bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract C107: [Advocate Abstract] Intermittent fasting for cancer patients
Authors: Stromer Nicole 
Published: August 2020

Abstract
When lab mice received chemotherapy and a fasted diet, the immune system was better able to target cancer cells. There is evidence from research that intermittent fasting in any form could slow cancer tumor growth, reduce treatment side effects, boost the immune system and increase survival rates.
Intermittent fasting refers to cycles of alternating eating and refraining from eating, or fasting. Some of the different types of intermittent fasting include:
24 Fasting….. This type of fasting means not eating at all for 24 hours. This is typically done once or twice a week.
The 5:2 Diet…… The 5:2 strategy modifies 24-hour fasting. It involves restricting calories for two 24-hour periods per week. On those two days women eat 500 calories and men 600 calories.
The 16/8 Fast…… This strategy involves not eating for 16 hours every day. Most people do this by skipping breakfast, and not eating between 8:00 at night and noon the next day.
Calorie Restriction…..Calorie restriction involves reducing calorie intake by 20 to 40% every day for an extended period of time. A guideline would be 1,200 calories per day for women and 1,400 calories per day for men.
Citation Format: Nicole Stromer. [Advocate Abstract] Intermittent fasting for cancer patients [abstract]. In: Proceedings of the Eleventh AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2018 Nov 2-5; New Orleans, LA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2020;29(6 Suppl):Abstract nr C107.
Abstract C126: Plant isolate dibenzyl trisulfide potently inhibits cytochrome P450 1 enzyme activity and the growth of breast cancer cells derived from African American patients
Authors: Wooten Jonathan V. , Wauchope Shaniece , Mavingire Nicole , Campbell Petreena , Watson JéAnn , Gossell-Williams Maxine , Delgoda Rupika , Brantley Eileen 
Published: August 2020

Abstract
Triple-negative breast cancer (TNBC), characterized by tumors that lack expression of the estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER2), carries a poor prognosis. African American women develop TNBC at disproportionately higher rates than women of other ethnic groups. Dibenzyl trisulfide (DTS), found expressed in the Jamaican plant Petiveria alliacea, has been shown to inhibit the growth of several cancer types. However, little is known about whether this plant isolate displays anticancer activity in TNBC cells from African American patients or modulates cytochrome P450 1 (CYP1) enzyme activity. This work, as part of an ongoing ethnopharmacology-based bioactivity screening, was designed to fill this deficit. African American TNBC (AA-TNBC) cells HCC1806 and MDA-MB-468 were treated with varying concentrations of DTS for 48 h and cell viability was assessed using the Alamar Blue assay. DTS potently inhibited the growth of HCC1806 and MDA-MB-468 cells, producing IC50 values of 10.6 ± 1.2μM and 10.3 ± 2.0μM, respectively. Additionally, we discovered that DTS induced apoptosis in these cells. Furthermore, we investigated the ability DTS to impact the activities of the CYP1 family of enzymes, which are known to convert procarcinogens to carcinogens. The IC50 values obtained for CYPs 1A1, 1A2 and 1B1 were 1.68 ± 0.3μM, 1.9 ± 0.2μM and 1.29 ± 0.3μM, respectively. These data indicate DTS exhibits potent inhibition of the activities of these enzymes. In particular, DTS was able to bind to CYP1A2 in accordance with irreversible kinetics. In addition, DTS reduced CYP1 mRNA expression in both cell lines. Our findings provide a rationale for in vivo evaluations of DTS as a potential candidate for chemoprevention and for treating AA-TNBC patients.
Citation Format: Jonathan V. Wooten, Shaniece Wauchope, Nicole Mavingire, Petreena Campbell, JéAnn Watson, Maxine Gossell-Williams, Rupika Delgoda, Eileen Brantley. Plant isolate dibenzyl trisulfide potently inhibits cytochrome P450 1 enzyme activity and the growth of breast cancer cells derived from African American patients [abstract]. In: Proceedings of the Eleventh AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2018 Nov 2-5; New Orleans, LA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2020;29(6 Suppl):Abstract nr C126.
Abstract IA08: Exploring social determinants of cancer outcomes using multilevel spatial analysis
Authors: Scribner Richard , Danos Denise , Leonardi Claudia , Ferguson Tekeda , Yu Qingzhao , Simonsen Neal , Wu Xiao-Cheng 
Published: August 2020

Abstract
Health disparities research increasingly relies on a social determinants of health approach, which focuses on identifying modifiable social and environmental factors that adversely affect health outcomes to create health disparities. We have used a multilevel framework that leverages cancer registry and US census data to examine the role of neighborhood social determinants in cancer incidence and survival in Louisiana. Multilevel studies of cases of colorectal, liver, and breast cancer reveal that differential exposure to unfavorable social and physical environments do contribute to racial disparities in cancer. In particular, we have observed that concentrated disadvantage, a robust measure of neighborhood environment, was positively associated with the incidence of colorectal cancer and hepatocellular carcinoma but not triple-negative breast cancer.
Citation Format: Richard Scribner, Denise Danos, Claudia Leonardi, Tekeda Ferguson, Qingzhao Yu, Neal Simonsen, Xiao-Cheng Wu. Exploring social determinants of cancer outcomes using multilevel spatial analysis [abstract]. In: Proceedings of the Eleventh AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2018 Nov 2-5; New Orleans, LA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2020;29(6 Suppl):Abstract nr IA08.
Abstract IA40: Advocate Perspective: Shaping survivorship in Hawaii
Authors: Matusmoto Lillian K. 
Published: August 2020

Abstract
As a person who has been diagnosed and treated four times for breast cancer, I have a deep value for the care of cancer warriors. I am especially interested in longer-term survivorship. What happens to cancer survivors after their formal care is complete? Today I will share some of my experience as well as discuss some work that the Hawaii Comprehensive Cancer Coalition has been conducting on behalf of cancer survivors. In the Hawaiian Islands we have a unique geography in that there are people living on many different islands and all in need of good care. Our work has been conducted by getting a firsthand look at what is needed throughout the primary Hawaiian Island chain, as the needs differ greatly depending on location. I also plan to talk about what has been helpful for me personally. Each of us has our own experience, and each experience is rich and adds to the landscape of cancer survivorship. I want to make sure people are not left behind, and I also want to do my part to try to ensure the best long-term care for cancer survivors, or as I like to call us, cancer warriors.
Citation Format: Lillian K. Matusmoto. Advocate Perspective: Shaping survivorship in Hawaii [abstract]. In: Proceedings of the Eleventh AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2018 Nov 2-5; New Orleans, LA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2020;29(6 Suppl):Abstract nr IA40.
Abstract IA43: Breast cancer and African ancestry
Authors: Newman Lisa A. 
Published: August 2020

Abstract
Variation in cancer incidence and outcome has well-documented correlations with racial-ethnic identity. In the United States, the possible genetic/ancestral hereditary explanations for these associations are confounded by socioeconomic, cultural, and lifestyle patterns. Differences in the breast cancer burden of African American (AA) compared to European/Caucasian (White) American (WA) women represent one of the most notable examples of disparities in oncology related to racial-ethnic identity. Elucidating the etiology of these associations is imperative in achieving the promise of the precision medicine initiatives. Population-based breast cancer mortality rates have been higher for AA compared to WA women since the early 1980s, likely reflecting declines in mortality among WA related to the advent of endocrine therapy, which is less effective in AA women because of the higher prevalence of estrogen receptor-negative disease. The increased risk of triple-negative breast cancer in AA women as well as western, sub-Saharan African women compared to WA, European, and east African women furthermore suggests that selected components of African ancestry are associated with hereditary susceptibility for specific patterns of mammary carcinogenesis. Oncologic anthropology represents a transdisciplinary field of research that can combine the expertise of population geneticists, translational oncologists, and behavioral scientists to elucidate breast cancer disparities related to racial-ethnic identity and to advance knowledge related to the pathogenesis of triple-negative breast cancer. This presentation will review associations between triple-negative/basal-like breast cancer and African ancestry, with a proposed mechanism based upon hereditary and population migration patterns.
Citation Format: Lisa A. Newman. Breast cancer and African ancestry [abstract]. In: Proceedings of the Eleventh AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2018 Nov 2-5; New Orleans, LA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2020;29(6 Suppl):Abstract nr IA43.
Abstract PR08: Higher expression of SATB2 gene in hepatocellular carcinoma of African American patients determines aggressiveness phenotypes than those in Caucasian Americans
Authors: Roy S.K. , Ma Y. , Danos D.M. , Shankar S. , Miele L. , Scribner R.A. , Srivastava R.K. 
Published: August 2020

Abstract
In the US, hepatocellular carcinoma (HCC) incidence has tripled over the past two decades. This trend indicates that social determinants, genetic and environmental factors are driving the epidemic at the population level. Furthermore, the disease has disproportionately affected minority and disadvantaged populations. SATB2 (special AT-rich binding protein-2), a transcription factor and epigenetic regulator, influences gene expression both by modulating chromatin architecture and by functioning as a transcriptional co-factor. SATB2 is highly expressed in embryonic stem cells and progenitor cells, whereas its expression is low or absent in human normal liver tissues. We have recently demonstrated that overexpression of SATB2 can transform normal epithelial cells to cancer stem-like cells in pancreatic, colorectal and breast cancer models, and the expression of SATB2 was significantly higher in cancer tissues compared to normal tissues. The purpose of this study was to examine the expression of SATB2 gene in HCC from AA and CA patients and assess its oncogenic potential by measuring cell viability, epithelial-mesenchymal transition (EMT), stem cell markers and pluripotency maintaining factors in cancer stem cells (CSCs). We compared the expression of SATB2 in primary hepatocytes, Hep3b (from AA), HepG2 (from CA) and HCC CSCs. Hep3b (higher), HepG2 (lower) and CSCs (highest) expressed SATB2 protein, whereas human primary normal hepatocytes did not express SATB2. Knockout of SATB2 in CSCs by Crispr/Cas9 technique significantly inhibited the expression of SATB2 gene, stem cell markers (CD24, CD44 and CD133), pluripotency maintaining factors (cMyc, KLF4, SOX2 and OCT4), and EMT compared to NTC control group. The expression of SATB2 was significantly higher in HCC tissues than adjacent normal controls. Furthermore, the expression of SATB2 was significantly higher in HCC tissues derived from AA compared to those in CA. These data suggest that SATB2 is an oncogenic factor and its expression, which is higher in in HCC tissues derived from AA, may explain the disparity in HCC outcomes among AA.
This abstract is also being presented as Poster B049.
Citation Format: S.K. Roy, Y. Ma, D.M. Danos, S. Shankar, L. Miele, R.A. Scribner, R.K. Srivastava. Higher expression of SATB2 gene in hepatocellular carcinoma of African American patients determines aggressiveness phenotypes than those in Caucasian Americans [abstract]. In: Proceedings of the Eleventh AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2018 Nov 2-5; New Orleans, LA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2020;29(6 Suppl):Abstract nr PR08.
Abstract 06: Streamlining data management for clinical trials
Authors: Norris Brook , Neighbors Lauren , Wale Lucas 
Published: August 2020

Abstract
The purpose of this study is to answer the FDA’s call to action for new research paradigms that rely on real-world data (RWD) to increase the efficiency of clinical trials and to conduct research using an approach that is less disruptive to the patient-provider clinical care setting. With the expansion of electronic health record (EHR) vendor structured data models, clinical study data can be directly captured using the patient’s EHR data as documented in the health care organization’s (HCOs) electronic medical record (EMR) system(s) and other electronic data sources (eSources). In partnership with HCOs, the Optum Digital Research Network is conducting a pilot to enable effective RWD extraction, normalization, and transcription from EMRs and other eSource to a read-only electronic data capture (EDC) system, effectively eliminating the need for duplicative data entry during the study. Optum is developing custom database queries to extract structured EMR data (including demographics, medications, labs, vitals, and encounters) from the respective domains of each EMR into a staging database. The raw data are then curated, normalized, and mapped into a common data model study database. In this case, the Observational Medical Outcomes Partnership (OMOP) data standard is employed as the clinical data management (CDM) model. The curated data are then mapped to Clinical Data Acquisition Standards Harmonization (CDASH) variables and transmitted to an EDC system using the EDC vendor’s application programming interface (API). The entire process is scheduled on a daily cadence (removing any duplicate data) to capture any updated visit information, medications, labs, or vitals. The EDC form fields are read-only. If there is a discrepancy or query, sites are notified requesting to confirm or correct their EHR data, which may result in an update to the respective read-only EDC form fields. Through this pilot project, Optum’s successful transfer of structured EMR data to a read-only EDC system has substantial implications for clinical research. Using data and technology, this methodology is projected to improve the efficiency (and lower costs) of clinical trials while minimizing the burden on HCOs.
Citation Format: Brook Norris, Lauren Neighbors, Lucas Wale. Streamlining data management for clinical trials [abstract]. In: Proceedings of the AACR Special Conference on Advancing Precision Medicine Drug Development: Incorporation of Real-World Data and Other Novel Strategies; Jan 9-12, 2020; San Diego, CA. Philadelphia (PA): AACR; Clin Cancer Res 2020;26(12_Suppl_1):Abstract nr 06.
Abstract 16: Landscape and outcome of TRK fusion-positive Cancers
Authors: Rosen Ezra Y. , Goldman Debra A. , Hechtman Jaclyn F. , Benayed Ryma , Schram Alison M. , Cocco Emiliano , Shifman Sophie , Gong Yixiao , Kundra Ritika , Solomon James P. , Bardelli Alberto , Scaltriti Maurizio , Drilon Alexander , Iasonos Alexia , Taylor Barry S. , Hyman David M. 
Published: August 2020

Abstract
TRK inhibitors achieve marked tumor-agnostic efficacy in TRK fusion-positive cancers and consequently are now an established standard of care. Little is known, however, about the demographics, clinical outcomes, response to alternative standard therapies, or genomic characteristics of TRK fusion-positive cancers. Utilizing a center-wide screening program involving more than 26,000 prospectively sequenced patients, genomic and clinical data from all cases with identified TRK fusions were extracted. An integrated analysis was performed of genomic, therapeutic, and phenomic outcomes. In total, we identified 76 cases with confirmed TRK fusions (0.27% overall prevalence) involving 48 unique rearrangements and 17 distinct cancer types. The presence of a TRK fusion was associated with depletion of concurrent oncogenic drivers (p=4.4E-7) and lower tumor mutation burden (p=4.2E-9), with the exception of colorectal cancer where TRK fusions co-occur with microsatellite instability (MSI-H). Longitudinal profiling in a subset of patients indicated that TRK fusions were present in all sampled timepoints in 82% (14/17) of cases. Progression-free survival on first-line therapy, excluding TRK inhibitors, administered for advanced disease was 9.6 months (95% CI: 4.8-13.2). The best ORR achieved with chemotherapy containing-regimens across all lines of therapy was 63% (95% CI: 41-81). Among 12 patients treated with checkpoint inhibitors, the only response observed was in an MSI-H colorectal patient. TRK fusion-positive cancers can respond to alternative standards of care, although efficacy of immunotherapy in the absence of other predictive biomarkers (MSI-H) appears limited. TRK fusions are present in tumors with simple genomes lacking in concurrent drivers that may partially explain the tumor-agnostic efficacy of TRK inhibitors.
Citation Format: Ezra Y. Rosen, Debra A. Goldman, Jaclyn F. Hechtman, Ryma Benayed, Alison M. Schram, Emiliano Cocco, Sophie Shifman, Yixiao Gong, Ritika Kundra, James P. Solomon, Alberto Bardelli, Maurizio Scaltriti, Alexander Drilon, Alexia Iasonos, Barry S. Taylor, David M. Hyman. Landscape and outcome of TRK fusion-positive Cancers [abstract]. In: Proceedings of the AACR Special Conference on Advancing Precision Medicine Drug Development: Incorporation of Real-World Data and Other Novel Strategies; Jan 9-12, 2020; San Diego, CA. Philadelphia (PA): AACR; Clin Cancer Res 2020;26(12_Suppl_1):Abstract nr 16.
Abstract 34: Improve decision making in clinical trials through machine learning and EHR
Authors: Shen LiMing , Sheng Tao , Luo Xaiodong 
Published: August 2020

Abstract
One of the key contributors to the failure of oncology trials is patient selection bias. A bias that results in a lower observed efficacy in phase II may lead to a premature decision to abort a trial, whereas a bias in the positive direction may result in an expensive failure in phase III. We propose an approach in which RWE is used to model a proxy endpoint that is available in RWE but is also related to the endpoint in clinical trial, on patient profile; the model is then used on clinical trial patients to predict their proxy endpoints, which in turn is used to quantitatively assess selection bias and infer the effect of bias on the observed efficacy of the trial. We used an ongoing metastatic breast cancer trial to demonstrate this approach. Medication, demography, vital signs, and time of death of the target patient population were extracted from Optum Humetica. These data were then used to train a ML survival model to predict OS based on patient profiles in a virtual trial. For this oncology trial, we chose OS as a proxy endpoint as it has a well-established strong correlation with the observed efficacy in terms of PFS and time on drug duration. OS is an endpoint. The term proxy is used here in the sense that it is not the endpoint used in the earlier-phase trial. The model is then used to predict risk profiles for patients in the actual trial, and the difference between risk profile of the trial patients and that of the RWE target population provides a quantitative assessment of selection bias of the trial population. The effectiveness of this approach depends on the predictive power of the model. A nonpredictive model obviously cannot detect bias even when it is present. To quantitatively assess the predictive power of the model, we subsampled the RWE population to simulate a trial population with different risk profiles and use the model to determine a threshold in risk difference beyond which the model can detect a significant difference. In this context, we also compared Cox PH, decision tree, and a neural network model with respect to their predictive power in term of concordance score. We then compared the risk profile of the clinical trial patients with that of the target patient population. As RWE data become more abundant and data interoperability and quality improve, the prediction model will become more accurate and bias detection will become more sensitive. We believe this approach will lead to an effective framework whereby RWE data can be used to improve the success rate of oncology clinical trials.
Citation Format: LiMing Shen, Tao Sheng, Xaiodong Luo. Improve decision making in clinical trials through machine learning and EHR [abstract]. In: Proceedings of the AACR Special Conference on Advancing Precision Medicine Drug Development: Incorporation of Real-World Data and Other Novel Strategies; Jan 9-12, 2020; San Diego, CA. Philadelphia (PA): AACR; Clin Cancer Res 2020;26(12_Suppl_1):Abstract nr 34.
A Rosetta Stone for eastern Pacific Caecidae (Gastropoda: Caenogastropoda)
Authors: RAINES BRET K. 
Published: August 2020

Nearly one hundred names have been proposed for Caecidae within the eastern Pacific. For the first time a comprehensive review of the extant members of Caecidae has been completed for this region. During this twelve year long deciphering effort, tens of thousands of specimens from Alaska to Chile were examined. All known type material was studied and whenever possible has been illustrated herein. Whenever possible the descriptions include details of each growth stage from the protoconch through to the final adult stage. Then, the growth stages have been reconstructed to show what the caecid might have looked like, if it had not discarded its previous stages. In doing so, a better understanding of the growth morphology is provided for each species. In addition, this effort shows that not only the apertures of late subadult stages can appear different from their adult stage, but there can also be multiple differences in the varices. The resulting product is a taxonomic resource for Caecidae identification and growth morphology. Forty-three species are treated herein. Neotypes have been designated for Caecum glabriforme, C. semilaeve and C. subaustrale, and a lectotype has been designated for C. mirificum. Five species are described as new to science, plus one replacement name: Caecum lightfootanum sp. nov., C. draperi sp. nov., C. shaskyi sp. nov., C. galapagoense sp. nov. and C. spiculum sp. nov. and C. adamsi nom. nov.