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PiggyBac transposon tools for recessive screening identify B-cell lymphoma drivers in mice
J. Weber, J. de la Rosa, CS. Grove, M. Schick, L. Rad, O. Baranov, A. Strong, A. Pfaus, MJ. Friedrich, T. Engleitner, R. Lersch, R. Öllinger, M. Grau, IG. Menendez, M. Martella, U. Kohlhofer, R. Banerjee, MA. Turchaninova, A. Scherger, GJ....
Jazyk angličtina Země Anglie, Velká Británie
Typ dokumentu časopisecké články, práce podpořená grantem
Perzistentní odkaz
https://www.medvik.cz/link/bmc19027682
Online
Plný text
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- MeSH
- B-buněčný lymfom genetika patologie MeSH
- buněčné klony MeSH
- CRISPR-Cas systémy genetika MeSH
- genetické asociační studie MeSH
- genetické testování metody MeSH
- genová dávka MeSH
- geny nádorové MeSH
- lidé MeSH
- myši inbrední C57BL MeSH
- myši transgenní MeSH
- receptory antigenů B-buněk metabolismus MeSH
- regulace genové exprese u nádorů MeSH
- reprodukovatelnost výsledků MeSH
- transpozibilní elementy DNA genetika MeSH
- tumor supresorové geny MeSH
- ztráta heterozygozity MeSH
- zvířata MeSH
- Check Tag
- lidé MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
B-cell lymphoma (BCL) is the most common hematologic malignancy. While sequencing studies gave insights into BCL genetics, identification of non-mutated cancer genes remains challenging. Here, we describe PiggyBac transposon tools and mouse models for recessive screening and show their application to study clonal B-cell lymphomagenesis. In a genome-wide screen, we discover BCL genes related to diverse molecular processes, including signaling, transcriptional regulation, chromatin regulation, or RNA metabolism. Cross-species analyses show the efficiency of the screen to pinpoint human cancer drivers altered by non-genetic mechanisms, including clinically relevant genes dysregulated epigenetically, transcriptionally, or post-transcriptionally in human BCL. We also describe a CRISPR/Cas9-based in vivo platform for BCL functional genomics, and validate discovered genes, such as Rfx7, a transcription factor, and Phip, a chromatin regulator, which suppress lymphomagenesis in mice. Our study gives comprehensive insights into the molecular landscapes of BCL and underlines the power of genome-scale screening to inform biology.
Center for Translational Cancer Research Heidelberg 69120 Germany
Comparative Experimental Pathology Technische Universität München Munich 81675 Germany
Divison of Chronic Inflammation and Cancer German Cancer Research Center Heidelberg 69120 Germany
Helmholtz Zentrum München Research Unit Gene Vectors Munich 81377 Germany
Helmholtz Zentrum München Research Unit Radiation Cytogenetics Neuherberg 85764 Germany
Instituto de Medicina Oncológica y Molecular de Asturias Universidad de Oviedo Oviedo 33006 Spain
The Wellcome Trust Sanger Institute Genome Campus Hinxton Cambridge CB10 1SA UK
Citace poskytuje Crossref.org
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