race, ethnicity or continental ancestry (inferred from self-report and/or genetic data) to describe training samples and target populations, but such labels run the risk of reinforcing biological determinist views of race and may not capture important aspects of the population that can affect polygenic model performance, such as region and socioeconomic status. Population descriptors may also be directly included in clinical risk models. The Polygenic RIsk MEthods in Diverse Populations (PRIMED) Consortium covened a multidisciplinary Population Descriptors Working Group to propose guidelines on conceptualizing, applying and communicating population descriptor information in the context of PRS development and application. These guidelines emphasize the importance of matching the chosen descriptors to the scientific and clinical goal; transparency; and engaging affected communities and subject matter experts to ensure that adequate considerations are given to ethical, legal, and social implications of their research and its communication. We present these guidelines and an accompanying data model designed to support transparency and flexibility.
Citation Format: Peter Kraft, Iain Konigsberg, Stephanie Gogarten. Guidelines from the PRIMED Consortium on the use of population descriptors in polygenic risk model development and application [abstract]. In: Proceedings of the 16th AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2023 Sep 29-Oct 2;Orlando, FL. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2023;32(12 Suppl):Abstract nr B109.
Abstract C015: Bridging the gap: A literature review of cancer mortality and incarcerated individuals
Authors: Isaacs Tamia , Oladeru Oluwadamilola , Li Jian , Iwai Yoshiko 
Published: December 2023

Abstract
There is a large and increasing rate of incarcerated individuals that face a risk of cancer. Cancer is the leading cause of death among the incarcerated population, resulting in a significantly shortened survival rate amongst said population. Very few studies have been conducted to truly assess the knowledge gap between incarceration and cancer outcomes. But, from the few that have been done, like the population-based study done by UF Radiation Oncology assistant professor, Dr. Oladeru, it was discovered that a higher risk of cancer mortality was prevalent in those who were diagnosed with cancer during their time incarcerated as well as one year post release than the general population. My goal and intent with this literature review is to open the conversation about possible ways to bridge the knowledge gap between cancer health disparities amongst incarcerated patients and contribution factors.
Citation Format: Tamia Isaacs, Oluwadamilola Oladeru, Jian Li, Yoshiko Iwai. Bridging the gap: A literature review of cancer mortality and incarcerated individuals [abstract]. In: Proceedings of the 16th AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2023 Sep 29-Oct 2;Orlando, FL. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2023;32(12 Suppl):Abstract nr C015.
Abstract C070: BACH1 regulates the hypoxia response and metastasis in triple negative breast cancer
Authors: Nguyen Long C. , Dann Christopher , Yang Dongbo , Shi Emily , Li Thomas , Stock Leticia , Henn Madeline , Khramtsova Galina , Liu Wenchao , Matsumoto Mitsuyo , Olopade Olufunmilayo , Igarashi Kazuhiko , Rosner Marsha 
Published: December 2023

Abstract
Triple-negative breast cancer (TNBC), the most aggressive subtype of breast cancer, is more prevalent among African American and underserved female populations. Hypoxia has recently been identified as one of the main drivers of TNBC, particularly within the African American cohort. Therefore, it is important to identify and target key regulators of hypoxia. Here we show that the pro-metastatic transcription factor BACH1 is induced by hypoxia and regulates the hypoxia response in TNBC tumor cells. BACH1 protein is destabilized via an oxygen-dependent prolyl-hydroxylation pathway, akin to Hypoxia-inducible Factors (HIFs). BACH1 mutants (BACH1M) resistant to hydroxylation exhibit heightened transcriptional activity and metastatic potential both in vitro and in vivo. TGCA analysis reveals that TNBC exhibits elevated BACH1 mRNA and hypoxia signature, irrespective of racial ancestry. Nevertheless, racial disparities in BACH1 mRNA expression exist across all breast cancer subtypes (Basal, Her, LumA, LumB). Our findings suggest that BACH1 is an oxygen-sensitive mediator of hypoxia and a promising therapeutic target for mitigating hypoxia-induced pro-metastatic signaling and treatment resistance. These results also highlight the necessity of accounting for racial differences in BACH1 expression and function as a means of developing targeted therapy that takes into account racial disparities in TNBC.
Citation Format: Long C. Nguyen, Christopher Dann, Dongbo Yang, Emily Shi, Thomas Li, Leticia Stock, Madeline Henn, Galina Khramtsova, Wenchao Liu, Mitsuyo Matsumoto, Olufunmilayo Olopade, Kazuhiko Igarashi, Marsha Rosner. BACH1 regulates the hypoxia response and metastasis in triple negative breast cancer [abstract]. In: Proceedings of the 16th AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2023 Sep 29-Oct 2;Orlando, FL. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2023;32(12 Suppl):Abstract nr C070.
Abstract C090: High GLUT1 membrane expression and low PSMA membrane expression in ductal adenocarcinoma and intraductal carcinoma of the prostate
Authors: Wang Xingming , Gao Xiaomei , Qi Lin , Zhang Ye , Yin Hongling , Gan Yu , Cai Yi 
Published: December 2023

Abstract
Background: Both Ductal Adenocarcinoma (DAC) and Intraductal Carcinoma (IDC) of the prostate are generally associated with aggressive clinical behavior and poor prognosis and can be lethal. Furthermore, previous studies linked aggressive clinical behavior and poor prognosis with discordant FDG positivity and low Prostate-specific membrane antigen (PSMA) expression. A recent study only cited a DAC patient with low 68Ga-PSMA-11 PET/CT uptake but high 18F-FDG PET/CT uptake, however, there is lack of directly compared articles nor large data sets. IDC-P has similar cribriform pattern in the pathological structure as a mean differential diagnosis for DAC. Hence, the objective of this study was to investigate the expression of PSMA and GLUT1 in DAC and IDC-P patients. Methods: The study was conducted on 87 DAC or IDCP patients without any treatment and 97 PAC patients with a Gleason score ≥ 8 of prostate biopsies and prostatectomy samples between August 2017 and August 2022. We performed immunohistochemical staining and scoring of various cancer component samples from the patients to reflect the protein expression levels of PSMA and GLUT1. Results: PSMA expression in PAC tissues was significantly higher than in DAC/IDC-P tissues (141.2 vs 78.6, p &lt; 0.001). There was no significant difference in PSMA membrane expression between DAC/IDC-P and adjacent acinar adenocarcinoma (78.6 vs 93.4, p = 0.166). GLUT1 expression was higher in DAC/IDC-P tissue than in acinar adenocarcinoma tissue adjacent to DAC/IDC-P (68.6 vs 51.3, p = 0.007), but was still lower than that in PAC tissue (68.6 vs 93.1, p = 0.0014). It is worth noting that GLUT1 membrane expression in DAC/IDC-P was significantly increased than in PAC (13.0 vs 6.6, p = 0.025), and in acinar adenocarcinoma adjacent to DAC/IDC-P (13.0 vs 2.0, p &lt; 0.001). Conclusions: In DAC and IDC-P tissues, PSMA membrane expression is low, while GLUT1 expression, especially GLUT1 membrane expression is high. These findings imply that DAC and IDC-P cells may have higher glucose metabolic and raise interest in targeting membrane GLUT1 as a novel anticancer strategy for DAC/IDC-P and other prostate cancer with high glucose metabolism.
Citation Format: Xingming Wang, Xiaomei Gao, Lin Qi, Ye Zhang, Hongling Yin, Yu Gan, Yi Cai. High GLUT1 membrane expression and low PSMA membrane expression in ductal adenocarcinoma and intraductal carcinoma of the prostate [abstract]. In: Proceedings of the 16th AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2023 Sep 29-Oct 2;Orlando, FL. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2023;32(12 Suppl):Abstract nr C090.
Abstract C103: Non-enzymatic glycoxidation reports on society, environment and biology to inform on enduring cancer disparities
Authors: Turner David P. 
Published: December 2023

Abstract
Disparities in overall cancer outcomes have been reduced across racial and ethnic divides, but still persist for some tumor types and have increased for others. This has stimulated significant debate regarding whether the enduring nature of cancer disparities arises solely out of inherent failings in addressing health inequities, or does an individual’s inherent biology also play an accompanying role. As a newly termed “bio-social determinant of health”, non-enzymatic glycoxidation profiles may represent an unexploited opportunity to consider how health inequity constructs combine to impact cancer outcomes across transdisciplinary studies. Resulting from the combined processes of glycation and oxidation, non-enzymatic glycoxidation is a complex series of reactions, leading to the irreversible posttranslational modification of peptides, lipids and nucleic acids by Advanced Glycation End Products (AGEs). Evidence is presented to support that health inequity constructs can serve to provide a superfluous source of the reactive substrates that sustains non-enzymatic glycoxidation resulting in a chronic cycle of AGE formation, bioavailability, and pathogenicity. AGEs are significant because: 1. Communities who bear the highest cancer burden are more likely to be exposed to health inequity risk factors that serve to increase AGE bioavailability 2. When health equity is compromised complex relationships are created between social and biological determinates of health that serve to overwhelm the fragile rheostat that maintains AGE homeostasis.; and 3. Increases in AGE bioavailability are associated with increased tumor growth and progression through their impact on the tumor microenvironment. Glycoxidation patterns visualized by AGE accumulation and pathogenic function may serve as a “bio-social determinant of health” as they may reflect the dynamic and varied nature of multiple health inequity constructs and their combined effects on cancer incidence and mortality. In turn this may allow a greater understanding of the complex relationships that exist between societal, ancestral, environmental, and biological constructs, and lifestyle associated risk factors associated with enduring cancer disparities. This would provide significant insight on novel cancer prevention and control strategies aimed at reducing AGE exposure due to health inequity.
Citation Format: David P. Turner. Non-enzymatic glycoxidation reports on society, environment and biology to inform on enduring cancer disparities [abstract]. In: Proceedings of the 16th AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2023 Sep 29-Oct 2;Orlando, FL. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2023;32(12 Suppl):Abstract nr C103.
Abstract C114: Indigenizing and ruralizing NCI’s Screen to Save Program: Resources, Optimizing Outreach, Teaching, Science (ROOTS)
Authors: Haring Rodney C. , Maybee William , Raphaelito Josie , Abrams Corrine 
Published: December 2023

Abstract
Resources, Optimizing Outreach, Teaching and Science (ROOTS) for Indigenous populations was a virtually adapted colorectal screening program to decrease cancer health disparities while increasing knowledge about culturally tailored screening processes. Indigenous and rural community outreach teams partnered with a community advisory board to provide an Indigenized/ruralized version of the NCI Screen to Save (S2S) program delivered to both Indigenous rural/sub-urban communities. 169 pre/post surveys were obtained from 82 participants. Findings demonstrated participants were able to identify smoking, tobacco use, and lack of physical activity as risk factors for colorectal cancer. Post intervention, participants were more likely to get screened for colorectal cancer and talk with family friends about their colorectal cancer screening experience increase physical activity. Additional adaptions were investigated for Two-Spirit and Native American lesbian, gay, bisexual, transgender, queer, questioning, intersex, asexual urban populations (n=6 virtual roundtables; n=14 participants). Findings from the overall ROOTS program suggested culturally tailored intervention messaging are an important means for increasing screening and decreasing cancer health disparities among both Indigenous and rural populations. Primary results from Two Spirit and LGBTQ+ adaption included understanding past mindsets and experiences of healthcare professionals; a need for continued lay translations, importance of community marketing beyond health centers; and more information on follow up details including central contact information.
Citation Format: Rodney C. Haring, William Maybee, Josie Raphaelito, Corrine Abrams. Indigenizing and ruralizing NCI’s Screen to Save Program: Resources, Optimizing Outreach, Teaching, Science (ROOTS) [abstract]. In: Proceedings of the 16th AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2023 Sep 29-Oct 2;Orlando, FL. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2023;32(12 Suppl):Abstract nr C114.