tbuckley/cabot-search huggingface dataset:
Abstract 877: Use of beta blockers and death from breast cancer in New Zealand breast cancer patients
Authors: Oliver William Scott, Sandar TinTin, Alana Cavadino, Mark Elwood
Journal: Cancer Research (2021)

Abstract Background Beta blockers (BB), used for a range of cardiovascular indications, have been associated with improved cancer outcomes in international studies. This study examines the association between the use of BBs and death from breast cancer in New Zealand women. Methods Women who were diagnosed with breast cancer between 2007 and 2016 were identified from four population-based regional NZ breast cancer registries and linked to pharmaceutical data, hospital discharges, and death records. Median follow up time was 3.96 years. Cox proportional hazard models were used to assess the hazard of breast cancer specific death (BCD) associated with BB use. Results Of the 14,971 women included in analysis, 21% used a BB after diagnosis. Although not significant, BB use increased the risk of BCD (adjusted hazard ratio: 1.15; 95% CI: 0.99-1.33). When considering subgroups however, the increased risk only remained in those with at least one cardiac condition, in patients under 80 years of age, and in those who were dispensed a BB in the last periods of life. When excluding dispensings in the six months prior to death/last follow up, the adjusted hazard ratio between BB use and BCD decreased to 0.95 (95% CI: 0.81-1.11). Risk was highest with short term use and decreased consistently with ever increasing doses. Conclusions The initial increased risk is likely to be due to confounding by indication, and there was a suggestion of a protective effect of long-term BB use on BCD. Citation Format: Oliver William Scott, Sandar TinTin, Alana Cavadino, Mark Elwood. Use of beta blockers and death from breast cancer in New Zealand breast cancer patients [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 877.
Abstract 704: Sex and age differences in telomere length and susceptibility to COVID-19
Authors: Manar Ahmed Kamal, Kareem Reda Alamiry, Mahmoud Zaki
Journal: Cancer Research (2021)

Abstract Background: Telomeres are the ends of a chromosome and play a fundamental role as vanguards contra the chromosomal decay. Due to the inability of DNA polymerase to replicate chromosomal ends, a reduction in telomeres length happens after each cell division. The existence of shorter telomeres in older people is related to diminished immune functions. Viral infections able to stimulate remodeling of cells, stress responses, and telomere shortening. Moreover, telomere shortening can be caused by extrinsic environmental variables which induce oxidative stress under conditions of inflammation. Aim: To identify the correlation between telomere shortening and susceptibility to Novel Coronavirus Disease 2019 (COVID-19). In addition to clarifying changes in telomere length according to the viral infection, the effect of sex and age differences in telomere length in confirmed positive COVID-19 cases are also reviewed. Conclusion: There is a correlation between telomere length and COVID-19 infection with higher susceptibly of elderly patients and males due to shortening in their telomere length. Approximately 53% of (111,428) infected cases (≥50) years old are males, and 47% of (111,428) infected cases (≥50) years old are females. Citation Format: Manar Ahmed Kamal, Kareem Reda Alamiry, Mahmoud Zaki. Sex and age differences in telomere length and susceptibility to COVID-19 [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 704.
The CXC-chemokine platelet factor 4 promotes monocyte survival and induces monocyte differentiation into macrophages
Authors: Barbara Scheuerer, Martin Ernst, Iris Dürrbaum-Landmann, Jens Fleischer, Evelin Grage-Griebenow, Ernst Brandt, Hans-Dieter Flad, Frank Petersen
Journal: Blood (2000)
Electrostatic Flocking of Insulative and Biodegradable Polymer Microfibers for Biomedical Applications
Authors: Alec McCarthy, Johnson V. John, Lorenzo Saldana, Hongjun Wang, Matthew Lagerstrom, Shixuan Chen, Yajuan Su, Mitchell Kuss, Bin Duan, Mark A. Carlson, Jingwei Xie
Journal: Advanced Healthcare Materials (2021)

Abstract Electrostatic flocking, a textile engineering technique, uses Coulombic driving forces to propel conductive microfibers toward an adhesive‐coated substrate, leaving a forest of aligned fibers. Though an easy way to induce anisotropy along a surface, this technique is limited to microfibers capable of accumulating charge. This study reports a novel method, utilizing principles from the percolation theory to make electrically insulative polymeric microfibers flockable. A variety of well‐mixed, conductive materials are added to multiple insulative and biodegradable polymer microfibers during wet spinning, which enables nearly all types of polymer microfibers to accumulate sufficient charges required for flocking. Biphasic, biodegradable scaffolds are fabricated by flocking silver nanoparticle (AgNP)‐filled poly( ε ‐caprolactone) (PCL) microfibers onto substrates made from 3D printing, electrospinning, and thin‐film casting. The incorporation of AgNP into PCL fibers and use of chitosan‐based adhesive enables antimicrobial activity against methicillin‐resistant Staphylococcus aureus . The fabricated scaffolds demonstrate both favorable in vitro cell response and new tissue formation after subcutaneous implantation in rats, as evident by newly formed blood vessels and infiltrated cells. This technology opens the door for using previously unflockable polymer microfibers as surface modifiers or standalone structures in various engineering fields.
Abstract 2688: The landscape of precision cancer combination therapy: a single-cell perspective
Authors: Saba Ahmadi, Pattara Sukprasert, Rahulsimham Vegesna, Sanju Sinha, Natalie Artzi, Samir Khuller, Alejandro A. Schäffer, Eytan Ruppin
Journal: Cancer Research (2021)

Abstract The availability of single-cell transcriptomics data opens new opportunities for rational design of combination cancer treatments in a systematic manner. Mining such data, we explore the landscape of optimal combination therapy targets in solid tumors (including brain, head and neck, melanoma, lung, breast and colon cancers). To this end, we developed MadHitter (https://github.com/ruppinlab/madhitter), which analyzes tumor single-cell transcriptomics data using combinatorial algorithms to identify precision combination of treatment targets that are predicted to maximize the killing of cancer cells while minimizing the killing of noncancerous ones. We started with a predefined set of 533 proteins that are lowly abundant across healthy tissues and thus may have low off-tumor targeting and toxicity if targeted via chimeric antigen receptors (CAR) T cell therapy. In most cancer types analyzed, we find that combinations composed of a single-digit number of targets are sufficient to kill at least 80% of the tumor cells while killing at most 10% of the non-tumor cells in each patient. We identify targets that are shared across datasets of the same cancer type (e.g., TNR) or across different cancer types (the SOX family, MAGE family, and KRT16). Next, we expanded our search for a set of 1269 known cell surface receptors, which may be precisely targeted by antibody or nanoparticles delivering a toxin into cells via receptor mediated endocytosis. The resulting optimal target sets are encouragingly also in the single-digit size. The gene PTPRZ1, a tyrosine phosphatase receptor, is frequently found in the optimal combinations for brain and head and neck cancers, and EGFR is a high-coverage target in multiple tumor types. Notably, requiring more stringent levels of cancer killing, the number of targets that need to be combined rises sharply in both search spaces described above. In sum, this analysis provides the first systematic characterization of potential combinatorial targets in solid tumors, uncovering promising future targets for both CAR therapy and conjugated toxin delivering antibodies and nanoparticles. Citation Format: Saba Ahmadi, Pattara Sukprasert, Rahulsimham Vegesna, Sanju Sinha, Natalie Artzi, Samir Khuller, Alejandro A. Schäffer, Eytan Ruppin. The landscape of precision cancer combination therapy: a single-cell perspective [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 2688.
Abstract 1942: Quantitative D2O proteomics reveals ATG9A-dependent autophagy substrates that are degraded independently of the LC3-lipidation machinery
Authors: Colten M. McEwan, David G. Broadbent, Ashari R. Kannangara, Daniel M. Poole, Bradley C. Naylor, John C. Price, Jens C. Schmidt, Josh L. Andersen
Journal: Cancer Research (2021)

Abstract Autophagy is an essential catabolic process that cancer cells use to survive metabolic stress and maintain basal cellular homeostasis via degradation of dysfunctional organelles and protein aggregates. One protein with an unclear, yet essential, role in autophagy is the multi-pass transmembrane protein ATG9A. ATG9A is an apical autophagy regulator that is hypothesized to help seed the formation of nascent autophagosomes by providing membrane through its own unique ATG9A vesicles. To understand the role ATG9A plays in autophagic protein turnover, we performed whole proteome deuterium exchange and quantitative mass spectrometry to measure protein degradation rates in Wild-Type (WT) and ATG9A Knock-Out (KO) cells. This experiment revealed that ATG9A KO cells display significantly decreased degradation rates of aggregation prone proteins and autophagy adapters, such as p62/SQSTM1. In an effort to understand the relationship between ATG9A and p62/SQSTM1, we found that ATG9A associates directly with p62/SQSTM1 and mediates the basal degradation of p62/SQSTM1-associated protein aggregates. This ATG9A-mediated degradation occurs in a non-canonical way, involving a subset of ATG proteins (e.g., ATG13, ATG101), but independent of the LC3-lipidation machinery ATG5 and ATG7. Taken together, our data suggests that ATG9A controls the degradation of p62 in an ATG5/ATG7-independent manner. Citation Format: Colten M. McEwan, David G. Broadbent, Ashari R. Kannangara, Daniel M. Poole, Bradley C. Naylor, John C. Price, Jens C. Schmidt, Josh L. Andersen. Quantitative D2O proteomics reveals ATG9A-dependent autophagy substrates that are degraded independently of the LC3-lipidation machinery [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 1942.
Abstract CT155: Role of Time intensity &amp; density curve for detecting early changes in pancreatic adenocarcinoma
Authors: Syed Rahmanuddin, Derek Cridebring, Ron Korn, Jordyn Brase, Pejman Motarjem, Wenli Kai, Vincent Chung, Erkut Borazanci, Ajay Goel, Daniel Von Hoff
Journal: Cancer Research (2021)

Abstract Purpose: Pancreatic cancer has limited options for early detection and this study tried to tackle that issue using TIDC (Time Intensity Density Curve), 3D volumetric and perfusion imaging. Experimental Design: This quantitative study was done by analyzing multi-phase CT images of patients undergoing treatment of different stages of pancreatic ductal adenocarcinoma (PDAC). Using advanced 3D imaging software we identified the perfusion and radiodensity of tumors at different stages. This analysis was done using 41 adult patients with unresectable treatment-naïve PDAC who were either enrolled in a clinical trial at HonorHealth Research Institute (Scottsdale, AZ) or treated at the City of Hope Comprehensive Cancer Center (Duarte, CA) as standard of care non study patients between 2015-2019. All patients were over the age of 18 and had been diagnosed with PDAC. We divided the participant sample into two groups, labeled Cohort 1 and Cohort 2. For image acquisition in both groups, we required to have multiphase CT images for the collection of images at both locations. Results: TIDC, 3D volumetric measurements and perfusion imaging proved useful in the quantification of tumor aggressiveness. Our results showed that perfusion in PDAC displayed delays in the venous phase which may be linked to vascular growth related activity and exhibits the active and viable part of the tumor. 3D volumetric analysis of the patient's multi-phase CT scan showed clear changes in arterial and venous perfusion and correlated with how rapidly patients progressed (e.g. tumor aggressiveness). Conclusion: TIDC and 3D volumetric analysis could play a significant role in defining the aggressiveness of the pancreatic ductal adenocarcinoma. Citation Format: Syed Rahmanuddin, Derek Cridebring, Ron Korn, Jordyn Brase, Pejman Motarjem, Wenli Kai, Vincent Chung, Erkut Borazanci, Ajay Goel, Daniel Von Hoff. Role of Time intensity &amp; density curve for detecting early changes in pancreatic 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 CT155.
Clinical and Germline Risk Factors for the Occurrence of Multiple Treatment Toxicities during Childhood Acute Lymphoblastic Leukemia (ALL) Therapy
Authors: Marion K Mateos, Toby N Trahair, Chelsea Mayoh, Pasquale M Barbaro, Carly George, Rosemary Sutton, Tamas Revesz, Draga Barbaric, Jodie Giles, Frank Alvaro, Francoise Marie Mechinaud, Daniel R Catchpoole, Rishi Sury Kotecha, Michael Cj Quinn, Georgia Chenevix-Trench, Stuart MacGregor, Luciano Dalla-Pozza, Glenn M Marshall
Journal: Blood (2017)
日本人男性におけるプリン作動性受容体P2Y,G蛋白質共役,2 (P2RY2)遺伝子と心筋梗塞との関係
Authors: Wang Zhao Xia, Nakayama Tomohiro, Sato Naoyuki, Izumi Yoichi, Kasamaki Yuji, Ohta Masakatsu, Soma Masayoshi, Aoi Noriko, Matsumoto Koichi, Ozawa Yukio, Ma Yi Tong, Doba Nobutaka, Hinohara Shigeaki
Journal: Circulation (2009)
Abstract 2150: High RRM1 expression as a potential poor prognosis factorin bladder cancer patients
Authors: Ziqiao Xu, Ting Bei, Wenzhuan Xie, Mengli Huang
Journal: Cancer Research (2021)

Abstract Background: RRM1 encodes the M1 subunit of Ribonucleotide Reductase (RNR), a complex participating in DNA replication and repairment. RRM1 expression level has been reported to be associated with prognosis in various cancers, such as non-small-cell lung cancer, pancreatic cancer, breast cancer, and biliary tract cancer. However, the prognosis value of RRM1 expression in bladder cancer (BLCA) has not been revealed. Method: Three bladder cancer cohorts with RNA-seq data including 2 cohorts from the GEO database and 1 from the TCGA database were used for investigating the overall survival (OS) of BLCA patients with differentiated RRM1 RNA expression. GSEA and CIBERSORT analyses were performed to study the potential mechanisms. The value of RRM1 RNA expression in predicting the clinical benefits of immune checkpoint inhibitors (ICIs) treated BLCA patients was also investigated using data from an ICI cohort (IMvigor210 cohort, n=348). Result: We found significant differences in OS between BLCA patients with high (top 25% RRM1 RNA expression patients) and low (lowest 25% RRM1 RNA expression patients) RRM1 RNA expression in all the three bladder cancer cohorts from the TCGA and the GEO database. The multiple-variables Cox regression analysis revealed that higher RRM1 expression was associated with worse survival outcomes (HR=1.65, 95% CI = 1.05 - 2.6, P = 0.03).GSEA analysis revealed that 20 out of 50 Hallmark gene sets were enriched in the RRM1 high expression group. Among these enriched gene sets, the interferon-gamma is a well-established immune-related pathway. Furthermore, CIBERSORT analysis showed that the RRM1 high expression group had higher scores in IFN-gamma response, intra-tumor heterogeneity, and leukocyte fraction than the RRM1 low expression group. Combining results from both CIBERSORT and GSEA analysis, we hypothesized that RRM1 expression may be an efficacious predictor for ICI treatment in BLCA patients. Overall survival analysis of another external ICI cohort revealed that ICI treated BLCA patients with high RRM1 expression tended to have better OS than those with low RRM1 expression (HR = 0.77, CI95 0.54 - 1.1), but this difference was not statistically significant (P = 0.152). Conclusion: Our study demonstrated that high RRM1 expression may serve as a poor prognostic biomarker in BLCA patients. Moreover, our study suggested that BLCA patients with high RRM1 expression may benefit more from ICIs therapies than those with low RRM1 expression. Citation Format: Ziqiao Xu, Ting Bei, Wenzhuan Xie, Mengli Huang. High RRM1 expression as a potential poor prognosis factorin bladder cancer patients [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 2150.
New Targeted Non–Small Cell Lung Cancer Therapy Approved
Authors: Bridget M. Kuehn
Journal: JAMA (2021)

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Abstract 1227: Oncofusion driven <i>de novo</i> enhancer assembly promotes malignancy in Ewing sarcoma<i>via</i> aberrant expression of the stereociliary protein LOXHD1
Authors: Qu Deng, Ramakrishnan Natesan, Florencia Cidre-Aranz, Shehbeel Arif, Ying Liu, Reyaz Rasool, Pei Wang, Zvi Crammer, Margaret Chou, Chandan Kumar, Kristy Weber, Karin Eisinger, Nicolas Grillet, Thomas Grünewald, Irfan Asangani
Journal: Cancer Research (2021)

Abstract Ewing sarcoma (EwS) is a highly aggressive tumor of bone and soft tissues that mostly affects children and adolescents. The pathognomonic oncofusion EWSR1-ETS (EWS-FLI1/EWS-ERG) transcription factors drive EwS by orchestrating an oncogenic transcription program through de novo enhancers. Pharmacological targeting of these oncofusions has been challenged by unstructured prion-like domains and common DNA binding motifs in the EWSR1 and ETS, respectively. Alternatively, identification and characterization of mediators and downstream targets of EWS-FLI1 dependent or independent function could offer novel therapeutic options. By integrative analysis of thousands of transcriptomic datasets representing pan-cancer cell lines, primary cancer, metastasis, and normal tissues, we have identified a 32 gene signature (ESS32) in EwS that could stratify EwS from pan-cancer. Of the ESS32, LOXHD1 - coding for a stereociliary protein was the most exquisite gene expressed in EwS. CRISPR-Cas9 mediated deletion or silencing of EWS-FLI1 bound upstream de novo enhancer elements in EwS cells led to the loss of LOXHD1 expression and altered the EWS-FLI1, MYC, and HIF1a pathway genes, resulting in decreased proliferation and invasion in vitro and in vivo. These observations open up new avenues for developing LOXHD1-targeted small molecules or cellular therapies for this deadly disease. Citation Format: Qu Deng, Ramakrishnan Natesan, Florencia Cidre-Aranz, Shehbeel Arif, Ying Liu, Reyaz Rasool, Pei Wang, Zvi Crammer, Margaret Chou, Chandan Kumar, Kristy Weber, Karin Eisinger, Nicolas Grillet, Thomas Grünewald, Irfan Asangani. Oncofusion driven de novo enhancer assembly promotes malignancy in Ewing sarcomavia aberrant expression of the stereociliary protein LOXHD1 [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 1227.
A Global Survey of Physicians Knowledge About Nonalcoholic Fatty Liver Disease
Authors: Zobair M. Younossi, Janus P. Ong, Hirokazu Takahashi, Yusuf Yilmaz, Yuichiro Eguc`hi, Mohamed El Kassas, Maria Buti, Moisés Diago, Ming-Hua Zheng, Jian-Gao Fan, Ming-Lung Yu, Vincent Wai-Sun Wong, Khalid Alswat, Wah-Kheong Chan, Nahum Mendez-Sanchez, Patrizia Burra, Elisabetta Bugianesi, Ajay K. Duseja, Jacob George, George V. Papatheodoridis, Hamid Saeed, Laurent Castera, Marco Arrese, Marcelo Kugelmas, Manuel Romero-Gomez, Saleh Alqahtani, Mariam Ziayee, Brian Lam, Issah Younossi, Andrei Racila, Linda Henry, Maria Stepanova
Journal: Clinical Gastroenterology and Hepatology (2021)