TY - JOUR
AU - Wierzbinska, Justyna Anna
AU - Toth, Reka
AU - Ishaque, Naveed
AU - Rippe, Karsten
AU - Mallm, Jan-Philipp
AU - Klett, Lara C
AU - Mertens, Daniel
AU - Zenz, Thorsten
AU - Hielscher, Thomas
AU - Seifert, Marc
AU - Küppers, Ralf
AU - Assenov, Yassen
AU - Lutsik, Pavlo
AU - Stilgenbauer, Stephan
AU - Roessner, Philipp M
AU - Seiffert, Martina
AU - Byrd, John
AU - Oakes, Christopher C
AU - Plass, Christoph
AU - Lipka, Daniel
TI - Methylome-based cell-of-origin modeling (Methyl-COOM) identifies aberrant expression of immune regulatory molecules in CLL.
JO - Genome medicine
VL - 12
IS - 1
SN - 1756-994X
CY - London
PB - BioMed Central
M1 - DKFZ-2020-00629
SP - 29
PY - 2020
N1 - Modyfied by adding this comment for testin purposes#EA:B340#LA:B340#
AB - In cancer, normal epigenetic patterns are disturbed and contribute to gene expression changes, disease onset, and progression. The cancer epigenome is composed of the epigenetic patterns present in the tumor-initiating cell at the time of transformation, and the tumor-specific epigenetic alterations that are acquired during tumor initiation and progression. The precise dissection of these two components of the tumor epigenome will facilitate a better understanding of the biological mechanisms underlying malignant transformation. Chronic lymphocytic leukemia (CLL) originates from differentiating B cells, which undergo extensive epigenetic programming. This poses the challenge to precisely determine the epigenomic ground state of the cell-of-origin in order to identify CLL-specific epigenetic aberrations.We developed a linear regression model, methylome-based cell-of-origin modeling (Methyl-COOM), to map the cell-of-origin for individual CLL patients based on the continuum of epigenomic changes during normal B cell differentiation.Methyl-COOM accurately maps the cell-of-origin of CLL and identifies CLL-specific aberrant DNA methylation events that are not confounded by physiologic epigenetic B cell programming. Furthermore, Methyl-COOM unmasks abnormal action of transcription factors, altered super-enhancer activities, and aberrant transcript expression in CLL. Among the aberrantly regulated transcripts were many genes that have previously been implicated in T cell biology. Flow cytometry analysis of these markers confirmed their aberrant expression on malignant B cells at the protein level.Methyl-COOM analysis of CLL identified disease-specific aberrant gene regulation. The aberrantly expressed genes identified in this study might play a role in immune-evasion in CLL and might serve as novel targets for immunotherapy approaches. In summary, we propose a novel framework for in silico modeling of reference DNA methylomes and for the identification of cancer-specific epigenetic changes, a concept that can be broadly applied to other human malignancies.
LB - PUB:(DE-HGF)16
C6 - pmid:32188505
DO - DOI:10.1186/s13073-020-00724-7
UR - https://inrepo02.dkfz.de/record/154170
ER -