tbuckley/cabot-search huggingface dataset:
Abstract LB183: Erythritol acts as tumor enhancer and suppressor depending on concentrations in brain tumor cell lines
Authors: Rayan Nassani, Hassan AlAmri, Bahauddeen M. Alrfaei
Journal: Cancer Research (2021)

Abstract Erythritol (ERT) is a simple four-carbon sugar alcohol, that is produced endogenously via pentose phosphate pathway from glucose in all human cells mainly erythrocytes with a plasma level of ∼9.8 μM. It can be obtained exogenously from diets as an FDA-artificial sweetener. It possesses hydroxyl groups that are responsible for hydroxyl radical scavenging effect (antioxidant property). Recent studies have pointed out an ERT protection based on concentration dependant effect on endothelial cells. The protection includes surviving death under high glucose conditions in diabetic patients. In addition, ERT has been reported in pre-diagnostic serum samples of glioblastoma patients, which was elevated. It was not known whether ERT elevation was defensive or harmful. We studied the cytotoxic activity of ERT on brain tumor cell lines (U87, Daoy) using metabolic activity assay (MTT) with different erythritol concentrations. We observed that on high concentrations (2.87 M, 1.43 M, 0.72 M), there was a significant growth inhibition (P&amp;lt;0.05). On the other hand, lower concentrations (0.36 M, 8 mM, 4 mM, 2 mM, 0.8 mM, 36 µM, 8.2 µM, 4.1µM, 8.2nM), showed growth enhancement. ERT is known with its antioxidant effect in a concentration dependent manner. Therefore, we studied the antioxidant activity of ERT using ROS-Glo H2O2 Assay. We observed that on the high concentrations of ERT there was a significant decrease in hydrogen peroxide concentration to less than 50%, this suggests that ERT has antioxidant effect against hydrogen peroxide. In contrast, low ERT concentrations (around physiological level) showed significant enhancement to tumor growth (P&amp;lt;0.05). In conclusion, we found that erythritol plays an important role in brain cancer development and hydrogen peroxide regulation through a concentration dependant manner. Since ERT is found normally in human plasma, controlling ERT concentration will grant ERT the ability to work as therapeutic enhancer for brain cancer treatment or even a biomarker for prognosis. Citation Format: Rayan Nassani, Hassan AlAmri, Bahauddeen M. Alrfaei. Erythritol acts as tumor enhancer and suppressor depending on concentrations in brain tumor cell lines [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2021; 2021 Apr 10-15 and May 17-21. Philadelphia (PA): AACR; Cancer Res 2021;81(13_Suppl):Abstract nr LB183.
Membranous urethral length (MUL) in patients who have had male sling or artificial urinary sphincter surgery for bothersome post prostatectomy stress incontinence
Authors: N.A. Faure Walker, P. Oza, G. Rottenberg, S. Malde, F. Macaskill, E. Solomon, C. Taylor, A. Sahai
Journal: European Urology (2021)
Abstract 1953: Q901, a selective CDK7 inhibitor, a potential new strategy for primary and CDK4/6 inhibitor resistant ER-positive breast cancer
Authors: Donghoon Yu, Yeejin Jeon, Dongsik Park, Mooyoung Seo, Wongyun Ahn, Jaeseung Kim, Kiyean Nam
Journal: Cancer Research (2021)

Abstract CDK4/6 inhibitors, in combination with hormone therapy, has made a breakthrough in treatment of hormone receptor-positive, HER2-negative metastatic breast cancers. However, in clinical practice, a substantial number of patients who responded to CDK4/6 inhibitors eventually develop resistance within 2-3 years. Current knowledge of the molecular mechanisms of CDK4/6 inhibitor resistance is under investigation , with the loss of function of the retinoblastoma (RB) protein the most frequently observed change in resistance to CDK4/6 inhibitors. RB loss of function by CDK4/6 inhibitors appears an irreversible mechanism of resistance while gain of cyclin E, and overexpression of CDK2 reducing cyclin D1-CDK4/6 dependency which results in the resistant cell to re-enter into s-phase. Thus, inhibition of the cyclin E-CDK2 axis may be effective in overcoming resistance to CDK4/6 inhibitors. We report a novel treatment strategy that targets Cyclin-dependent kinase 7 (CDK7) in CDK4/6 inhibitor-resistant, ER+ breast cancer. Q901 is a novel highly-selective inhibitor against CDK7 and demonstrates good functional inhibition of CDK activating kinase (CAK) activities leading to activation of CDK4, 6 and CDK2 in vitro and in vivo. Q901, monotherapy, effectively inhibited tumor growth in ER+ breast cancer xenograft model as well as CDK4/6 inhibitor resistant PDX model. The results suggest a potential for Q901 in treatment of hormone receptor-positive, HER2-negative metastatic breast cancer, regardless of resistance status to CDK4/6 inhibitors. Citation Format: Donghoon Yu, Yeejin Jeon, Dongsik Park, Mooyoung Seo, Wongyun Ahn, Jaeseung Kim, Kiyean Nam. Q901, a selective CDK7 inhibitor, a potential new strategy for primary and CDK4/6 inhibitor resistant ER-positive breast cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2021; 2021 Apr 10-15 and May 17-21. Philadelphia (PA): AACR; Cancer Res 2021;81(13_Suppl):Abstract nr 1953.
Unexpected Hepatitis B Virus Infection After Liver Transplantation — United States, 2014–2019
Authors: Danae Bixler, Pallavi Annambhotla, Martha P. Montgomery, Tonya Mixon-Hayden, Ben Kupronis, Marian G. Michaels, Ricardo M. La Hoz, Sridhar V. Basavaraju, Saleem Kamili, Anne Moorman
Journal: MMWR Morbidity and Mortality Weekly Report (2021)

TABLE. (Continued) Demographic and clinical characteristics and risk behaviors of deceased organ donors* reported to
Abstract 3133: Clonal facilitation drives estrogen receptor positive (ER+) breast cancer growth and survival
Authors: Rena Emond, Vince K. Grolmusz, Jason Griffiths, Jinfeng Chen, Frederick R. Adler, Andrea Bild
Journal: Cancer Research (2021)

Abstract Competition between different lineages of cells within a tumor has been included in thinking about cancer evolution and progression, but positive interactions like cooperation have received far less study. We have developed isogenic estrogen positive breast cancer cell lineages sensitive and resistant to CDK4/6 inhibition in order to investigate the mechanisms cell interactions under selective pressure. When these sensitive and resistant lineages are grown in co-culture under ribociclib treatment, sensitive survive and proliferate better than in mono-culture despite the effects of competition. Conditioned media taken from resistant cells grown in monoculture conditions reproduces this advantage, suggesting that secretion of some factor from resistant cells underlies the effect. Liquid chromatography-tandem mass spectrometry (LC-MS/MS) assays were used to identify factors secreted by cell lineages. While the less active estrone metabolite was detected in all lineages, the highly active estradiol was only detectable in mono- or coculture with resistant cells. As sensitive cells are more dependent on estrogen signaling than resistant cells, they benefit more from the increase in local estradiol, leading to facilitative growth when cocultured. Cooperative signaling between isogenic cancer cells is enhanced through addition of estradiol and blocked by small molecule inhibitors targeting estrogen signaling pathways. We have developed mathematical models that quantify the strength of competition and facilitation between cell lines and evaluated the effects of treatments that modify these interactions. These analyses support the conclusion that these heterogeneous cell lineages cooperate to survive during therapy through the increased production and sharing of local estradiol. This multidisciplinary approach reveals interactions between ER+ cancer lineages during treatment and provides insight into cell cooperation and competition during treatment, and how these interactions promote cancer cell growth and survival during treatment. Citation Format: Rena Emond, Vince K. Grolmusz, Jason Griffiths, Jinfeng Chen, Frederick R. Adler, Andrea Bild. Clonal facilitation drives estrogen receptor positive (ER+) breast cancer growth and survival [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2021; 2021 Apr 10-15 and May 17-21. Philadelphia (PA): AACR; Cancer Res 2021;81(13_Suppl):Abstract nr 3133.
Myeloma Cell Addiction to the Transcription Factor TCF11
Authors: Valentina Caputo, Katerina Goudevenou, Nikolaos Trasanidis, Kyriaki Petevi, Xiaolin Xiao, Kanagaraju Ponnusamy, Deena Iskander, David Pitcher, Antonia Rotolo, Holger W. Auner, Aristeidis Chaidos, Anastasios Karadimitris
Journal: Blood (2017)
Robotic prostate sparing cystectomy with intracorporeal neobladder - single tertiary care institution experience
Authors: J.I. Perez Reggeti, C. Ferreiro Pareja, P. De Pablos-Rodríguez, N. Picola Brau, M. Serrallach Orejas, J.F. Suárez Novo, F. Vigues Julià
Journal: European Urology (2021)
Abstract 722: The hallmark of COVID-19 cancer disparities: Cellular sequelae
Authors: Eva McGhee, Mengtao LI, Yi-Ling Lin, Nefertari Carr, Chinelo Njubigbo, Rohun Sadeghi, Brooke Su-Velez, Julian Handler, Adin Handler, Judith Okoro, Sebhat Afework, Jay Vadgama
Journal: Cancer Research (2021)

Abstract Coronavirus disease-19 (COVID-19). Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) is a novel coronavirus resulting in a severe threat to safety and public health. Genetic analyses suggest that SARS-COV-2 belongs to the Betacoronavirus group and Middle East respiratory syndrome coronavirus (MERS-CoV). Like most viruses, some are oncogenic, and genetic instability is involved in the initiating factor for tumor progression that is known to lead to malignancy, resulting in disease sequelae. Genomic instability is characterized by the increased rate of acquisition of alterations in the mammalian genome. These changes encompass a diverse set of biological end points including gene mutation and amplification, cellular transformation, clonal heterogeneity and delayed reproductive cell death. The loss of stability of the genome is becoming accepted as one of the most important aspects of viral induced carcinogenesis, and the numerous genetic changes associated with cancer cell implicate genomic stability as contributing to the neoplastic phenotype. The aim of this study is to analyze the influence of COVID-19 cancer related diseases and determine the epigenetic-genomic profiles in these diseases. In our experimental procedures, we will use oral epithelium cells as a model for this cancer study. We proposed a novel approach to study COVID-19-induced genetic changes with oral epithelium cells. We used these cells with COVID-19 co treatment to determine mechanisms that lead cells into crisis. Preliminary data using oral viral infected cells show that the viral infection can trigger certain gatekeeper proteins like p53 and pRB to be degraded and forcing cells to go into crises, and telomerase is turned on. In this study we will determine if COVID-19 transfected cells can follow the process using the Hayflick model, which show cells that are in crises, and some may progress to cancer. In summary, preliminary data show that viral infected cells that are none cancerous and are telomerase positive, may use a similar mechanism to send cells into crisis that turn telomerase on resulting in cellular malignancy. Citation Format: Eva McGhee, Mengtao LI, Yi-Ling Lin, Nefertari Carr, Chinelo Njubigbo, Rohun Sadeghi, Brooke Su-Velez, Julian Handler, Adin Handler, Judith Okoro, Sebhat Afework, Jay Vadgama. The hallmark of COVID-19 cancer disparities: Cellular sequelae [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2021; 2021 Apr 10-15 and May 17-21. Philadelphia (PA): AACR; Cancer Res 2021;81(13_Suppl):Abstract nr 722.
Abstract 871: KYNU expression is a prognostic factor in KEAP1/STK11 co-mutated lung adenocarcinoma
Authors: Ling Cai, Thomas J. Rogers, Huiyu Li, Jiyeon Kim, Yang Xie, Guanghua Xiao, John Minna, Ralph J. DeBerardinis
Journal: Cancer Research (2021)

Abstract We searched for gene expression prognostic markers with bimodal distribution in lung adenocarcinoma (LUAD) that might help specify molecular subtypes and identified a highly consistent biomarker KYNU, an enzyme in the pathway that converts tryptophan to nicotinamide adenine dinucleotide (NAD+). KYNU performed better in predicting LUAD outcomes than genes in related pathways. High KYNU expression is particularly observed in tumors with mutations in the tumor suppressor genes KEAP1 and STK11, but not in the oncogene KRAS. From clinical data of LUAD, we found more frequent co-mutation of KEAP1 and STK11 than KRAS with either KEAP1 or STK11. Tumors with mutations in both KEAP1 and STK11 had poorer outcomes than tumors with mutations in neither or only one of these genes, regardless of KRAS status. Importantly, KYNU expression associated with poor outcomes regardless of KEAP1/STK11 status and other covariates. We also assessed clinical features associated with KEAP1/STK11 mutations with AACR GENIE data. By examining co-expression of KYNU with other genes, we determined that high KYNU expression had low expression of gene sets related to macrophages. Citation Format: Ling Cai, Thomas J. Rogers, Huiyu Li, Jiyeon Kim, Yang Xie, Guanghua Xiao, John Minna, Ralph J. DeBerardinis. KYNU expression is a prognostic factor in KEAP1/STK11 co-mutated lung adenocarcinoma [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2021; 2021 Apr 10-15 and May 17-21. Philadelphia (PA): AACR; Cancer Res 2021;81(13_Suppl):Abstract nr 871.
Abstract 2149: Subgroups of early-stage microsatellite stability endometrial, colorectal and stomach tumors based on transcriptomics have distinct disease-free survival
Authors: Shi Zhang, Xinyi Liu, Lan Zhang, Mengli Huang
Journal: Cancer Research (2021)

Abstract Background: Microsatellite stability (MSS) is a biomarker for worse prognosis than microsatellite instability (MSI) in non-metastatic tumors. Tumors with MSS status are more probable to occur postoperative recurrence and metastasis. Some studies had revealed that endometrial and gastrointestinal tumors have distinct MSI-related features compared with other types of cancers, indicating there are potential similarities in these cancer types. The proportion of MSS population in non-metastatic endometrial and gastrointestinal tumors were about 90% and 75%. There are high heterogeneity in such wide range of patient population. The status of immune microenvironment based on immunohistochemistry or RNA-Seq profiling had been proved effective prognostic biomarker in some previous investigation. Therefore, we assume a subtype model of immune microenvironment based on transcriptomics features in endometrial and gastrointestinal tumors. Method: 128 patients with I-III stage MSS endometrial and gastrointestinal tumors from TCGA project were included as training cohort and a meta cohort of 603 patients of colorectal and stomach cancers from GEO datasets (GSE39582,GSE62254) were included as validation cohort in our study. The RNA-Seq profiling data and disease-free survival (DFS) of patients were collected. CIBERSORT tool was conducted to evaluate the immune-related cells' enrichment. A lasso-cox model of DFS was developed based on the CIBERSORT features. Patients in training cohort were scored the recurrence risk by the model. We further investigate the differentially expressed genes between high-risk and low-risk patients. Log-rank test was used to evaluate the difference of DFS. Result: 76 immune-related genes were identified to be differentially expressed significantly. The patients in training cohort were divided into two groups (group1 n=81, group2 n=41) based on non-negative matrix factorization (NMF) method. The DFS of group1 and group2 were significantly different (log-rank p=0.005). In validation cohort, patients were divided into group1 and group2 (group1 n=401, group2 n=202) using clustering method above. A significant difference between subgroups was also tested (log-rank p&amp;lt;0.0001). Conclusion: We identified 76 immune-related genes using CIBERSORT tool. Based on this gene set, early stage MSS endometrial and gastrointestinal tumors could be divided into two subgroups with distinct disease-free survival. Citation Format: Shi Zhang, Xinyi Liu, Lan Zhang, Mengli Huang. Subgroups of early-stage microsatellite stability endometrial, colorectal and stomach tumors based on transcriptomics have distinct disease-free survival [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2021; 2021 Apr 10-15 and May 17-21. Philadelphia (PA): AACR; Cancer Res 2021;81(13_Suppl):Abstract nr 2149.
Scaling Metal‐Elastomer Composites toward Stretchable Multi‐Helical Conductive Paths for Robust Responsive Wearable Health Devices
Authors: Yue Zhao, Yu Jun Tan, Weidong Yang, Shaohua Ling, Zijie Yang, Ju Teng Teo, Hian Hian See, David Kwok Hung Lee, Dingjie Lu, Shihao Li, Xianting Zeng, Zhuangjian Liu, Benjamin C.K. Tee
Journal: Advanced Healthcare Materials (2021)

Abstract Stretchable electronics have advanced rapidly and many applications require high repeatability and robustness under various mechanical deformations. It has been described here that how a highly stretchable and reliable conductor composite made from helical copper wires and a soft elastomer, named eHelix, can provide mechanically robust and strain‐insensitive electronic conductivity for wearable devices. The reversibility of the mechanical behavior of the metal‐elastomer system has been studied using finite element modeling methods. Optimal design parameters of such helical metal‐elastomer structures are found. The scaling of multiple copper wires into such helical shapes to form a Multi‐eHelix system is further shown. With the same elastomer volume, Multi‐eHelix has more conductive paths and a higher current density than the single‐eHelix. Integrations of these eHelix stretchable conductors with fabrics showed wearable displays that can survive machine‐washes and hundreds of mechanical loading cycles. The integration of the eHelix developed by us with a wearable optical heart rate sensor enabled a wearable health monitoring system that can display measured heart rates on clothing. Furthermore, Multi‐eHelix conductors are used to connect flexible printed circuit boards and piezoresistive sensors on a tactile sensing glove for the emerging sensorized prosthetics.
腎乏血の高感度標識としての尿脂肪酸結合タンパク質(FABP):移植後ヒト腎臓に対する生体内ビデオCCD分析による直接証拠
Authors: Sugaya T, Yamamoto T, Noiri E, Ono Y, Hattori R
Journal: Journal of the American Society of Nephrology (2003)
Abstract 1030: CENP-E inhibition generates micronucleus formation activating the cGAS-STING pathway in cancer cells
Authors: Yumi Hakozaki, Yukie Kashima, Tomoko Y. Morita, Kosuke Tanaka, Susumu S. Kobayashi, Akihiro Ohashi
Journal: Cancer Research (2021)

Abstract Background: Micronuclear formation has been reported to activate innate immune response in tumor through the cGAS-STING pathway, which monitors cytosolic DNA primarily to detect bacteria or virus infection. We have developed a novel small molecule inhibitor targeting CENP-E, termed Cmpd-A, which intensively generate micronucleus formation in a broad range of cancer cells, causing a potent antiproliferation by aneuploid-mediated cellular stresses. In this study, using Cmpd-A as a tool compound, we aim to determine that micronucleus formation induced by CENP-E inhibitor could activate the cGAS-STING pathway in cancer cells, which may potentially induce an immunological conversion from cold to hot in cancer cells. Method: We generated micronuclear formation in cancer cells by Cmpd-A treatment. Phosphorylations of TBK1 and IRF3, indexes of the cGAS-STING pathway activation, were determined by immunoblotting. Gene set enrichment analysis of RNA-seq data was performed, comparing DMSO (control) and Cmpd-A treatment. Reporter assays for IRF and NF-kB were also performed. Results: Immunoblotting revealed that phosphorylations of TBK1 and IRF3 were remarkably upregulated in Cmpd-A-treated cells concordantly with micronuclear formation. Transcriptome analysis revealed that the down-stream genes in the cGAS-STING pathway (innate immune pathways) are elevated: IL6, IP10, CXCL1, IL8, TNF, IFNA families, and IFNB1. The Gene Set Enrichment Analysis (GSEA) also demonstrated that innate immune-associated pathways were significantly enriched in Cmpd-A-treated cells: cytosolic DNA sensing pathway, cytokine-cytokine receptor interaction pathway, and Toll-like receptor signaling pathway. Furthermore, the IRF-Lucia and NF-kB-SEAP reporter activity assays revealed that both IRF and NF-kB were significantly activated in Cmpd-A-treated cells in a time-dependent manner. Conclusions: The CENP-E inhibitor generates micronucleus formation to activate the cGAS-STING pathway in cancer cells. These findings suggest the CENP-E inhibitor could potentially induce the immunological conversion from cold to hot in cancer cells. Citation Format: Yumi Hakozaki, Yukie Kashima, Tomoko Y. Morita, Kosuke Tanaka, Susumu S. Kobayashi, Akihiro Ohashi. CENP-E inhibition generates micronucleus formation activating the cGAS-STING pathway in cancer cells [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2021; 2021 Apr 10-15 and May 17-21. Philadelphia (PA): AACR; Cancer Res 2021;81(13_Suppl):Abstract nr 1030.
Three-dimensional printing technology to create a high-fidelity ureteroscopy simulator: Development and evaluation
Authors: A. de Hauteclocque, C. Michiels, J. Sarrazin, M. Faessel, M. Percot, J-P. Le Paih, A. Guillaume, E. Alezra, L. Dupitout, N.S. Vuong, N. Grenier, G. Capon, P. Blanc, H. Bensadoun, G. Robert, F. Bladou, J.M. Ferriere, F. Bos, V. Estrade, J-C. Bernhard
Journal: European Urology (2021)
Abstract 1375: Activity of pemetrexed in patients with driver oncogene positive non-small cell lung cancer and squamous histology
Authors: Yunan Nie, Tejas Patil, David Ross Camidge
Journal: Cancer Research (2021)

Abstract Pemetrexed, a multi-targeted antifolate chemotherapy agent, has been used both as a single agent chemotherapy as well as in combination given its favorable side effect profile, and has been the only effective continuation maintenance chemotherapy regimen after initial doublet use associated with increased overall survival (OS) among non-squamous non-small cell lung cancers. The current labelled indications for pemetrexed in NSCLC are restricted to those with non-squamous histology due to previous studies that showed worse outcomes in patients with squamous histology when compared to non-squamous histology. More recently, however, in the era of increased molecular profiling of NSCLC, it has been observed that patients with ALK, ROS1, and RET gene fusions have demonstrated marked sensitivity to pemetrexed. This retrospective case series, therefore, evaluated the response to pemetrexed among a cohort of 9 oncogene-driven patients with squamous (or adenosquamous) histologies who did receive pemetrexed based chemotherapy. Response rates, progression free survival (PFS), and OS for these patients were compared to a historical group of patients published in previous studies that examined pemetrexed response. The results indicated a positive response to pemetrexed in patients with an actionable driver oncogene occurring in the context of squamous or adenosquamous histology. Patients in the oncogene-driven adenosquamous/squamous group had significantly higher response rates as compared to the historical squamous cell group and no significant difference in response rates as compared to the historical adenocarcinoma comparison group. In summary, contrary to prior studies, this case series does suggest that pemetrexed may be a viable treatment option in patients with squamous cell histology who also have a targetable mutation. Citation Format: Yunan Nie, Tejas Patil, David Ross Camidge. Activity of pemetrexed in patients with driver oncogene positive non-small cell lung cancer and squamous histology [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2021; 2021 Apr 10-15 and May 17-21. Philadelphia (PA): AACR; Cancer Res 2021;81(13_Suppl):Abstract nr 1375.