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Long-term Aspirin Use and Epigenetic Mitotic Clocks for Cancer Risk Prediction: Findings in Healthy Colon Mucosa and Recommendations for Future Epigenetic Aging Studies

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Epigenetics communications 2021年第1期1卷 5-5页

作者： Jamaji C Nwanaji-Enwerem Chijioke Nze Andres Cardenas Department of Environmental Health Harvard T.H. Chan School of Public Health and MD/PhD Program Harvard Medical School Boston MA USA. Division of Environmental Health Sciences School of Public Health and Center for Computational Biology University of California Berkeley Berkeley CA USA. The University of Texas MD Anderson Cancer Center Houston TX USA.

Background:Despite the known role of mitosis in colorectal cancer, previous associations of long-term aspirin use with suppressed cancer-related epigenetic aging did not involve epigenetic mitotic clocks. We investigated these relationships using three epigenetic mitotic clocks developed for cancer risk prediction: EpiTOC, EpiTOC2, and MiAge. We utilized publicly available HumanMethylationEPIC BeadChip data from 112 healthy colon (proximal and distal) mucosal samples taken at baseline (T1) and at 10-years follow-up (T2) from a screening cohort of 28 Polish women (11 non-users and 17 long-term [≥ 2 years] aspirin users). Mitotic clock values were divided by chronological age at each timepoint to obtain intrinsic rates (IRs). We evaluated differences in residuals of the mitotic clock IRs taken from linear mixed effects models adjusted for BMI, polyp status, and DNA methylation batch. Findings:EpiTOC, EpiTOC2 and MiAge were significantly correlated with chronological age ( < 0.05) with correlations ranging from 0.41 to 0.63. The EpiTOC, EpiTOC2 and MiAge clocks were strongly correlated with each other in proximal and distal samples (r > 0.79, < 0.0001). We observed proximal within group median clock IR deceleration for EpiTOC (-0.0004 DNAm, = 0.008), EpiTOC2 (-16 cell divisions, = 0.009), and MiAge (-3 cell divisions, = 0.002) for long-term aspirin users from T1 to T2 but not for non-users. In distal samples, only the long-term user MiAge IR was significantly deaccelerated (-3 cell divisions, = 0.009). Conclusions:Our observed findings support previously reported longitudinal associations of aspirin use with deceleration of other epigenetic age measures in the proximal colon. Our mitotic clock results suggest that cell proliferation could play a role in some aspirin relationships with epigenetic aging. Furthermore, the findings provide added impetus for establishing gold standards for epigenetic aging and consensus guidelines for more comprehensive reporting in fu

关键词： Colorectal cancer DNA methylation Disparities EpiTOC2 Epigenetic age MiAge Mitotic clock

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Machine learning for early prediction of circulatory failure in the intensive care unit

arXiv

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arXiv 2019年

作者： Hyland, Stephanie L. Faltys, Martin Hüser, Matthias Lyu, Xinrui Gumbsch, Thomas Esteban, Cristóbal Bock, Christian Horn, Max Moor, Michael Rieck, Bastian Zimmermann, Marc Bodenham, Dean Borgwardt, Karsten Rätsch, Gunnar Merz, Tobias M. Department of Computer Science ETH Zürich Zürich Switzerland Computational Biology Program Memorial Sloan Kettering Cancer Center New York United States Tri-Institutional PhD Program in Computational Biology and Medicine Weill Cornell Medicine New York United States Medical Informatics Group Zürich University Hospital Zürich Switzerland Department of Intensive Care Medicine University Hospital University of Bern Bern Switzerland Department of Biosystems and Engineering ETH Zürich Basel Switzerland Department of Biology ETH Zürich Zürich Switzerland Swiss Institute for Bioinformatics Lausanne Switzerland Cardiovascular Intensive Care Unit Auckland City Hospital Auckland New Zealand

Intensive care clinicians are presented with large quantities of patient information and measurements from a multitude of monitoring systems. The limited ability of humans to process such complex information hinders physicians to readily recognize and act on early signs of patient deterioration. We used machine learning to develop an early warning system for circulatory failure based on a high-resolution ICU database with 240 patient-years of data. This automatic system predicts 90.0% of circulatory failure events (prevalence 3.1%), with 81.8% identified more than two hours in advance, resulting in an area under the receiver operating characteristic curve of 94.0% and area under the precision recall curve of 63.0%. The model was externally validated in a large independent patient cohort. Copyright © 2019, The Authors. All rights reserved.

关键词： Intensive care units

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Author Correction: Multiplexed CRISPR-based microfluidic platform for clinical testing of respiratory viruses and identification of SARS-CoV-2 variants

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Nature medicine 2024年第1期30卷 307页

作者： Nicole L Welch Meilin Zhu Catherine Hua Juliane Weller Marzieh Ezzaty Mirhashemi Tien G Nguyen Sreekar Mantena Matthew R Bauer Bennett M Shaw Cheri M Ackerman Sri Gowtham Thakku Megan W Tse Jared Kehe Marie-Martine Uwera Jacqueline S Eversley Derek A Bielwaski Graham McGrath Joseph Braidt Jeremy Johnson Felecia Cerrato Gage K Moreno Lydia A Krasilnikova Brittany A Petros Gabrielle L Gionet Ewa King Richard C Huard Samantha K Jalbert Michael L Cleary Nicholas A Fitzgerald Stacey B Gabriel Glen R Gallagher Sandra C Smole Lawrence C Madoff Catherine M Brown Matthew W Keller Malania M Wilson Marie K Kirby John R Barnes Daniel J Park Katherine J Siddle Christian T Happi Deborah T Hung Michael Springer Bronwyn L MacInnis Jacob E Lemieux Eric Rosenberg John A Branda Paul C Blainey Pardis C Sabeti Cameron Myhrvold Broad Institute of MIT and Harvard Cambridge MA USA. nicole_welch@g.harvard.edu. Harvard Program in Virology Division of Medical Sciences Harvard Medical School Boston MA USA. nicole_welch@g.harvard.edu. Broad Institute of MIT and Harvard Cambridge MA USA. Department of Biological Engineering Massachusetts Institute of Technology Cambridge MA USA. Division of Infectious Diseases Department of Medicine Massachusetts General Hospital Boston MA USA. Wellcome Sanger Institute Wellcome Genome Campus Hinxton UK. Harvard Program in Biological and Biomedical Sciences Harvard Medical School Boston MA USA. Division of Health Sciences and Technology Harvard Medical School and Massachusetts Institute of Technology Cambridge MA USA. Department of Organismic and Evolutionary Biology Harvard University Cambridge MA USA. Harvard/Massachusetts Institute of Technology MD-PhD Program Harvard Medical School Boston MA USA. Department of Systems Biology Harvard Medical School Boston MA USA. State Health Laboratories Rhode Island Department of Health Providence RI USA. Massachusetts Department of Public Health Boston MA USA. Influenza Division National Center for Immunization and Respiratory Diseases Centers for Disease Control and Prevention Atlanta GA USA. African Centre of Excellence for Genomics of Infectious Diseases Redeemer's University Ede Nigeria. Department of Biological Sciences College of Natural Sciences Redeemer's University Ede Nigeria. Molecular Biology Department and Center for Computational and Integrative Biology Massachusetts General Hospital Boston MA USA. Department of Immunology and Infectious Disease Harvard T.H. Chan School of Public Health Harvard University Boston MA USA. Department of Pathology Massachusetts General Hospital and Harvard Medical School Boston MA USA. Koch Institute for Integrative Cancer Research at Massachusetts Institute of Technology Cambridge MA USA. Broad Institute of MIT and Harvard Cambridge MA USA. pardis

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Patterns of somatic structural variation in human cancer genomes (vol 578, pg 112, 2020)

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NATURE 2023年第7948期614卷 E38-E38页

作者： Li, Yilong Roberts, Nicola D. Wala, Jeremiah A. Shapira, Ofer Schumacher, Steven E. Kumar, Kiran Khurana, Ekta Waszak, Sebastian Korbel, Jan O. Haber, James E. Imielinski, Marcin Weischenfeldt, Joachim Beroukhim, Rameen Campbell, Peter J. Cancer Genome Project Wellcome Trust Sanger Institute Hinxton UK Totient Inc Cambridge MA USA Wellcome Sanger Institute Wellcome Genome Campus Hinxton UK Department of Haematology University of Cambridge Cambridge UK Cambridge University Hospitals NHS Foundation Trust Cambridge UK Korea Advanced Institute of Science and Technology Daejeon South Korea Department of Zoology Genetics and Physical Anthropology University of Santiago de Compostela Santiago de Compostela Spain Centre for Research in Molecular Medicine and Chronic Diseases (CIMUS) University of Santiago de Compostela Santiago de Compostela Spain The Biomedical Research Centre (CINBIO) University of Vigo Vigo Spain Centre for Research in Molecular Medicine and Chronic Diseases (CiMUS) Universidade de Santiago de Compostela Santiago de Compostela Spain Department of Zoology Genetics and Physical Anthropology (CiMUS) Universidade de Santiago de Compostela Santiago de Compostela Spain The Biomedical Research Centre (CINBIO) Universidade de Vigo Vigo Spain The Broad Institute of Harvard and MIT Cambridge MA USA Bioinformatics and Integrative Genomics Harvard University Cambridge MA USA Department of Cancer Biology Dana-Farber Cancer Institute Boston MA USA Broad Institute of MIT and Harvard Cambridge MA USA Department of Medical Oncology Dana-Farber Cancer Institute Boston MA USA Harvard Medical School Boston MA USA Massachusetts General Hospital Center for Cancer Research Charlestown MA USA Dana-Farber Cancer Institute Boston MA USA Department of Biostatistics and Computational Biology Dana-Farber Cancer Institute and Harvard Medical School Boston MA USA Weill Cornell Medical College New York NY USA Department of Physiology and Biophysics Weill Cornell Medicine New York NY USA Institute for Computational Biomedicine Weill Cornell Medicine New York NY USA Controlled Department and Institution New York NY USA Englander Institute for Precision Medicine Weill Cornell Medicine Ne

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TET proteins safeguard bivalent promoters from de novo methylation in human embryonic stem cells (vol 50, pg 83, 2017)

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NATURE GENETICS 2018年第5期50卷 764-764页

作者： Verma, Nipun Pan, Heng Dore, Louis C. Shukla, Abhijit Li, Qing V. Pelham-Webb, Bobbie Teijeiro, Virginia Gonzalez, Federico Krivtsov, Andrei Chang, Chan-Jung Papapetrou, Eirini P. He, Chuan Elemento, Olivier Huangfu, Danwei Developmental Biology Program Sloan Kettering Institute New York NY USA Weill Graduate School of Medical Sciences at Cornell University/The Rockefeller University/Sloan Kettering Institute Tri-Institutional MD-PhD Program New York NY USA Department of Physiology and Biophysics Englander Institute for Precision Medicine Institute for Computational Biomedicine Weill Cornell Medical College New York NY USA Weill Cornell Graduate School of Medical Sciences Weill Cornell Medical College New York NY USA Department of Chemistry Department of Biochemistry and Molecular Biology Institute for Biophysical Dynamics Howard Hughes Medical Institute University of Chicago Chicago IL USA Louis V. Gerstner Jr. Graduate School of Biomedical Sciences Memorial Sloan Kettering Cancer Center New York NY USA Cancer Biology and Genetics Program Sloan Kettering Institute New York NY USA Department of Oncological Sciences and Black Family Stem Cell Institute Icahn School of Medicine at Mount Sinai New York NY USA

TET enzymes oxidize 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC), which can lead to DNA demethylation. However, direct connections between TET-mediated DNA demethylation and transcriptional output are difficult to establish owing to challenges in distinguishing global versus locus-specific effects. Here we show that TET1, TET2 and TET3 triple-knockout (TKO) human embryonic stem cells (hESCs) exhibit prominent bivalent promoter hypermethylation without an overall corresponding decrease in gene expression in the undifferentiated state. Focusing on the bivalent PAX6 locus, we find that increased DNMT3B binding is associated with promoter hypermethylation, which precipitates a neural differentiation defect and failure of PAX6 induction during differentiation. dCas9-mediated locus-specific demethylation and global inactivation of DNMT3B in TKO hESCs partially reverses the hypermethylation at the PAX6 promoter and improves differentiation to neuroectoderm. Taking these findings together with further genome-wide methylation and TET1 and DNMT3B ChIP-seq analyses, we conclude that TET proteins safeguard bivalent promoters from de novo methylation to ensure robust lineage-specific transcription upon differentiation.

关键词： Epigenetics Stem cells

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Author Correction: Low-intensity pulsed ultrasound stimulation (LIPUS) modulates microglial activation following intracortical microelectrode implantation

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Nature communications 2024年第1期15卷 7618页

作者： Fan Li Jazlyn Gallego Natasha N Tirko Jenna Greaser Derek Bashe Rudra Patel Eric Shaker Grace E Van Valkenburg Alanoud S Alsubhi Steven Wellman Vanshika Singh Camila Garcia Padilla Kyle W Gheres John I Broussard Roger Bagwell Maureen Mulvihill Takashi D Y Kozai Department of Bioengineering University of Pittsburgh Pittsburgh PA USA. Center for Neural Basis of Cognition Pittsburgh PA USA. Computational Modeling and Simulation PhD Program University of Pittsburgh Pittsburgh PA USA. Department of Biochemistry and Molecular Biology Pennsylvania State University University Park PA USA. Actuated Medical Bellefonte PA USA. Washington University in St. Louis St. Louis MO USA. Department of Neuroscience University of Pittsburgh Pittsburgh PA USA. Columbia University New York NY USA. Department of Bioengineering University of Pittsburgh Pittsburgh PA USA. TK.Kozai@pitt.edu. Center for Neural Basis of Cognition Pittsburgh PA USA. TK.Kozai@pitt.edu. Center for Neuroscience University of Pittsburgh Pittsburgh PA USA. TK.Kozai@pitt.edu. McGowan Institute of Regenerative Medicine University of Pittsburgh Pittsburgh PA USA. TK.Kozai@pitt.edu. NeuroTech Center University of Pittsburgh Brain Institute Pittsburgh PA USA. TK.Kozai@pitt.edu.

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The anatomic determinants of conductive hearing loss secondary to tympanic membrane perforation

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Journal of Otology 2017年第3期12卷 125-131页

作者： David J.Carpenter Debara L.Tucci David M.Kaylie Dennis O.Frank-Ito Division of Head and Neck Surgery & Communication Sciences Department of Surgery Duke University Medical Center Durham NC USA Computational Biology & Bioinformatics PhD Program Duke University Durham NC USA Department of Mechanical Engineering and Materials Science Duke University Durham NC USA

Objectives: Recent studies have introduced middle ear volume(MEV) as a novel determinant of perforation-induced conductive hearing loss(CHL) in a mechanism driven by trans-tympanic membrane pressure differences. The primary aims of this preliminary report are to: 1) correlate CHL with perforation size; 2) describe the relationship between CHL and MEV; and 3) compare CHL across a range of cholesteatoma ***: A retrospective pilot study was performed in 31 subjects with audiometry indicative of conductive hearing loss, temporal bone CT scans,and no prior middle ear surgery. Perforation size and MEV were analyzed with respect to CHL in a cohort of 10 perforated ears with no cholesteatoma. CHLs were compared in 3 groups defined by extent of cholesteatoma ***: Ears with large and small perforations showed mean ABG values of 32.0 ± 15.7 dB and 16.0 ± 16.4 dB, respectively. A direct relationship was observed between MEV and CHL for ears with large perforations across all frequencies, whereas this relationship for small perforations was frequency-dependent. Finally, a statistically significant increase in CHL was found across ears with increasing cholesteatoma involvement at 1000 Hz(X^2(2) = 9.786, p = 0.008),2000 Hz(x^2(2) = 8.455, p = 0.015),and 4000 Hz(x^2(2)= 8.253, p = 0.016).Conclusions: These pilot data suggest that greater perforation-induced conductive hearing losses may be associated with larger perforation sizes and cholesteatoma. The correlation between MEV and CHL may require additional study.

关键词： Perforation-induced hearing loss Conductive hearing loss Middle ear volume Three-dimensional volume reconstruction

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Disagreement in middle ear volume estimation between tympanometry and three-dimensional volume reconstruction in the context of tympanic membrane perforation

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Journal of Otology 2017年第2期12卷 74-79页

作者： David J.Carpenter Debara L.Tucci David M.Kaylie Dennis O.Frank-Ito Division of Head and Neck Surgery&Communication Sciences Department of SurgeryDuke University Medical CenterDurhamNCUSA Computational Biology&Bioinformatics PhD Program Duke UniversityDurhamNCUSA Department of Mechanical Engineering and Materials Science Duke UniversityDurhamNCUSA

Introduction: Middle ear volume(MEV) is a clinically relevant parameter across middle ear diseases. MEV values between these techniques have never before been tested for agreement in ears with perforated tympanic membranes(TMs).Methods: Middle ears were identified from 36 patients ranging 18-89 years of age with TM perforations who underwent tympanometry and temporal bone computed tomography(CT) between 2005 and 2015. MEVs calculated by both tympanometry and three-dimensional volume reconstruction(3DVR) were analyzed for agreement using Bland Altman plots. The differences between tympanometric and 3DVR MEV values for each given middle ear were characterized across MEV quartiles(1= smallest; 4= largest) and across increasing states of middle ear disease using Kruskale Wallis and Wilcoxon testing with Bonferroni ***: Bland Altman plots demonstrated significant disagreement between MEV measurement techniques. Differences between tympanometric(T) and 3DVR MEV values were significantly greater with increasing average(i.e.(Tt3DVR)/2)) MEV per linear regression(p < 0.0001). Significance was demonstrated between fourth and first average MEV quartiles(p= 0.0024), fourth and second quartiles(p= 0.0024), third and first quartiles(p= 0.0048), and third and second quartiles(p= 0.048). Absolute MEV difference was not significantly different across varying states of middle ear disease(p= 0.44).Conclusion: Statistically and clinically significant disagreement was demonstrated between tympanometric and 3DVR MEV values. Studies that vary in MEV estimation techniques may be expected to demonstrate significantly different results. These preliminary results suggest that clinicians should endeavor to seek further confirmation when interpreting high tympanometric MEV values.

关键词： Middle ear volume Tympanometry Three-dimensional volume reconstruction Tympanic membrane perforation

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The evolutionary history of 2,658 cancers (vol 578, pg 122, 2020)

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NATURE 2023年第7948期614卷 E42-E42页

作者： Gerstung, Moritz Jolly, Clemency Leshchiner, Ignaty Dentro, Stefan C. Gonzalez, Santiago Rosebrock, Daniel Mitchell, Thomas J. Rubanova, Yulia Anur, Pavana Yu, Kaixian Tarabichi, Maxime Deshwar, Amit Wintersinger, Jeff Kleinheinz, Kortine Vazquez-Garcia, Ignacio Haase, Kerstin Jerman, Lara Sengupta, Subhajit Macintyre, Geoff Malikic, Salem Donmez, Nilgun Livitz, Dimitri G. Cmero, Marek Demeulemeester, Jonas Schumacher, Steven Fan, Yu Yao, Xiaotong Lee, Juhee Schlesner, Matthias Boutros, Paul C. Bowtell, David D. Zhu, Hongtu Getz, Gad Imielinski, Marcin Beroukhim, Rameen Sahinalp, S. Cenk Ji, Yuan Peifer, Martin Markowetz, Florian Mustonen, Ville Yuan, Ke Wang, Wenyi Morris, Quaid D. Spellman, Paul T. Wedge, David C. Van Loo, Peter European Molecular Biology Laboratory European Bioinformatics Institute (EMBL-EBI) Cambridge UK European Molecular Biology Laboratory Genome Biology Unit Heidelberg Germany Wellcome Sanger Institute Cambridge UK Genome Biology Unit European Molecular Biology Laboratory (EMBL) Heidelberg Germany University of Ljubljana Ljubljana Slovenia The Francis Crick Institute London UK Big Data Institute University of Oxford Oxford UK Wellcome Sanger Institute Wellcome Genome Campus Hinxton UK Big Data Institute Li Ka Shing Centre University of Oxford Oxford UK University of Cambridge Cambridge UK Cambridge University Hospitals NHS Foundation Trust Cambridge UK Department of Applied Mathematics and Theoretical Physics Centre for Mathematical Sciences University of Cambridge Cambridge UK Department of Epidemiology and Biostatistics Memorial Sloan Kettering Cancer Center New York NY USA Department of Statistics Columbia University New York NY USA Department of Haematology University of Cambridge Cambridge UK University of Leuven Leuven Belgium Broad Institute of MIT and Harvard Cambridge MA USA Center for Cancer Research Massachusetts General Hospital Charlestown MA USA Department of Pathology Massachusetts General Hospital Boston MA USA Harvard Medical School Boston MA USA Center for Cancer Research Massachusetts General Hospital Boston MA USA Dana-Farber Cancer Institute Boston MA USA Department of Medical Oncology Dana-Farber Cancer Institute Boston MA USA Department of Cancer Biology Dana-Farber Cancer Institute Boston MA USA Oxford NIHR Biomedical Research Centre Oxford UK Oxford NIHR Biomedical Research Centre University of Oxford Oxford UK University of Toronto Toronto Ontario Canada Vector Institute Toronto Ontario Canada Vector Institute Toronto ON Canada Department of Computer Science University of Toronto Toronto ON Canada Ontario Institute for Cancer Research Toronto Ontario Canada University of California Los Angeles

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Author Correction: Genomic footprints of activated telomere maintenance mechanisms in cancer (Dec, 10.1038/s41467-019-13824-9, 2022)

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NATURE COMMUNICATIONS 2022年第1期13卷 1-1页

作者： Sieverling, Lina Hong, Chen Koser, Sandra D. Ginsbach, Philip Kleinheinz, Kortine Hutter, Barbara Braun, Delia M. Cortes-Ciriano, Isidro Xi, Ruibin Kabbe, Rolf Park, Peter J. Eils, Roland Schlesner, Matthias Brors, Benedikt Rippe, Karsten Jones, David T. W. Feuerbach, Lars Division of Applied Bioinformatics German Cancer Research Center (DKFZ) 69120 Heidelberg Germany Faculty of Biosciences Heidelberg University 69120 Heidelberg Germany Division of Applied Bioinformatics German Cancer Research Center (DKFZ) Heidelberg Germany Faculty of Biosciences Heidelberg University Heidelberg Germany Division of Theoretical Bioinformatics German Cancer Research Center (DKFZ) 69120 Heidelberg Germany Department for Bioinformatics and Functional Genomics Institute for Pharmacy and Molecular Biotechnology (IPMB) and BioQuant 69120 Heidelberg Germany Division of Theoretical Bioinformatics German Cancer Research Center (DKFZ) Heidelberg Germany Institute of Pharmacy and Molecular Biotechnology and BioQuant Heidelberg University Heidelberg Germany German Cancer Consortium (DKTK) Heidelberg Germany National Center for Tumor Diseases (NCT) Heidelberg Heidelberg Germany Heidelberg Center for Personalized Oncology (DKFZ-HIPO) German Cancer Research Center (DKFZ) Heidelberg Germany German Cancer Consortium (DKTK) German Cancer Research Center (DKFZ) Heidelberg Germany Division of Chromatin Networks German Cancer Research Center (DKFZ) and BioQuant 69120 Heidelberg Germany Department of Biomedical Informatics Harvard Medical School Boston Massachusetts 02115 USA Department of Chemistry Centre for Molecular Science Informatics University of Cambridge Cambridge CB2 1EW UK Ludwig Center at Harvard Medical School Boston Massachusetts 02115 USA Department of Biomedical Informatics Harvard Medical School Boston MA USA Department of Chemistry Centre for Molecular Science Informatics University of Cambridge Cambridge UK Ludwig Center at Harvard Medical School Boston MA USA School of Mathematical Sciences and Center for Statistical Science Peking University Beijing 100871 China Heidelberg University Heidelberg Germany New BIH Digital Health Center Berlin Institute of Health (BIH) and Charité - Universitätsmedizin Berlin Berlin Germany Bioi

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