tbuckley/cabot-search huggingface dataset:
Integrative Analysis of miRNAs Identifies Clinically Relevant Epithelial and Stromal Subtypes of Head and Neck Squamous Cell Carcinoma
Authors: Jeremiah Holt, Vonn Walter, Xiaoying Yin, David Marron, Matthew D. Wilkerson, Hyo Young Choi, Xiaobei Zhao, Heejoon Jo, David Neil Hayes, Yoon Ho Ko
Journal: Clinical Cancer Research (2020)

Abstract Purpose: The objective of this study is to characterize the role of miRNAs in the classification of head and neck squamous cell carcinoma (HNSCC). Experimental Design: Here, we analyzed 562 HNSCC samples, 88 from a novel cohort and 474 from The Cancer Genome Atlas, using miRNA microarray and miRNA sequencing, respectively. Using an integrative correlations method followed by miRNA expression–based hierarchical clustering, we validated miRNA clusters across cohorts. Evaluation of clusters by logistic regression and gene ontology approaches revealed subtype-based clinical and biological characteristics. Results: We identified two independently validated and statistically significant (P &amp;lt; 0.01) tumor subtypes and named them “epithelial” and “stromal” based on associations with functional target gene ontology relating to differing stages of epithelial cell differentiation. miRNA-based subtypes were correlated with individual gene expression targets based on miRNA seed sequences, as well as with miRNA families and clusters including the miR-17 and miR-200 families. These correlated genes defined pathways relevant to normal squamous cell function and pathophysiology. miRNA clusters statistically associated with differential mutation patterns including higher proportions of TP53 mutations in the stromal class and higher NSD1 and HRAS mutation frequencies in the epithelial class. miRNA classes correlated with previously reported gene expression subtypes, clinical characteristics, and clinical outcomes in a multivariate Cox proportional hazards model with stromal patients demonstrating worse prognoses (HR, 1.5646; P = 0.006). Conclusions: We report a reproducible classification of HNSCC based on miRNA that associates with known pathologically altered pathways and mutations of squamous tumors and is clinically relevant.
MRI-traceable theranostic nanoparticles for targeted cancer treatment
Authors: Tareq Anani, Shiva Rahmati, Nayer Sultana, Allan E. David
Journal: Theranostics (2020)

Current cancer therapies, including chemotherapy and radiotherapy, are imprecise, non-specific, and are often administered at high dosages - resulting in side effects that severely impact the patient's overall well-being. A variety of multifunctional, cancer-targeted nanotheranostic systems that integrate therapy, imaging, and tumor targeting functionalities in a single platform have been developed to overcome the shortcomings of traditional drugs. Among the imaging modalities used, magnetic resonance imaging (MRI) provides high resolution imaging of structures deep within the body and, in combination with other imaging modalities, provides complementary diagnostic information for more accurate identification of tumor characteristics and precise guidance of anti-cancer therapy. This review article presents a comprehensive assessment of nanotheranostic systems that combine MRI-based imaging (T1 MRI, T2 MRI, and multimodal imaging) with therapy (chemo-, thermal-, gene- and combination therapy), connecting a range of topics including hybrid treatment options (e.g. combined chemo-gene therapy), unique MRI-based imaging (e.g. combined T1-T2 imaging, triple and quadruple multimodal imaging), novel targeting strategies (e.g. dual magnetic-active targeting and nanoparticles carrying multiple ligands), and tumor microenvironment-responsive drug release (e.g. redox and pH-responsive nanomaterials). With a special focus on systems that have been tested in vivo, this review is an essential summary of the most advanced developments in this rapidly evolving field.
<i>QuickStats:</i> Percentage Distribution of Deaths Involving Injuries from Recreational and Nonrecreational Use of Watercraft,* by Month — United States, 2015–2017
Journal: MMWR Morbidity and Mortality Weekly Report (2019)

During 2015-2017, there were 1,389 deaths involving injuries from recreational and nonrecreational use of watercraft.Deaths were identified using International Classification of Diseases, Tenth Revision (ICD-10) underlying cause of death codes V90-V94 (water transport).Water transport includes both recreational and nonrecreational use of motorized (e.g., merchant ship, ferry, passenger ship, fishing boat, and jet ski) and nonmotorized (e.g., canoe, kayak, inflatable craft, surfboard, and windsurfer) watercraft.Deaths resulted from drowning, submersion, and other types of injuries.All water transport deaths are unintentional.During 2015-2017, there were 1,389 deaths involving injuries from recreational and nonrecreational use of watercraft (an average of 463 deaths per year).The percentage of deaths that occurred by month ranged from 2.7% in December to 18.2% in July.The majority of deaths (57%) occurred during May-August.
Acquired Mutations within the JAK2 Kinase Domain Confer Resistance to JAK Inhibitors in an <i>in Vitro</i> model of a High-Risk Acute Lymphoblastic Leukemia
Authors: Charlotte EJ Downes, Barbara J McClure, Jacqueline Rehn, James Breen, John B Bruning, David T Yeung, Deborah L White
Journal: Blood (2020)
ITP World Impact Survey (I-WISh) 2.0: Further Exploration of the Impact of ITP on Patients
Authors: Waleed Ghanima, Drew Provan, Nichola Cooper, Axel Matzdorff, Ming Hou, Cristina Santoro, Mervyn Morgan, Caroline Kruse, Francesco Zaja, Leron Lahav, Yoshiaki Tomiyama, Michal Winograd, Barbara Lovrencic, Tom Bailey, Jens Haenig, James B. Bussel
Journal: Blood (2020)
Innate-like Chemokine Receptor Profile and Migratory Behaviour By Terminally Differentiated and Educated NK Cells
Authors: Mieszko Lachota, Daniel Alfredo Palacios, Dennis Clement, Eivind Heggernes Ask, Hanna Julie Hoel, Merete Thune Wiiger, Marianna Vincenti, Magdalena Winiarska, Radoslaw Zagozdzon, Karl-Johan Malmberg
Journal: Blood (2020)
TP53 in Acute Myeloid Leukemia: Evolving from Just Another Prognostic Marker to an Actionable Biomarker Informing Treatment
Authors: Peter Riccelli, Marieke Hoefsmit, Wendy Moore, Adam Idica, Jirawas Sornkom, Bethany Slifko, Sabit Delic, Kevin Entwistle, Susanne Munksted, Jordan Clark
Journal: Blood (2020)
Abstract 501: Hydrogen Sulfide Protects the Heart Against Ferroptotic Cell Death in Diabetic Cardiomyopathy
Authors: Sumit Kar, Hamid Shahshahan, Paras K Mishra
Journal: Circulation Research (2020)

Hyperglycemia-induced death of terminally differentiated cardiomyocytes in diabetic cardiomyopathy (DMCM) leads to heart failure. Ferroptosis is a newly discovered form of cell death triggered by intracellular iron and oxidative stress. While little is known about ferroptosis in DMCM, hyperinsulinemia stimulates intracellular iron uptake, which would be predicted to increase ferroptosis. H 2 S is an endogenous gaseous signaling molecule which may inhibit ferroptosis. H 2 S donors increase glutathione substrate for glutathione peroxidase 4 (GPX4), which removes lipid peroxidation and is the primary inhibitor of ferroptosis. However, no study has investigated the role of H 2 S in ferroptosis. We tested the hypothesis that increased ferroptosis contributes to DMCM, which is ameliorated by restoring H 2 S levels, by measuring ferroptosis in the hearts of db/db mice with DMCM and high glucose treated primary neonatal cardiomyocytes after H 2 S donor treatment. GPX4 expression was decreased (3.21±0.41 GPX4/total protein in db/+ control mice vs. 1.84±0.26 in db/db, P&lt;0.05, n=6/group) and 4-HNE lipid peroxide was increased (7.37±0.98 μg 4-HNE/total protein in db/+ control mice vs. 8.73±0.84 in db/db, P&lt;0.05, n=3/group) in the left ventricle of db/db mice indicating increased ferroptosis in DMCM. GPX4 activity was also decreased along with increased 4-HNE in high glucose cultured cardiomyocytes. Treatment with the ferroptosis inhibitor ferrostatin-1 prevented hyperglycemia induced ferroptosis. Treatment of cardiomyocytes with the H 2 S donor GYY4137 in hyperglycemia also decreased 4-HNE. We also validated the anti-ferroptotic potential of H 2 S by treating cardiomyocytes with the ferroptosis inducer RSL3 and GYY4137. H 2 S donor treatment reduced reactive oxygen species and 4-HNE lipid peroxide seen after ferroptosis induction with RSL3. This study establishes ferroptosis as a new, non-apoptotic, form of cell death in DMCM, and H 2 S as a novel regulator of cardiac ferroptosis.
R-Nanochop Incorporating a TFR1-Targeted Doxorubicin Nanocarrier Is Superior to R-CHOP in a PDX Model of Diffuse Large B-Cell Lymphoma
Authors: Artavazd Arumov, Piumi Y. Liyanage, Asaad Trabolsi, Evan R. Roberts, Braulio C. L. B. Ferreira, Austin D. Newsam, Daniel Bilbao, Roger M. Leblanc, Jonathan H. Schatz
Journal: Blood (2020)
Abstract 11452: Are Patients With Caseous Calcification of the Mitral Annulus But Without Atrial Fibrillation at Increased Risk of Cerebral Embolization?
Authors: Charles A Dietl, Christopher M Hawthorn, Veena Raizada
Journal: Circulation (2014)

Background: Caseous calcification of the mitral annulus (CCMA) is very uncommon, and is frequently misdiagnosed as an intracardiac tumor, thrombus, abscess, or simply as mitral annular calcification (MAC). These masses are generally believed to have a benign prognosis. The aims of this study are to increase the awareness of this unusual variant of MAC, and to determine whether patients with CCMA are at increased risk of cerebral embolization in patients with or without atrial fibrillation (AF). Methods: A comprehensive literature search was done to determine whether patients with CCMA are at increased risk of cerebral embolization, using the following search modules: caseous calcification of the mitral annulus, mitral annular calcification, cerebral embolization with mitral annulus calcification, risk of stroke with mitral annular calcification. Results: Among the 496 articles listed in PubMed.gov, ScienceDirect.com, and Google Scholar, a total of 129 patients with CCMA were identified in 85 publications, and 31 articles were reviewed to evaluate the incidence of stroke in 1800 patients with MAC. Literature review revealed that the incidence of cerebrovascular events (CVE) associated with CCMA is 18.6% (24 of 129) which is even higher than the risk of embolic CVE reported in patients with MAC, 11.6% (209 of 1800) (range 4.8% to 24.1%). Only 2 of 24 patients (8.3%) with CCMA who suffered a CVE had history of AF, whereas the majority (22 of 24, or 91.7%) of CCMA patients with a CVE did not have AF. Conclusions: Despite the fact that several reports suggest that CCMA is a benign condition, CCMA may be potentially serious, because of the increased risk of cerebral embolization, even in patients without atrial fibrillation.
Isorhapontigenin protects against doxorubicin-induced cardiotoxicity via increasing YAP1 expression
Authors: Panxia Wang, Minghui Wang, Yuehuai Hu, Jianxing Chen, Yanjun Cao, Cui Liu, Zhongkai Wu, Juan Shen, Jing Lu, Peiqing Liu
Journal: Acta Pharmaceutica Sinica B (2020)

As an effective anticancer drug, the clinical limitation of doxorubicin (Dox) is the time- and dose-dependent cardiotoxicity. Yes-associated protein 1 (YAP1) interacts with transcription factor TEA domain 1 (TEAD1) and plays an important role in cell proliferation and survival. However, the role of YAP1 in Dox-induced cardiomyopathy has not been reported. In this study, the expression of YAP1 was reduced in clinical human failing hearts with dilated cardiomyopathy and Dox-induced in vivo and in vitro cardiotoxic model. Ectopic expression of Yap1 significantly blocked Dox-induced cardiomyocytes apoptosis in TEAD1 dependent manner. Isorhapontigenin (Isor) is a new derivative of stilbene and responsible for a wide range of biological processes. Here, we found that Isor effectively relieved Dox-induced cardiomyocytes apoptosis in a dose-dependent manner in vitro. Administration with Isor (30 mg/kg/day, intraperitoneally, 3 weeks) significantly protected against Dox-induced cardiotoxicity in mice. Interestingly, Isor increased Dox-caused repression in YAP1 and the expression of its target genes in vivo and in vitro. Knockout or inhibition of Yap1 blocked the protective effects of Isor on Dox-induced cardiotoxicity. In conclusion, YAP1 may be a novel target for Dox-induced cardiotoxicity and Isor might be a new compound to fight against Dox-induced cardiotoxicity by increasing YAP1 expression.
Targeting microglial autophagic degradation in NLRP3 inflammasome-mediated neurodegenerative diseases
Authors: An-Guo Wu, Xiao-Gang Zhou, Gan Qiao, Lu Yu, Yong Tang, Lu Yan, Wen-Qiao Qiu, Rong Pan, Chong-Lin Yu, Betty Yuen-Kwan Law, Da-Lian Qin, Jian-Ming Wu
Journal: Ageing Research Reviews (2020)
Firearm Policy and Youth Suicide—In Pursuit of Mechanistic Explanations
Authors: Ali Rowhani-Rahbar, Miriam J. Haviland, Alice M. Ellyson
Journal: JAMA Network Open (2020)

Apurva Bhatt, MD; Xi Wang, MS; An-Lin Cheng, PhD; Kalee L. Morris, MS; Luke Beyer, BS; Abbie Chestnut, JD; Kristy Steigerwalt, MLS, PharmD; Jeffrey Metzner, MD
Long-Term Follow-up of a Randomized Trial of Two Dose Levels of Antithymocyte Globulin in Haploidentical Hematopoietic Stem Cell Transplantation
Authors: Yu Wang, Ren Lin, Lan-Ping Xu, Kai-Yan Liu, Xiao-Hui Zhang, Qi-Fa Liu, Xiao-Jun Huang
Journal: Blood (2020)
Erythropoiesis Failure in Diamond-Blackfan Anemia Starts at the Oligopotent Common Myeloid and Megakaryocyte-Erythroid Progenitor Stage
Authors: Richard N Armstrong, Mariana Benicio, Houtan Moshiri, Hongbing Li, Bozana Zlateska, Olga I. Gan, Eric R Lechman, John E. Dick, Yigal Dror
Journal: Blood (2020)
THU0100 Interleukin-17 increased the production of matrix metalloproteinase-3 in cultured rheumatoid arthritis synoviocytes
Authors: K Sung, K Ihm Soo, R Ha Yeon, K Yu Sun
Journal: Annals of the Rheumatic Diseases (2001)

<h3>Background</h3> <h3>Objectives</h3> To investigate the effect of interleukin-17 (IL-17) on production of matrix metalloproteinase-3 (MMP-3) in rheumatoid arthritis synoviocytes. <h3>Methods</h3> Fibroblast-like synovial cell (FLS) were prepared from the synovial tissue of rheumatoid arthritis patients and cultured in the presence of various concentration of IL-17. MMP-3 levels were determined in the culture supernatants by sandwitch ELISA according to culturing periods. <h3>Results</h3> Stimulation of FLS by IL-17 with 5, 10, 20, 40 ng/ml concentrations increased the production of MMP-3 by 2.7, 2.7, 3, 3.4 fold after 24 h and 8.7, 8.7, 8.1, 10.2 fold after 48 h over the constitutive levels of unstimulated FLS. <h3>Conclusion</h3> IL-17, a T cell-derived proinflammatory cytokine produced by rheumatoid synovium, may be involved in the cartilage degradation in rheumatoid arthritis by enhancing the production of MMP-3 from rheumatoid arthritis synoviocytes.
Comprehensive Characterization of the Epigenetic Landscape in Multiple Myeloma
Authors: Elina Alaterre, Laurie Herviou, Hugues De Boussac, Giorgio Papadopoulos, Stéphanie Boireau, Nicolas Robert, Guilhem Requirand, Angelique Bruyer, Sara Ovejero-Merino, Laure Vincent, Anne Marie Martinez, Giacomo Cavalli, Jerome Moreaux
Journal: Blood (2020)
Rational design of adjuvants for subunit vaccines: The format of cationic adjuvants affects the induction of antigen-specific antibody responses
Authors: Giulia Anderluzzi, Signe Tandrup Schmidt, Robert Cunliffe, Stuart Woods, Craig W. Roberts, Daniele Veggi, Ilaria Ferlenghi, Derek T. O'Hagan, Barbara C. Baudner, Yvonne Perrie
Journal: Journal of Controlled Release (2020)
Allogeneic Hematopoietic Stem-Cell Transplantation in Patients with GATA 2 Deficiency: Influence of Donor Stem Cell Source and Post-Transplantation Cyclophosphamide
Authors: Diana X. Nichols-Vinueza, Nirali N. Shah, Jennifer Cuellar-Rodriguez, Thomas R. Bauer, Katherine R. Calvo, Luigi D. Notarangelo, Steven M. Holland, Dennis D. Hickstein
Journal: Blood (2020)
<i>Prdm16</i> Is a Critical Regulator of Adult Long-Term Hematopoietic Stem Cell Quiescence
Authors: Kristbjorn Orri Gudmundsson, Yang Du, Nhu Nguyen, Kevin Oakley, Yufen Han, Bjorg Gudmundsdottir, Pentao Liu, Lino Tessarollo, Nancy Jenkins, Neal Copeland
Journal: Blood (2020)
Initial Clinical Activity and Safety of BFCR4350A, a FcRH5/CD3 T-Cell-Engaging Bispecific Antibody, in Relapsed/Refractory Multiple Myeloma
Authors: Adam D. Cohen, Simon J Harrison, Amrita Krishnan, Rafael Fonseca, Peter A Forsberg, Andrew Spencer, Jesus G. Berdeja, Jacob P. Laubach, Mengsong Li, Voleak Choeurng, Anjali Vaze, Divya Samineni, Teiko Sumiyoshi, James Cooper, Bernard M Fine, Suzanne Trudel
Journal: Blood (2020)
Identification of m6a Methyltransferase KIAA1429 As a Potential Prognostic Biomarker in Diffuse Large B-Cell Lymphoma
Authors: Xiaomin Chen, Shuai Ren, Mengfei Ding, Yiqing Cai, Shunfeng Hu, Yi Zhao, Yang Han, Xiangxiang Zhou, Xin Wang
Journal: Blood (2020)
Disruption of the Oral Microbiota Predicts Poor Outcomes after Allogeneic Hematopoietic Stem Cell Transplantation
Authors: Vinicius Campos de Molla, Vitor Heidrich, Julia Bruno, Franciele Knebel, Wanessa Miranda-Silva, Paula Asprino, Luciana Tucunduva, Vanderson Rocha, Yana Novis, Anamaria Camargo, Eduardo Fregnani, Celso Arrais-Rodrigues
Journal: Blood (2020)
Phase I Trial of MB-CART2019.1, a Novel CD20 and CD19 Targeting Tandem Chimeric Antigen Receptor, in Patients with Relapsed or Refractory B-Cell Non-Hodgkin Lymphoma
Authors: Peter Borchmann, Anja Jühling, Philipp Gödel, Hyatt Balke-Want, Christoph Schmid, Francis A. Ayuk, Silke Holtkamp, Liane Preussner, Gregor Zadoyan, Linda Hanssens, Andrew Kaiser, Marion Jurk, Iris Bürger, Dina Schneider, Boro Dropulic, Toon Overstijns, Christof Scheid, Udo Holtick, Stefan Miltenyi, Michael Hallek
Journal: Blood (2020)
SAT0080 Insight into the structural basis of selective cyclooxygenase-2 inhibition
Authors: G Trummlitz, H Wittneben
Journal: Annals of the Rheumatic Diseases (2001)

<h3>Background</h3> Cyclooxygenase-1 and -2 (COX-1/COX-2) catalyse the rate-limiting step in prostaglandin (PG) synthesis and are the targets of non-steroidal anti-inflammatory drugs (NSAIDs). The evidence is strong that the selective COX-2 inhibitors have reduced GI side effects in patients treated for rheumatic conditions, including osteoarthritis. <h3>Objectives</h3> The molecular basis of binding affinities and COX-2/COX-1 selectivity are explored using an approach that combines experimental results from X-ray analyses and docking experiments from computational chemistry. <h3>Methods</h3> The reported X-ray structures of COX-1 and COX-2 were used for computational optimisation of the interaction between the different NSAIDs and COX isoforms using the established computer program Sybyl/Molcad. <h3>Results</h3> The inhibition of COX can occur by compounds with high degree of structural diversity and various types of mechanisms. The results show that COX-2 selective inhibitors are belonging to several different, structural distinct classes: arylalkanoic acids, enolcarboxamids, acidic sulfonamids and diarylheterocycles. Two fundamental differences between the active site of COX-2 and COX-1 are responsible for the COX-2 selectivity and are caused by several amino acid substitution in COX-2 vs. COX-1: The volume of the COX-2 channel is extended by the substitution of Iso 523 by Val 523, Iso 434 by Val 434, His 513 by Arg 513 and Phe 503 by Leu 503. COX-selective diaryl-heterocycles (DuP 697, celecoxib, rofecoxib) are exploiting the side pocket and enolcarboxamid (meloxicam) and acidic sulfonamids (L745,733, NS 398, nimesulide) the extra space at the top of the channel. <h3>Conclusion</h3> This work illustrates the value of novel docking procedure for determining the binding of NSAIDs to the COX-enzyme. The structural insights into the binding mechanism indicate that COX-2 selectivity can be obtained by at least three chemically distinct classes of NSAIDs of which meloxicam, nimesulide and celecoxib are representatives.
AB0027 Tnf-alfa responses induced by different enterobacteria and gram-positive cell walls of normal intestinal microbiota in early rheumatoid arthritis
Authors: RK Luukkainen, T Cheng, M Rimpiläinen, T Möttönen, U Yli-Kerttula, R Saario, P Toivanen
Journal: Annals of the Rheumatic Diseases (2001)

<h3>Background</h3> The aetiology of the rheumatoid arthritis (RA) is unknown. A variety of infective agents have been proposed to be the etiological factor of the disease. <h3>Objectives</h3> To study whether enterobacteria and Gram-positive bacterial cell walls (BCW) derived from normal intestinal microbiata are involved in the etiopathogenesis of early rheumatoid arthritis. <h3>Methods</h3> Peripheral blood mononuclear cells (PBMC) and synovial fluid mononuclear cells (SFMC) were isolated from patients with early RA (the average duration of 3 months). The tumour necrosis factor-alpha (TNF-alfa) responses to heat-killed Salmonella enteritidis, Yersinia enterocolitica and Escherichia coli, and to Gram-positive BCW derived from four common intestinal indigenous bacteria, Eubacterium aerofaciens, Eubacterium limosum, Lactobacillus casei and Lactobacillus fermentum, and a BCW derived from a pathogen, Streptococcus pyogenes were investigated. <h3>Results</h3> The results obtained indicate that these bacterial antigens induce TNF-alfa responses of PBMC and SFMC from at least some patients with early RA. However, the responses are not spesific for any particular bacterial antigen tested. The responses observed are similar to those observed in the patients with other inflammatory arthritides. <h3>Conclusion</h3> These results suggest that SFMC reacting with BCW exist in some patients with early RA. They are in agreement with the hypothesis that BCW derived from normal intestinal microbiota might be involved in the etiopathogenesis of chronic arthritides, including RA.
Abstract PO-104: Phenotypic mapping of pathological crosstalk between glioblastoma and innate immune cells by synthetic genetic tracing
Authors: Matthias Jürgen Schmitt, Carlos Company, Yuliia Dramaretska, Iros Barozzi, Andreas Göhrig, Sonia Kertalli, Melanie Großmann, Heike Naumann, Jikke Wierikx, Danielle Hulsman, Rainer Glass, Massimo Squatrito, Michela Serresi, Gaetano Gargiulo
Journal: Cancer Research (2020)

Abstract Glioblastoma is a lethal brain tumor with a high degree of heterogeneity and resistance to therapy. The lack of genetic tracing approaches to selectively identify tumor states and fate transitions limited our understanding of tumor homeostasis. By translating glioblastoma subtype signatures into synthetic genetic tracing cassettes, we investigated tumor heterogeneity at cellular and molecular level, in vitro and in vivo. Synthetic genetic tracing demonstrated that proneural glioblastoma is a hardwired identity, whereas the mesenchymal glioblastoma is an adaptive and metastable state downstream pro-inflammatory and differentiation cues, similarly wired in breast and lung tumors. Importantly, we discovered that innate immune cells divert glioblastoma cells into a proneural-to-mesenchymal transition causal to therapeutic resistance. Systematic phenotypic mapping using synthetic locus control regions (sLCRs) is a simple, automated, and scalable strategy for genetic tracing, generally applicable to study developmental and disease homeostasis. In glioblastoma, it uncovered causality between various (micro)environmental, genetic and pharmacological perturbations and mesenchymal commitment. Citation Format: Matthias Jürgen Schmitt, Carlos Company, Yuliia Dramaretska, Iros Barozzi, Andreas Göhrig, Sonia Kertalli, Melanie Großmann, Heike Naumann, Jikke Wierikx, Danielle Hulsman, Rainer Glass, Massimo Squatrito, Michela Serresi, Gaetano Gargiulo. Phenotypic mapping of pathological crosstalk between glioblastoma and innate immune cells by synthetic genetic tracing [abstract]. In: Proceedings of the AACR Virtual Special Conference on Tumor Heterogeneity: From Single Cells to Clinical Impact; 2020 Sep 17-18. Philadelphia (PA): AACR; Cancer Res 2020;80(21 Suppl):Abstract nr PO-104.