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Loss of PRDM11 promotes MYC-driven lymphomagenesis

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Harvard

Fog, CK, Asmar, F, Côme, C, Jensen, KT, Johansen, JV, Kheir, TB, Jacobsen, LM, Friis, C, Louw, A, Rosgaard, LS, Øbro, NF, Marquart, HV, Anthonsen, K, Braat, AK, van Lohuizen, M, Ralfkiaer, E, Grønbæk, K & Lund, AH 2015, 'Loss of PRDM11 promotes MYC-driven lymphomagenesis' Blood, bind 125, nr. 8, s. 1272-81. https://doi.org/10.1182/blood-2014-03-560805

APA

Fog, C. K., Asmar, F., Côme, C., Jensen, K. T., Johansen, J. V., Kheir, T. B., ... Lund, A. H. (2015). Loss of PRDM11 promotes MYC-driven lymphomagenesis. Blood, 125(8), 1272-81. https://doi.org/10.1182/blood-2014-03-560805

CBE

Fog CK, Asmar F, Côme C, Jensen KT, Johansen JV, Kheir TB, Jacobsen LM, Friis C, Louw A, Rosgaard LS, Øbro NF, Marquart HV, Anthonsen K, Braat AK, van Lohuizen M, Ralfkiaer E, Grønbæk K, Lund AH. 2015. Loss of PRDM11 promotes MYC-driven lymphomagenesis. Blood. 125(8):1272-81. https://doi.org/10.1182/blood-2014-03-560805

MLA

Vancouver

Fog CK, Asmar F, Côme C, Jensen KT, Johansen JV, Kheir TB o.a. Loss of PRDM11 promotes MYC-driven lymphomagenesis. Blood. 2015 feb 19;125(8):1272-81. https://doi.org/10.1182/blood-2014-03-560805

Author

Fog, Cathrine Kolster ; Asmar, Fazila ; Côme, Christophe ; Jensen, Klaus Thorleif ; Johansen, Jens Vilstrup ; Kheir, Tony Bou ; Jacobsen, Linda Mosegaard ; Friis, Carsten ; Louw, Alison ; Rosgaard, Louise Skørbæk ; Øbro, Nina Friesgaard ; Marquart, Hanne Vibeke ; Anthonsen, Kristian ; Braat, Arie Koen ; van Lohuizen, Maarten ; Ralfkiaer, Elisabeth ; Grønbæk, Kirsten ; Lund, Anders Henrik. / Loss of PRDM11 promotes MYC-driven lymphomagenesis. I: Blood. 2015 ; Bind 125, Nr. 8. s. 1272-81.

Bibtex

@article{6f88a4af337d41148484108288c10208,
title = "Loss of PRDM11 promotes MYC-driven lymphomagenesis",
abstract = "The PR-domain (PRDM) family of genes encodes transcriptional regulators, several of which are deregulated in cancer. By using a functional screening approach, we sought to identify novel tumor suppressors among the PRDMs. Here we demonstrate oncogenic collaboration between depletion of the previously uncharacterized PR-domain family member Prdm11 and overexpression of MYC. Overexpression of PRDM11 inhibits proliferation and induces apoptosis. Prdm11 knockout mice are viable, and loss of Prdm11 accelerates MYC-driven lymphomagenesis in the Eµ-Myc mouse model. Moreover, we show that patients with PRDM11-deficient diffuse large B-cell lymphomas (DLBCLs) have poorer overall survival and belong to the nongerminal center B-cell-like subtype. Mechanistically, genome-wide mapping of PRDM11 binding sites coupled with transcriptome sequencing in human DLBCL cells evidenced that PRDM11 associates with transcriptional start sites of target genes and regulates important oncogenes such as FOS and JUN. Hence, we characterize PRDM11 as a putative novel tumor suppressor that controls the expression of key oncogenes, and we add new mechanistic insight into B-cell lymphomagenesis.",
keywords = "Animals, Carrier Proteins, Cell Transformation, Neoplastic, Cells, Cultured, Embryo, Mammalian, Gene Deletion, Gene Expression Regulation, Neoplastic, Gene Knockout Techniques, HEK293 Cells, HeLa Cells, Humans, Lymphoma, Lymphoma, Large B-Cell, Diffuse, Mice, Molecular Sequence Data, Proto-Oncogene Proteins c-myc, Tumor Suppressor Proteins",
author = "Fog, {Cathrine Kolster} and Fazila Asmar and Christophe C{\^o}me and Jensen, {Klaus Thorleif} and Johansen, {Jens Vilstrup} and Kheir, {Tony Bou} and Jacobsen, {Linda Mosegaard} and Carsten Friis and Alison Louw and Rosgaard, {Louise Sk{\o}rb{\ae}k} and {\O}bro, {Nina Friesgaard} and Marquart, {Hanne Vibeke} and Kristian Anthonsen and Braat, {Arie Koen} and {van Lohuizen}, Maarten and Elisabeth Ralfkiaer and Kirsten Gr{\o}nb{\ae}k and Lund, {Anders Henrik}",
note = "{\circledC} 2015 by The American Society of Hematology.",
year = "2015",
month = "2",
day = "19",
doi = "10.1182/blood-2014-03-560805",
language = "English",
volume = "125",
pages = "1272--81",
journal = "Blood",
issn = "0006-4971",
publisher = "American Society of Hematology",
number = "8",

}

RIS

TY - JOUR

T1 - Loss of PRDM11 promotes MYC-driven lymphomagenesis

AU - Fog, Cathrine Kolster

AU - Asmar, Fazila

AU - Côme, Christophe

AU - Jensen, Klaus Thorleif

AU - Johansen, Jens Vilstrup

AU - Kheir, Tony Bou

AU - Jacobsen, Linda Mosegaard

AU - Friis, Carsten

AU - Louw, Alison

AU - Rosgaard, Louise Skørbæk

AU - Øbro, Nina Friesgaard

AU - Marquart, Hanne Vibeke

AU - Anthonsen, Kristian

AU - Braat, Arie Koen

AU - van Lohuizen, Maarten

AU - Ralfkiaer, Elisabeth

AU - Grønbæk, Kirsten

AU - Lund, Anders Henrik

N1 - © 2015 by The American Society of Hematology.

PY - 2015/2/19

Y1 - 2015/2/19

N2 - The PR-domain (PRDM) family of genes encodes transcriptional regulators, several of which are deregulated in cancer. By using a functional screening approach, we sought to identify novel tumor suppressors among the PRDMs. Here we demonstrate oncogenic collaboration between depletion of the previously uncharacterized PR-domain family member Prdm11 and overexpression of MYC. Overexpression of PRDM11 inhibits proliferation and induces apoptosis. Prdm11 knockout mice are viable, and loss of Prdm11 accelerates MYC-driven lymphomagenesis in the Eµ-Myc mouse model. Moreover, we show that patients with PRDM11-deficient diffuse large B-cell lymphomas (DLBCLs) have poorer overall survival and belong to the nongerminal center B-cell-like subtype. Mechanistically, genome-wide mapping of PRDM11 binding sites coupled with transcriptome sequencing in human DLBCL cells evidenced that PRDM11 associates with transcriptional start sites of target genes and regulates important oncogenes such as FOS and JUN. Hence, we characterize PRDM11 as a putative novel tumor suppressor that controls the expression of key oncogenes, and we add new mechanistic insight into B-cell lymphomagenesis.

AB - The PR-domain (PRDM) family of genes encodes transcriptional regulators, several of which are deregulated in cancer. By using a functional screening approach, we sought to identify novel tumor suppressors among the PRDMs. Here we demonstrate oncogenic collaboration between depletion of the previously uncharacterized PR-domain family member Prdm11 and overexpression of MYC. Overexpression of PRDM11 inhibits proliferation and induces apoptosis. Prdm11 knockout mice are viable, and loss of Prdm11 accelerates MYC-driven lymphomagenesis in the Eµ-Myc mouse model. Moreover, we show that patients with PRDM11-deficient diffuse large B-cell lymphomas (DLBCLs) have poorer overall survival and belong to the nongerminal center B-cell-like subtype. Mechanistically, genome-wide mapping of PRDM11 binding sites coupled with transcriptome sequencing in human DLBCL cells evidenced that PRDM11 associates with transcriptional start sites of target genes and regulates important oncogenes such as FOS and JUN. Hence, we characterize PRDM11 as a putative novel tumor suppressor that controls the expression of key oncogenes, and we add new mechanistic insight into B-cell lymphomagenesis.

KW - Animals

KW - Carrier Proteins

KW - Cell Transformation, Neoplastic

KW - Cells, Cultured

KW - Embryo, Mammalian

KW - Gene Deletion

KW - Gene Expression Regulation, Neoplastic

KW - Gene Knockout Techniques

KW - HEK293 Cells

KW - HeLa Cells

KW - Humans

KW - Lymphoma

KW - Lymphoma, Large B-Cell, Diffuse

KW - Mice

KW - Molecular Sequence Data

KW - Proto-Oncogene Proteins c-myc

KW - Tumor Suppressor Proteins

U2 - 10.1182/blood-2014-03-560805

DO - 10.1182/blood-2014-03-560805

M3 - Journal article

VL - 125

SP - 1272

EP - 1281

JO - Blood

JF - Blood

SN - 0006-4971

IS - 8

ER -

ID: 45690474