tbuckley/cabot-search huggingface dataset:
Combination studies of Trifluorothymidine with Oxaliplatin in colon cancer cell lines
Authors: Olaf H. Temmink, Henk-Jan Prins, Jennette A. Sakoff, Stephen P. Ackland, Masakazu Fukushima, Godefridus J. Peters
Journal: Cancer Research (2005)

4941  Trifluorothymidine (TFT) is part of the formulation TAS-102 which currently undergoes clinical trials and also contains the thymidine phosphorylase inhibitor TPI. TFT is activated by thymidine kinase to TFT-MP which inhibits thymidylate synthase (TS) leading to dTTP depletion in the cell causing dUTP (and also TFT-TP) to be misincorporated into DNA, resulting in DNA damage and possibly cell death. This may enhance the effect of DNA damaging agents, such as oxaliplatin (OHP). We studied the effect of TFT on OHP induced cytotoxicity in colon cancer cells, using growth inhibition experiments in which TFT was combined with OHP in different combination schedules. A panel of 5 colon cancer cell lines (H630, WiDr, Colo320, SNU-C4, SW1116) was used for the experiments. To evaluate the effects multiple drug effect analysis was performed using Calcusyn software and expressed as mutually nonexclusive combination index (CI): synergism, CI 1.1. For H630, WiDr and SW1116 we also investigated whether there was an increase in DNA damage induction, Pt-DNA adduct formation and/or cell cycle delay when the drugs were combined. The effect of the combinations of TFT-OHP showed synergism in all cell lines when the drugs were combined simultaneously (0.4   10%). Exposure to [IC75] of TFT or OHP for 48 hr induced a clear cell cycle S-phase arrest, although dose-schedule and cell line-dependent. More decrease in G1-population was observed after TFT exposure compared to OHP alone. After exposure to TFT-OHP at their [IC75]s a stronger S-phase arrest was seen, for all cell lines (> 6.2%), but was hardly influenced by a 4 hr TFT pre-incubation period. We currently determine basal protein levels of DNA repair enzymes to be evaluated in relation to DNA damage that was induced in these cell lines. In conclusion, the combination of TFT with the DNA synthesis inhibitor OHP can induce synergistic effects when the drugs are given simultaneously and that DNA damage induction by OHP can be enhanced when combined with TFT but is dependent on the dose-schedule used.
Molecular Characterization of Clinical Response and Relapse in Patients with IDH1-Mutant Newly Diagnosed Acute Myeloid Leukemia Treated with Ivosidenib and Azacitidine
Authors: Scott R. Daigle, Sung Choe, Courtney D. DiNardo, Anthony S. Stein, Eytan M. Stein, Amir T. Fathi, Olga Frankfurt, Andre C. Schuh, Hartmut Döhner, Giovanni Martinelli, Prapti A. Patel, Emmanuel Raffoux, Peter Tan, Amer M. Zeidan, Stephane De Botton, Richard M. Stone, Mark Frattini, Aleksandra Franovic, Emily Xu, Thomas Winkler, Bin Wu, Paresh Vyas
Journal: Blood (2020)
Single-Cell Multi-Omics Reveals Distinct Paths to Survival of Admixed BTKC481 Mutant Vs. Wild-Type Cells in Clinically Progressing Chronic Lymphocytic Leukemia
Authors: Andrew Lipsky, Danny Luan, Shirley Chen, Ronan Chaligne, Neville Dusaj, Erica B Bhavsar, Chelston Ang, Anna S Nam, Federico Gaiti, Paulina Chamely, Nathaniel D. Omans, Preeti Trisal, Anita K Gandhi, Kyu-Tae Kim, Rafael Schulman, Joshua S. Schiffman, Franco Izzo, Gregory Mullokandov, Chingiz Underbayev, Adrian Wiestner, John N. Allan, Richard R. Furman, Dan A. Landau
Journal: Blood (2020)
Rates of Thrombotic Events in Hypereosinophilic Syndrome and the Effect of Molecular Aberrations in Thrombotic Risk
Authors: Orly Leiva, Olesya Baker, Andrew M. Brunner, Hanny Al-Samkari, Rebecca Karp Leaf, Rachel P. Rosovsky, Amir T. Fathi, James I Weitzman, Larissa Bornikova, Valentina Nardi, Gabriela S. Hobbs
Journal: Blood (2020)
Zeb1 modulates hematopoietic stem cell fates required for suppressing acute myeloid leukemia
Authors: Alhomidi Almotiri, Hamed Alzahrani, Juan Bautista Menendez-Gonzalez, Ali Abdelfattah, Badi Alotaibi, Lubaid Saleh, Adelle Greene, Mia Georgiou, Alex Gibbs, Amani Alsayari, Sarab Taha, Leigh-anne Thomas, Dhruv Shah, Sarah Edkins, Peter Giles, Marc P. Stemmler, Simone Brabletz, Thomas Brabletz, Ashleigh S. Boyd, Florian A. Siebzehnrubl, Neil P. Rodrigues
Journal: Journal of Clinical Investigation (2020)

Zeb1, a zinc finger E-box binding homeobox epithelial-mesenchymal transition (EMT) transcription factor, confers properties of "stemness," such as self-renewal, in cancer. Yet little is known about the function of Zeb1 in adult stem cells. Here, we used the hematopoietic system as a well-established paradigm of stem cell biology to evaluate Zeb1-mediated regulation of adult stem cells. We employed a conditional genetic approach using the Mx1-Cre system to specifically knock out (KO) Zeb1 in adult hematopoietic stem cells (HSCs) and their downstream progeny. Acute genetic deletion of Zeb1 led to rapid-onset thymic atrophy and apoptosis-driven loss of thymocytes and T cells. A profound cell-autonomous self-renewal defect and multilineage differentiation block were observed in Zeb1-KO HSCs. Loss of Zeb1 in HSCs activated transcriptional programs of deregulated HSC maintenance and multilineage differentiation genes and of cell polarity consisting of cytoskeleton-, lipid metabolism/lipid membrane-, and cell adhesion-related genes. Notably, epithelial cell adhesion molecule (EpCAM) expression was prodigiously upregulated in Zeb1-KO HSCs, which correlated with enhanced cell survival, diminished mitochondrial metabolism, ribosome biogenesis, and differentiation capacity and an activated transcriptomic signature associated with acute myeloid leukemia (AML) signaling. ZEB1 expression was downregulated in AML patients, and Zeb1 KO in the malignant counterparts of HSCs - leukemic stem cells (LSCs) - accelerated MLL-AF9- and Meis1a/Hoxa9-driven AML progression, implicating Zeb1 as a tumor suppressor in AML LSCs. Thus, Zeb1 acts as a transcriptional regulator in hematopoiesis, critically coordinating HSC self-renewal, apoptotic, and multilineage differentiation fates required to suppress leukemic potential in AML.
A Population-Based Study of Chronic Myelomonocytic Leukemia in the United States from 2004-2015
Authors: Gordon Ruan, Caleb J. Smith, Courtney Day, William Harmsen, Abhishek A. Mangaonkar, Hassan B. Alkhateeb, Kebede H. Begna, Aref Al-Kali, Mark Litzow, William J Hogan, Naseema Gangat, Animesh Pardanani, Michelle A Elliott, Ayalew Tefferi, Ronald S. Go, Mrinal M. Patnaik, Mithun Vinod Shah
Journal: Blood (2020)
Health State Utility Valuation in Patients with Triple-Class-Exposed Relapsed and Refractory Multiple Myeloma Treated with the Bcma-Directed CAR T Cell Therapy, Idecabtagene Vicleucel (ide-cel, bb2121): Results from the Karmma Trial
Authors: Michel Delforge, Nina Shah, Paula Rodriguez-Otero, Parameswaran Hari, Julia Braverman, Andrew Trigg, Payal Patel, Liping Huang, Kristen Hege, Sujith Dhanasiri
Journal: Blood (2020)
Abstract PO-038: DCE-MRI of tumor hypoxia in cervical carcinoma and pancreatic ductal adenocarcinoma xenografts
Authors: Jon-Vidar Gaustad, Anette Hauge, Catherine S. Wegner, Lise Mari K. Hansem, Einar K. Rofstad
Journal: Cancer Research (2020)

Abstract Tumor hypoxia is associated with resistance to treatment, aggressive growth, and poor clinical outcome in many cancer types, and is a result of an imbalance between oxygen supply and oxygen consumption. We have previously shown that Ktrans and ve images derived by dynamic contrast-enhanced magnetic resonance imaging (DCE-MRI) reflect blood perfusion and cell density which are important determinants of oxygen supply and oxygen consumption respectively. The purpose of the current study was to investigate whether Ktrans and/or ve images can be used to produce images of tumor hypoxia. Cervical carcinoma and pancreatic ductal adenocarcinoma xenografts were used as models of human cancer, and xenografted tumors were subjected to antiangiogenic treatment or left untreated. Ktrans and ve images were derived from DCE-MRI data by using Tofts standard pharmacokinetic model, and images of tumor hypoxia were produced by applying threshold values to Ktrans and/or ve. Tumor hypoxia was also assessed by immunohistochemistry by using pimonidazole as a hypoxia marker. Ktrans and ve images were highly heterogeneous. Strong correlations were found between hypoxic fractions determined by immunohistochemistry and hypoxic fractions calculated by using Ktrans but not ve images. Importantly, hypoxia images produced by using Ktrans images reflected both naturally occurring and treatment-induced hypoxia. Moreover, hypoxia images produced by combining Ktrans and ve images were not superior to the hypoxia images produced by using only Ktrans images. These observations imply that Ktrans images reflected blood perfusion and oxygen supply, and that the heterogeneity in hypoxia was caused by heterogeneity in oxygen supply rather than heterogeneity in cell density and oxygen consumption in these tumor models. Citation Format: Jon-Vidar Gaustad, Anette Hauge, Catherine S. Wegner, Lise Mari K. Hansem, Einar K. Rofstad. DCE-MRI of tumor hypoxia in cervical carcinoma and pancreatic ductal adenocarcinoma xenografts [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-038.
Clinical Utility of Plasma Cell-Free DNA for Detection and Quantification of Clonal Hematopoiesis
Authors: Fernanda Gutierrez-Rodrigues, Isabel Beerman, Emma M. Groarke, Bhavisha A Patel, Nina Spitofsky, Diego Quinones Raffo, Sachiko Kajigaya, Luigi Ferrucci, Neal S. Young
Journal: Blood (2020)
SAT0008 Bone mass evaluation using quantitative computed tomography in ankylosing spondylitis
Authors: A El Maghraoui, S Chaouir, A Bezza, F Tabache, D Ghafir, V Ohayon, MI Archane
Journal: Annals of the Rheumatic Diseases (2001)

<h3>Background</h3> Osteoporosis (OP) is now a well recognised feature of ankylosing spondylitis (AS). Dual energy x-ray absorptiometry, which is the most routinely used method to assess OP, fails to demonstrate spine OP in patients with late stage disease (syndesmophytes and facet joints ankylosis). Therefore, quantitative computed tomography (QCT) is the only method that can evaluate correctly the spinal OP in patients with advanced spinal changes. <h3>Objectives</h3> To study OP prevalence in AS using QCT and relationship between OP and AS symptomatic and structural severity. <h3>Methods</h3> 27 patients with AS were enrolled prospectively: 24 men (88.8%) and 3 women with mean age of 37.7 ± 9.2 years [17–66] and mean disease duration of 7.6 ± 4.7 years [0.4–19]. The patients were studied clinically, radiologically and by QCT. <h3>Results</h3> OP at the lumbar spine as defined by Z score &lt; -1 was observed in 11 patients (40.7%). Osteoporotic patients were older than normals (42.3 yrs (9.8) vs 34.6 (7.6); p = 0.03) and had more severe disease as showed the significant statistical differences in symptomatic and structural parameters (chest expansion, BASMI, BASRI, and syndesmophyte score). There was a negative significant statistical correlation between Z score and Schöber index, chest expansion, BASMI and radiological indexes (syndesmophytes score, BASRI). <h3>Conclusion</h3> OP is frequent in AS. Patients with AS are more susceptible to develop OP when they have active and severe disease.
Treatment and Outcome of Patients with Follicular Lymphoma Relapsed or Progressed after Frontline Lenalidomide and Rituximab
Authors: Paolo Strati, Felipe Samaniego, Mariana Gallardo, Mansoor Noorani, F. B. B. Hagemeister, Jason R. Westin, Hun Ju Lee, Maria Alma Rodriguez, Sattva S. Neelapu, Jillian R. Gunther, Rashmi Kanagal-Shamanna, Francisco Vega, Nathan H Fowler, Chris R. Flowers, Loretta J. Nastoupil
Journal: Blood (2020)
SAT0050 Osteoarthritis of the fingers. evaluation of a 4 months treatment with diacerein (verboril)
Authors: AE Georgiadis, C Berberidis, I Koulouris, B Tataridis, A Lagoudakis, P Alexiou, E Koutris, B Papadakos, X Rifiotis, E Lyritsis
Journal: Annals of the Rheumatic Diseases (2001)

<h3>Background</h3> Diacerein (Verboril) is a symptomatic slow-acting drug for the treatment of Hip and/or Knee Osteoarthritis (OA). Although Osteoarthritis of the fingers (OAF) is a very common form of OA and according to the epidemiological studies affects the 60% of the population, clinical studies concerning its treatment are very rare. <h3>Objectives</h3> In order to determine if Diacerein has a beneficial effect on the clinical symptoms of OAF, we performed a prospective open multicenter study involving 30 doctors (rheumatologists or orthopaedics) in 5 Greek towns. <h3>Methods</h3> 477 righthand female patients (MA = 57,4 ± 8,9 yrs), suffering from OAF according to ACR criteria, were enrolled in this study. All patients received 100 mg/day of Diacerein for 4 ms and if needed NSAIDs and/or simple analgesics. All patients were evaluated at inclusion and at the end of 4 ms: a) for the presence of inflammatory and/or mechanical pain, b) for the presence and duration of morning stiffness, c) with the functional index of Dreiser d) for the concomitant consumption of analgesics and/or NSAIDs. We have used the t-test and chi-test in our statistical analysis and a probability level of 0,05 was considered to be statistically significant. <h3>Results</h3> 225 patients have completed till now the 4 ms treatment and the analysis of their results showed a statistically significant improovement in clinical data, especially in Dreiser functional index (p &lt; 0,005) and in the presence of inflammatory symptoms (p &lt; 0,001). The concomitant consumption of NSAIDs and/or analgesics was significantly lower at the end of 4 ms (p &lt; 0,05). The overall assessment of therapy was good and very good for the 68% of patients and for the 72% of doctors. The safety profile of the drug was very good throughout the study period. <h3>Conclusion</h3> These data suggest that Diacerein appears to be very useful in the treatment of Osteoarthritis of the fingers. <h3>Reference</h3> Dreiser RL, <i>et al</i>. <i>Rev Rheum</i> 1995;<b>62</b>:129–139S
Abstract PO-085: Mass spectrometry imaging of N-glycans identifies racial discrepancies in human prostate tumors
Authors: Lindsey R. Conroy, Lyndsay E.A. Young, Grant L. Austin, Alexandra E. Stanback, Derek B. Allison, Matthew S. Gentry, Richard R. Drake, Ramon C. Sun
Journal: Cancer Research (2020)

Abstract Prostate cancer is the most commonly diagnosed cancer in men worldwide. A critical knowledge gap in prostate cancer biology is the molecular events underlining higher incidence and mortality rate in Black men. Identifying molecular features that separate racial disparities is a critical step in prostate cancer research that could lead to predictive biomarkers and personalized therapy. N-linked glycosylation is a required co-translational event during protein folding that modulates many biological processes, such as cell adhesion, immune modulation, cell-matrix interactions, and cell proliferation. Recently, aberrant N-linked glycosylation has been reported in prostate cancers. However, the full clinical implications of dysregulated glycosylation in prostate cancer has yet to be explored. Matrix-assisted laser desorption/ionization-mass spectrometry imaging (MALDI-MSI) is a new and innovative technique that combines mass spectrometry with imaging, enabling the detection of glycans with spatial distribution. Herein, we performed MALDI-MSI analysis to characterize the N-glycan profile from tissue microarrays of over 100 patient tumors banked at the University of Kentucky with over 10 years of follow-up data. Additionally, we performed MALDI-MSI analysis on large sections of prostate cancer to define the regional distribution of N-glycans within the tumor microenvironment. We successfully identified 46 unique glycans from readily available formalin-fixed paraffin-embedded prostate tissue, and found significant N-glycan dysregulation between benign and prostate tumor tissue across all patient groups. High mannose as well as tri- and tetra-antennary N-glycans were predominantly found in tumor tissue and correlate with increased tumor grade. Surprisingly, several species of N-glycans were profoundly different between early grade prostate tumors resected from White and Black patients. Further, these glycans predict opposing overall survival between White and Black patients with prostate cancer. These data suggest differential N-linked glycosylation underline the racial disparity of prostate cancer prognosis. Our study highlights the potential clinical applications of MALDI-MSI for digital pathology and biomarker applications, and reveals molecular features that contribute to the racial disparity in diagnosis and survival of prostate cancer patients. Citation Format: Lindsey R. Conroy, Lyndsay E.A. Young, Grant L. Austin, Alexandra E. Stanback, Derek B. Allison, Matthew S. Gentry, Richard R. Drake, Ramon C. Sun. Mass spectrometry imaging of N-glycans identifies racial discrepancies in human prostate tumors [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-085.
Abstract 542: Chronic Doxorubicin Cardiotoxicity Assessed in Engineered Cardiac Tissues Generated in Biowire™ II Platform
Authors: Roozbeh Aschar-sobbi, Julia E Napolitano, Danielle R Bogdanowicz, Michael P Graziano
Journal: Circulation Research (2020)

The anthracycline doxorubicin is an effective anti-tumor agent widely used in both adults and children. One major adverse effect of doxorubicin therapy is dose-dependent cardiotoxicity, ranging from asymptomatic reduction in left ventricular ejection fraction to more serious, potentially fatal symptoms including arrythmias and congestive heart failure. The exact mechanism of doxorubicin-induced cardiotoxicity remains unknown. Recently, human induced pluripotent stem cells (hiPSC) have emerged as a potential tool to model cardiac toxicity, but their fetal-like phenotype raises concerns about the translatability of in vitro data to in vivo cardiotoxicity. To overcome this limitation, Biowire™ II platform was used to generate 3D engineered cardiac tissues (ECTs) from hiPSC-derived cardiomyocytes and human cardiac fibroblasts. Using long-term electrical stimulation, ECTs with a phenotype approaching that of adult human myocardium were obtained. The ECTs were then exposed to 1 μM doxorubicin for 8 days followed by 7 days of washout. Measurements of contractile force amplitude at 1 Hz stimulation showed a transient increase in force within 24 hours of doxorubicin exposure followed by decrease in force after 2 days. Intracellular recordings of action potential (AP) showed a decrease in maximum upstroke velocity (dV/dt), AP amplitude (APA), and resting membrane potential (RMP) after 8 days of doxorubicin treatment. In addition, action potential duration (APD) at 30% (APD30) repolarization was increased in doxorubicin-treated ECTs, whereas APD50 and APD90 were decreased. Following 7 days of washout, no difference in force or AP parameters was found between doxorubicin and vehicle-treated ECTs with the exception of APD50 and APD90 which remained abbreviated. A global untargeted analysis of the conditioned media from doxorubicin-treated ECTs identified 204 analytes and revealed an upregulation of redox homeostasis, differential fatty acid metabolism, altered glycolysis and TCA cycle metabolites, and decreased nucleoside metabolism compared to vehicle-treated ECTs. These results show that doxorubicin not only increases oxidative stress, but also irreversibly affects action potential duration which may predispose to cardiac arrhythmias.
Prospective Pilot Study of Telehealth As Domiciliary Follow-up after Hematopoietic Cell Transplantation during the COVID19 Pandemic
Authors: Alberto Mussetti, Maria Queralt Salas Gay, Maria Condom, Maite Antonio, Cristian Ochoa, Iulia Ivan, David Jiménez Ruiz De La Torre, Gabriela Isabel Sanz-Linares, Belen Ansoleaga, Rocio Parody, Ali Bazarbachi, Anna Sureda Balari
Journal: Blood (2020)
A Multicenter Real-Life Study of Polatuzumab Vedotin Combined with Immunochemotherapy in Patients with R/R DLBCL: Preliminary Data on Efficacy and Safety in Chinese Cohort
Authors: Jianqiu Wu, Yanyan Liu, Li Fei, Zhi-Jun Wuxiao, Fancong Kong, Zhihua Yao, Weilun Zhou, Jifeng Feng
Journal: Blood (2020)
Efficacy and Safety of Voxelotor in Adolescents and Adults with Sickle Cell Disease: HOPE Trial 72-Week Analysis
Authors: Jo Howard, Kenneth I. Ataga, R. Clark Brown, Maureen Achebe, Videlis Nduba, Amal El-Beshlawy, Hoda Hassab, Irene Agodoa, Margaret Tonda, Sarah Gray, Joshua Lehrer-Graiwer, Elliott Vichinsky
Journal: Blood (2020)
Abstract MP152: Smad1 Activation in Infarct Macrophages Restrains Angiogenesis and Accentuates Adverse Remodeling of the Infarcted Myocardium
Authors: Bijun Chen, Ya Su, Nikolaos G Frangogiannis
Journal: Circulation Research (2020)

Macrophages play multiple roles in repair and remodeling of the infarcted heart, contributing to phagocytosis of dead cells, regulation of inflammation, fibrosis and angiogenesis. TGF-β superfamily members are critically involved in regulation of macrophage phenotype through the Smad cascades. In most cell types, TGF-βs signal predominantly by activating Smad2/3 signaling, whereas BMPs act through Smad1/5-mediated pathways. We previously showed that TGF-β/Smad3 signaling in macrophages protects the infarcted heart from adverse remodeling by mediating phagocytotic activity and anti-inflammatory transition. However, the in vivo role of Smad1/5 signaling in macrophages remains unknown. We examined the role of macrophage-specific Smad1 signaling in a mouse model of myocardial infarction (MI). Smad1 is activated in a subset of myeloid cells infiltrating the infarcted myocardium. In vitro, TGF-β1, TGF-β3, BMP4, BMP7, but not TGF-β2, BMP2, BMP6 markedly activated Smad1/5 signaling in macrophages. In order to examine the role of Smad1 in regulation of macrophage phenotype we generated myeloid cell-specific Smad1 KO mice (MyS1KO). MyS1KO mice had better survival compared to S1fl/fl controls 28 days post MI ( p =0.0009, n=26-27). Echocardiographic data showed that MyS1KO mice had reduced left ventricular dilation and attenuated systolic dysfunction 28 days after MI. Although scar size was comparable between groups at the 7 day timepoint, MyS1KO animals had significantly smaller scars 28 days after MI, suggesting improved scar remodeling. MyS1KO mice exhibited increased microvessel density in the infarct, suggesting that Smad1 activation in macrophages may restrain angiogenesis. In order to explore the mechanisms, we isolated infarct macrophages from MyS1KO and S1fl/fl hearts and compared angiogenesis-related protein expression by performing a proteomic array. Smad1 loss in macrophages did not affect VEGF-A expression, but significantly increased levels of the angiogenic chemokine CXCL12. Our findings suggest that Smad1 is directly activated by TGF-βs in macrophages, and that Smad1 activation in infarct macrophages may promote adverse remodeling by restraining angiogenic effects through suppression of angiogenic chemokines.
Ifnα Attenuates the Disease Phenotype and Extends Survival in Mouse Models of MPN
Authors: Harini Nivarthi, Andrea Majoros, Eva Hug, Ruochen Jia, Sarada Achyutuni, Roland Jäger, Raimund Holly, Beatrice Grabner, Felix Rosebrock, Shin-Jye Lee, Chung-Wei Lee, Robert Kralovics
Journal: Blood (2020)
Retrospective Chart Review of Gastrointestinal Bleeding in Patients with Von Willebrand Disease
Authors: Jonathan C. Roberts, Miguel A. Escobar, Suchitra Acharya Acharya, Nina Hwang, Michael Wang, Sarah A Hale, Abiola Oladapo, Sohaib Asghar, Syed Mehdi, Peter A. Kouides
Journal: Blood (2020)
Regulatory effects of noncoding RNAs on the interplay of oxidative stress and autophagy in cancer malignancy and therapy
Authors: Pei-Feng Liu, Ammad Ahmad Farooqi, Sheng-Yao Peng, Tzu-Jung Yu, Hans-Uwe Dahms, Cheng-Hsin Lee, Jen-Yang Tang, Sheng-Chieh Wang, Chih-Wen Shu, Hsueh-Wei Chang
Journal: Seminars in Cancer Biology (2020)