bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract D021: Chinese E-Women Project: A community-based approach to improving breast cancer knowledge among Chinese American women
Authors: Lee Alice W , Puga Cindy , Tsai Michelle , Huang Sherry 
Published: September 2020

Abstract
Background: Breast cancer is the most common cancer for Chinese women living in the United States (U.S.). Despite overall rates being significantly lower than other races and ethnicities, incidence has steadily increased over the last few decades. This is concerning given that Asian Americans are the fastest growing racial group in the U.S. and Chinese Americans constitute the largest Asian American ethnic population. In addition, mammography screening rates are low among Chinese American women, and this may be attributable to a lack of breast cancer knowledge and awareness. Methods: The Chinese E-Women Project (CEWP) is a breast health education and engagement program developed by the Orange County Herald Center (OCHC), a non-profit organization that serves the Chinese American community in Orange County, California. Two key CEWP components are the Community Gatekeeper Education Session (CGES), which is a formal education session led by trained OCHC staff to engage and educate Chinese American community leaders, and the E-Women Tea Time (EWTT), which is an informal peer group education session led by a past CGES participant. All CGES and EWTT events presented information on breast cancer epidemiology, biology, and screening. Questionnaires testing breast cancer knowledge were administered before and after the education session at each event. We pooled data across the CGES and EWTT events separately and used Wilcoxon signed rank test to evaluate change in participants’ overall knowledge. We also examined change in knowledge by question using McNemar’s test. Results: Our analysis included a total of 94 CGES and 149 EWTT female participants. For both CGES and EWTT, we observed significant improvements in overall breast cancer knowledge after the education session (both p&lt;0.0001). Although we did identify one question related to mammography and another question related to personal breast health that did not show significant improvement after the session, knowledge for all other questions significantly improved (all p&lt;0.05). Conclusions: These findings highlight community-based education sessions as effective ways of both informing Chinese American women about breast cancer and engaging them to become advocates of breast health wellness in their community. Future research should evaluate whether these types of sessions can lead to positive individual changes in behavior and screening practice.
Citation Format: Alice W Lee, Cindy Puga, Michelle Tsai, Sherry Huang. Chinese E-Women Project: A community-based approach to improving breast cancer knowledge among Chinese American women [abstract]. In: Proceedings of the Twelfth AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2019 Sep 20-23; San Francisco, CA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2020;29(6 Suppl_2):Abstract nr D021.
Abstract D091: The impact of distance to hospital on cervical cancer outcomes
Authors: Park Hyungkyung , Wang Zhixin , Wang Chenguang , Huh Warner , Bae Sejong 
Published: September 2020

Abstract
Objective – To determine the impact of distance on cervical cancer outcomes in addition to identifying potential factors by exploring age-specific differences Methods –Using the National Cancer Database (NCDB) for the years 2004 to 2013, cervical cancer incidence and mortality rates were calculated, and potential factors were investigated by using multivariable logistic regression analysis. Results – A total of 90,076 white and black women (≥20 years old) were diagnosed with cervical cancer from 2004 to 2013 (82.7% and 17.3% respectively). Race, region, insurance, income, facility type, comorbidity, cancer stage, age, and year of diagnosis were significantly associated with cervical cancer mortality. Only cancer stage was significantly associated with mortality for both white and black women across age groups. Race, insurance, facility type, comorbidity, cancer stage, distance to hospital, and age were significantly associated with five-year survival rates. Conclusions – This study confirmed the impact of distance to hospital on five-year survival rates. Both white and black women living more than 50 miles away showed significant lower five-year survival rates than those who lived in less than 10 miles (OR=0.82, 95% CI 0.73 to 0.91; OR=0.59, 95% CI 0.45 to 0.77 respectively).
Citation Format: Hyungkyung Park, Zhixin Wang, Chenguang Wang, Warner Huh, Sejong Bae. The impact of distance to hospital on cervical cancer outcomes [abstract]. In: Proceedings of the Twelfth AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2019 Sep 20-23; San Francisco, CA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2020;29(6 Suppl_2):Abstract nr D091.
Abstract IA25: Using cancer registry data for geospatial and disparity research
Authors: Sherman Recinda 
Published: September 2020

Abstract
This talk will provide an overview on how to use cancer registry data in geospatial analysis. Our national cancer surveillance system comprises a set of international data collection standards overseen by individual state registries. While there are highly detailed geospatial data available from each state registry, not all registries release these data and each have separate data release procedures, regulations, and cost. This presentation will discuss how the cancer surveillance community geocodes cancer incidence data and creates geocoded data quality measures. This presentation will also detail the current area-based social measures available to researchers in the national CiNA (Cancer in North America) cancer incidence dataset. Release procedures and limitations of the data will be described, and the move towards a national geographic dataset for cancer incidence data will be presented.
Citation Format: Recinda Sherman. Using cancer registry data for geospatial and disparity research [abstract]. In: Proceedings of the Twelfth AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2019 Sep 20-23; San Francisco, CA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2020;29(6 Suppl_2):Abstract nr IA25.
Abstract IA27: Metformin use and pancreatic cancer survival: Are there racial differences?
Authors: Carson Kenneth R. , Toriola Adetunji T. , Luo Suhong , Thomas Theodore , Drake Bettina F. , Chang Su-Hsin , Sanfilippo Kristen M. 
Published: September 2020

Abstract
Background: The effect of metformin use on survival among pancreatic ductal adenocarcinoma (PDAC) patients is controversial. Further, there are no data on African American patients. To address these, we analyzed data from the United States Veterans Health Administration (VHA).
Methods: We performed a population-based retrospective cohort study evaluating survival among 3,811 PDAC patients with pre-existing diabetes mellitus (DM), diagnosed with PDAC within the VHA between 1998 and 2013. We calculated hazard ratios (HRs) and 95% confidence intervals (CIs) using multivariable adjusted conventional Cox proportional hazards regression as well as the time-varying Cox proportional hazards regression to control for immortal time bias and confounders. All statistical tests were two-sided.
Results: In multivariable adjusted analyses using the conventional Cox model, there was an artificial survival benefit associated with metformin use: HR= 0.89 (95%CI 0.83-0.98, p-value=0.01). In multivariable adjusted analyses using the time-varying Cox model, metformin use was not associated with survival: HR=1.05 (95%CI 0.92-1.14, p-value=0.28). Results were similar among non-Hispanic white patients: HR=1.05 (95%CI 0.96-1.14, p-value=0.26) and African American patients: HR=1.01 (95%CI 0.86-1.19, p-value=0.88). Among patients who were metformin naïve at the time of PDAC diagnosis (N=1158), metformin use was associated with improved survival in non-Hispanic white: HR=0.78 (95%CI 0.61-0.99, p-value=0.04), but not African American patients: HR=1.20 (95%CI 0.75-1.93, p-value=0.45). The survival benefit among non-Hispanic whites was limited to patients with metastatic disease: HR=0.67 (95%CI 0.44-1.01, p-value=0.055). Among African American patients with metastatic disease, HR was 1.30 (95%CI 0.77-2.53, p-value=0.28). There was an interaction between race and metformin use in patients with metastatic disease (p-interaction=0.05).
Conclusions: Although metformin use was not associated with survival in patients with PDAC, the survival benefit limited to non-Hispanic white patients who were metformin naïve at the time of diagnosis deserves further study in a racially diverse study population.
Citation Format: Kenneth R. Carson, Adetunji T. Toriola, Suhong Luo, Theodore Thomas, Bettina F. Drake, Su-Hsin Chang, Kristen M. Sanfilippo. Metformin use and pancreatic cancer survival: Are there racial differences? [abstract]. In: Proceedings of the Twelfth AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2019 Sep 20-23; San Francisco, CA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2020;29(6 Suppl_2):Abstract nr IA27.
Abstract IA39: Inspiring hope, help, and healing: The hard work and heart work of cancer survivorship
Authors: Brown Jameisha 
Published: September 2020

Abstract
Cancer is the leading cause of disease-related death in children and teens. However, medical milestones advance cancer treatments that help nearly 85% of children diagnosed with cancer live at least five years following diagnosis. Some children are ultimately considered cured. Consequently, there is an increasing interest in childhood cancer survivorship. The current aim is to increase quality of life by decreasing treatment toxicity and proactive surveillance of potential late effects through long-term follow-up. Brown will share her challenges and triumphs experienced from more than 20 years of childhood cancer survivorship, long-term follow-up, and patient and research advocacy.
Citation Format: Jameisha Brown. Inspiring hope, help, and healing: The hard work and heart work of cancer survivorship [abstract]. In: Proceedings of the Twelfth AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2019 Sep 20-23; San Francisco, CA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2020;29(6 Suppl_2):Abstract nr IA39.
Abstract A03: Generation of primary sarcoma mouse models through CRISPR/Cas9 mediated activation of Yap1
Authors: Huang Jianguo , Xu Eric , Van Mater David , Kirsch David G 
Published: September 2020

Abstract
Soft tissue sarcomas (STSs) are rare heterogeneous cancers arising from diverse connective tissues. Undifferentiated pleomorphic sarcomas (UPSs), the most common sarcomas diagnosed in adult patients, are complex karyotypes of nonspecific genetic alterations. To date, the molecular mechanisms by which UPSs develop in patients are still poorly understood, which hinders precision medicine to treat the disease. Primary UPS mouse model generated by conditional activation of KrasG12D and mutation of Trp53 (KP mouse model) is currently used for studying sarcoma biology, imaging, and preclinical trials. However, Kras mutation is rarely identified in human UPSs. We recently showed that injury can replace KrasG12D to induce primary UPSs in mouse models of conditional mutation of Trp53. Furthermore, our whole-exome sequencing determined Yap1 amplification in some injury-induced sarcomas. Moreover, it is also shown that a subset of human UPSs may be driven by Hippo pathway. In addition, it is reported that activation of mutant Yap1 induced primary rhabdomyosarcomas (RMSs) in mouse models. CRISPR/Cas9-mediated genetic mutation has been applied to rapidly create mouse models of cancers, including sarcoma, with spatial and temporal control. However, rare studies have been performed to investigate whether CRISPR/Cas9-mediated activation of endogenous oncogenes could generate primary cancer models. Thus, we applied CRISPR/Cas9 technology to test whether activation of endogenous Yap1 can induce cell transformation or even generate primary UPSs in mouse models. Our results showed that CRISPR/dCas9-p300-mediated activation of endogenous Yap1 resulted in transformation of KrasG12D immortalized mouse embryonic fibroblasts (MEFs) as well as Trp53 knockout MEFs. Moreover, we are currently applying our recently developed in vivo CRISPR/Cas9 delivery method combined with Sleeping Beauty transposon system to investigate whether we are able to develop primary UPSs in mouse models by activating Yap1. If successful, it will further allow us to perform CRISPR/Cas9-mediated direct in vivo activation screen to identify other oncogene drivers for sarcomagenesis. In conclusion, primary sarcoma mouse models generated by CRISPR/Cas9-mediated activation will be an indispensable platform for studying sarcoma biology and precision medicine.
Citation Format: Jianguo Huang, Eric Xu, David Van Mater, David G Kirsch. Generation of primary sarcoma mouse models through CRISPR/Cas9 mediated activation of Yap1 [abstract]. In: Proceedings of the AACR Special Conference on the Hippo Pathway: Signaling, Cancer, and Beyond; 2019 May 8-11; San Diego, CA. Philadelphia (PA): AACR; Mol Cancer Res 2020;18(8_Suppl):Abstract nr A03.
Abstract A04: Genetic and pharmacologic inhibition of HES1 reduces YAP1 expression, impairing rhabdomyosarcoma cell growth
Authors: Kovach Alexander R. , Linardic Corinne M. 
Published: September 2020

Abstract
Rhabdomyosarcoma (RMS) is a mesenchymal cancer with skeletal muscle histogenesis and the most common soft-tissue sarcoma of childhood. High-risk patient groups continue to have a poor survival (&lt;30%) and novel therapeutic targets are needed. In our studies of Hippo signaling in RMS, we found that expression of YAP1 in a human myoblast-based model of RMS is permissive for bypass of senescence, tolerance of oncogenic RAS expression, and full transformation to cells able to grow as xenografts mimicking the embryonal variant of RMS (ERMS). In parallel, we found that YAP1 engages in a positive feedback loop with the Notch signaling pathway, suggesting that Notch effectors must impact downstream YAP1. Here we show that shRNA-mediated suppression of the basic helix-loop-helix transcriptional repressor and Notch effector, HES1, inhibits ERMS cell growth in vitro. Mechanistically, HES1 suppression causes decreased levels of YAP1 mRNA and protein, and increased mRNA and protein levels of the cell cycle regulator and tumor suppressor CDKN1C (P57kip2) across three different cell lines. Additionally, HES1 suppression results in cell line-specific increases in the myogenic markers MYOD1, MYOG, and MYF6. Recently, Perron et al. reported that the small molecule JI051 inhibits HES1 by stabilizing its interaction (doi:10.1074/jbc.RA118.002316) with the protein chaperone prohibitin-2, thus sequestering HES1 outside the nucleus. We demonstrate that JI051 inhibits ERMS cell growth in vitro with EC50 values in the low nanomolar range. Preclinical in vivo studies combining HES1 inhibition and YAP1 inhibition are planned, with the hypothesis that their coinhibition could prove effective in mitigating treatment resistance. A full understanding of the relationship between HES1 and YAP1 signaling will be paramount in moving compounds such as JI051 from the laboratory to the clinic.
Citation Format: Alexander R. Kovach, Corinne M. Linardic. Genetic and pharmacologic inhibition of HES1 reduces YAP1 expression, impairing rhabdomyosarcoma cell growth [abstract]. In: Proceedings of the AACR Special Conference on the Hippo Pathway: Signaling, Cancer, and Beyond; 2019 May 8-11; San Diego, CA. Philadelphia (PA): AACR; Mol Cancer Res 2020;18(8_Suppl):Abstract nr A04.
Abstract A23: Verteporfin as a new treatment paradigm for platinum-resistant ovarian cancer cells
Authors: Gogoi Radhika P. , Dasari Venkata Ramesh 
Published: September 2020

Abstract
Ovarian cancer is the most lethal of the gynecologic malignancies and has poor survival rates due to a combination of diagnosis at advanced stages and disease recurrence due to platinum chemotherapy resistance. It is of utmost importance that novel chemotherapeutic agents are identified to increase or restore chemosensitization to platinum-based chemotherapy. Verteporfin (VP, VisudyneTM) is a benzoporphyrin derivative used for treating adult macular degeneration. Verteporfin has recently been identified as an inhibitor of YAP/TEAD interaction. Yes-associated protein (YAP), the main downstream target of the HIPPO pathway, plays an important role in cell proliferation and apoptosis. We investigated the efficacy of VP alone or in combination with cisplatin (CDDP) or carboplatin (CP) or paclitaxel (Taxol) on two serous ovarian cancer cell lines (OV90, COV504). The effect of VP, CDDP, CP or Taxol was studied either alone or in combination after 72 hours of treatment. Cell viability-based cytotoxicity measurements indicate dose-dependent increase in cytotoxicity for all the drugs. IC50 values of the drugs were calculated based on dose-effect curves using Compusyn software following the Chou-Talalay method. For OV90 cells, the calculated IC50 values were 29.33μM for VP, 2.17μM for cisplatin, 96.21μM for carboplatin, and 89.05μM for paclitaxel. For COV504 cells, the calculated IC50 values were 8.37μM for VP, 1.79μM for cisplatin, 117.23μM for carboplatin, and 7.16μM for paclitaxel. Based on the IC50 values of single agents, we performed cell proliferation assay using VP and CDDP/CP/Taxol in combination. We observed synergistic effects of VP with CDDP/CP/Taxol based on combination index plots. Based on the dose-reduction index (DRI) values of the drugs in combination treatments, we performed cytotoxicity and invasion assays. The combination treatments of these drugs at DRI values induced cytotoxicity and inhibited invasion of cancer cells. To check the chemosensitization of VP in cancer cells, we used cisplatin-resistant ovarian cancer cells, A2780Cis. Similar to ovarian cancer cells, VP effectively inhibited proliferation of A2780Cis cells. Based on these results, we hypothesize that VP is inducing chemosensitivity in platinum resistant ovarian cancer cells and increasing the efficacy of either platin drugs or Taxol. We suggest that our preclinical data in combination with previously available human safety data support the study of VP in combination with platinum in a clinical phase 2 trial of serous ovarian cancer patients.
Note: This abstract was not presented at the conference.
Citation Format: Radhika P. Gogoi, Venkata Ramesh Dasari. Verteporfin as a new treatment paradigm for platinum-resistant ovarian cancer cells [abstract]. In: Proceedings of the AACR Special Conference on the Hippo Pathway: Signaling, Cancer, and Beyond; 2019 May 8-11; San Diego, CA. Philadelphia (PA): AACR; Mol Cancer Res 2020;18(8_Suppl):Abstract nr A23.
Abstract A24: Functional annotation of the Hippo somatic mutations in human cancer
Authors: Han Han , Wang Wenqi 
Published: September 2020

Abstract
The Hippo pathway plays a crucial role in organ size control and tissue homeostasis, whose downstream targets YAP and TAZ are frequently activated in various types of human cancers. However, inactivation of this key tumor suppressor pathway in human cancers has not been fully characterized. In this study, we comprehensively annotate the somatic mutations for 23 Hippo core components in The Cancer Genome Atlas, which includes 11,706 patient samples across 32 major human cancer types. To determine the role of these patient-derived mutations in Hippo pathway regulation, we reconstituted each Hippo component mutant into the corresponding knockout (KO) cells and performed an immunofluorescence screen by using YAP cellular localization as a readout. Through it, we identified a number of somatic mutations that are able to suppress Hippo signaling and activate YAP. In addition, we elucidated the underlying mechanism for several identified somatic mutations and revealed novel regulatory mechanisms for the Hippo pathway. Taken together, our study not only systematically profiled the somatic mutations for the Hippo pathway components, but also generated a valuable resource to further characterize of this key signaling pathway in human cancer development.
Citation Format: Han Han, Wenqi Wang. Functional annotation of the Hippo somatic mutations in human cancer [abstract]. In: Proceedings of the AACR Special Conference on the Hippo Pathway: Signaling, Cancer, and Beyond; 2019 May 8-11; San Diego, CA. Philadelphia (PA): AACR; Mol Cancer Res 2020;18(8_Suppl):Abstract nr A24.
Abstract A35: Regulation of the Hippo signaling pathway through ubiquitin-mediated degradation of TEAD transcription factors
Authors: Lin Eva , Martin Scott , Modrusan Zora , Dey Anwesha , Pham Trang H. , Ho-Lee June , Chang Matt , Lacap Jennifer , Rose Chris , Pham Victoria , Lill Jennie 
Published: September 2020

Abstract
The Hippo pathway is an evolutionarily conserved signaling pathway that plays a key role in the development and homeostasis of tissues and organs. Studies over the past few years have demonstrated that the pathway is deregulated in a spectrum of cancers, making it a promising target for therapeutic intervention. YAP and TAZ, the two important transcriptional coactivators of the Hippo pathway, are highly activated in human cancers. Together with the transcription factor TEAD, the activation is essential for cancer initiation, progression, and metastasis. Regulating protein levels in cancer cells is very critical for their homeostasis, especially for the oncoproteins and tumor suppressors. Several Hippo pathway components including YAP and TAZ have been shown to be targeted for proteasomal degradation via ubiquitination by E3 ligases. Here, we design our studies to characterize the degradation of TEAD transcription factors. YAP and TAZ mainly function via interaction with TEADs as promoters, enhancers, and super-enhancers. Therefore, the level of TEAD proteins is very critical in Hippo-driven tumorigenesis. Thus, understanding how TEAD degradation is regulated can inform future therapeutic strategies.
Citation Format: Eva Lin, Scott Martin, Zora Modrusan, Anwesha Dey, Trang H. Pham, June Ho-Lee, Matt Chang, Jennifer Lacap, Chris Rose, Victoria Pham, Jennie Lill. Regulation of the Hippo signaling pathway through ubiquitin-mediated degradation of TEAD transcription factors [abstract]. In: Proceedings of the AACR Special Conference on the Hippo Pathway: Signaling, Cancer, and Beyond; 2019 May 8-11; San Diego, CA. Philadelphia (PA): AACR; Mol Cancer Res 2020;18(8_Suppl):Abstract nr A35.