An Oncogenic Role for Alternative NF-κB Signaling in DLBCL Revealed upon Deregulated BCL6 Expression

Baochun Zhang; Dinis Pedro Calado; Zhe Wang; Sebastian Fröhler; Karl Köchert; Yu Qian; Sergei B. Koralov; Marc Schmidt-Supprian; Yoshiteru Sasaki; Christine Unitt; Scott Rodig; Wei Chen; Riccardo Dalla-Favera; Frederick W. Alt; Laura Pasqualucci; Klaus Rajewsky

doi:10.1016/j.celrep.2015.03.059

An Oncogenic Role for Alternative NF-κB Signaling in DLBCL Revealed upon Deregulated BCL6 Expression

Baochun Zhang, Dinis Pedro Calado, Zhe Wang, Sebastian Fröhler, Karl Köchert, Yu Qian, Sergei B. Koralov, Marc Schmidt-Supprian, Yoshiteru Sasaki, Christine Unitt, Scott Rodig, Wei Chen, Riccardo Dalla-Favera, Frederick W. Alt, Laura Pasqualucci, Klaus Rajewsky

Publikation: Beitrag in Fachzeitschrift › Artikel › Begutachtung

67 Zitate (Scopus)

Abstract

Diffuse large B cell lymphoma (DLBCL) is a complex disease comprising diverse subtypes and genetic profiles. Possibly because of the prevalence of genetic alterations activating canonical NF-κB activity, a role for oncogenic lesions that activate the alternative NF-κB pathway in DLBCL has remained elusive. Here, we show that deletion/mutation of TRAF3, a negative regulator of the alternative NF-κB pathway, occurs in ~15% of DLBCLs and that it often coexistswith BCL6 translocation, which prevents terminalBcell differentiation. Accordingly, in a mouse modelconstitutive activation of the alternative NF-κB pathway cooperates with BCL6 deregulation in DLBCL development. This work demonstrates a key oncogenic role for the alternative NF-κB pathway in DLBCL development.

Originalsprache	Englisch
Seiten (von - bis)	715-726
Seitenumfang	12
Fachzeitschrift	Cell Reports
Jahrgang	11
Ausgabenummer	5
DOIs	https://doi.org/10.1016/j.celrep.2015.03.059
Publikationsstatus	Veröffentlicht - 2015
Extern publiziert	Ja

Zugriff auf Dokument

10.1016/j.celrep.2015.03.059

Andere Dateien und Links

Verknüpfung zur Publikation in Scopus

Dieses zitieren

Zhang, B., Calado, D. P., Wang, Z., Fröhler, S., Köchert, K., Qian, Y., Koralov, S. B., Schmidt-Supprian, M., Sasaki, Y., Unitt, C., Rodig, S., Chen, W., Dalla-Favera, R., Alt, F. W., Pasqualucci, L., & Rajewsky, K. (2015). An Oncogenic Role for Alternative NF-κB Signaling in DLBCL Revealed upon Deregulated BCL6 Expression. Cell Reports, 11(5), 715-726. https://doi.org/10.1016/j.celrep.2015.03.059

@article{65e29c14710d43d3a7e774f23f8f3644,

title = "An Oncogenic Role for Alternative NF-κB Signaling in DLBCL Revealed upon Deregulated BCL6 Expression",

abstract = "Diffuse large B cell lymphoma (DLBCL) is a complex disease comprising diverse subtypes and genetic profiles. Possibly because of the prevalence of genetic alterations activating canonical NF-κB activity, a role for oncogenic lesions that activate the alternative NF-κB pathway in DLBCL has remained elusive. Here, we show that deletion/mutation of TRAF3, a negative regulator of the alternative NF-κB pathway, occurs in ~15% of DLBCLs and that it often coexistswith BCL6 translocation, which prevents terminalBcell differentiation. Accordingly, in a mouse modelconstitutive activation of the alternative NF-κB pathway cooperates with BCL6 deregulation in DLBCL development. This work demonstrates a key oncogenic role for the alternative NF-κB pathway in DLBCL development.",

author = "Baochun Zhang and Calado, {Dinis Pedro} and Zhe Wang and Sebastian Fr{\"o}hler and Karl K{\"o}chert and Yu Qian and Koralov, {Sergei B.} and Marc Schmidt-Supprian and Yoshiteru Sasaki and Christine Unitt and Scott Rodig and Wei Chen and Riccardo Dalla-Favera and Alt, {Frederick W.} and Laura Pasqualucci and Klaus Rajewsky",

note = "Publisher Copyright: {\textcopyright} 2015 The Authors.",

year = "2015",

doi = "10.1016/j.celrep.2015.03.059",

language = "English",

volume = "11",

pages = "715--726",

journal = "Cell Reports",

issn = "2211-1247",

publisher = "Cell Press",

number = "5",

}

Zhang, B, Calado, DP, Wang, Z, Fröhler, S, Köchert, K, Qian, Y, Koralov, SB, Schmidt-Supprian, M, Sasaki, Y, Unitt, C, Rodig, S, Chen, W, Dalla-Favera, R, Alt, FW, Pasqualucci, L & Rajewsky, K 2015, 'An Oncogenic Role for Alternative NF-κB Signaling in DLBCL Revealed upon Deregulated BCL6 Expression', Cell Reports, Jg. 11, Nr. 5, S. 715-726. https://doi.org/10.1016/j.celrep.2015.03.059

TY - JOUR

T1 - An Oncogenic Role for Alternative NF-κB Signaling in DLBCL Revealed upon Deregulated BCL6 Expression

AU - Zhang, Baochun

AU - Calado, Dinis Pedro

AU - Wang, Zhe

AU - Fröhler, Sebastian

AU - Köchert, Karl

AU - Qian, Yu

AU - Koralov, Sergei B.

AU - Schmidt-Supprian, Marc

AU - Sasaki, Yoshiteru

AU - Unitt, Christine

AU - Rodig, Scott

AU - Chen, Wei

AU - Dalla-Favera, Riccardo

AU - Alt, Frederick W.

AU - Pasqualucci, Laura

AU - Rajewsky, Klaus

PY - 2015

Y1 - 2015

N2 - Diffuse large B cell lymphoma (DLBCL) is a complex disease comprising diverse subtypes and genetic profiles. Possibly because of the prevalence of genetic alterations activating canonical NF-κB activity, a role for oncogenic lesions that activate the alternative NF-κB pathway in DLBCL has remained elusive. Here, we show that deletion/mutation of TRAF3, a negative regulator of the alternative NF-κB pathway, occurs in ~15% of DLBCLs and that it often coexistswith BCL6 translocation, which prevents terminalBcell differentiation. Accordingly, in a mouse modelconstitutive activation of the alternative NF-κB pathway cooperates with BCL6 deregulation in DLBCL development. This work demonstrates a key oncogenic role for the alternative NF-κB pathway in DLBCL development.

AB - Diffuse large B cell lymphoma (DLBCL) is a complex disease comprising diverse subtypes and genetic profiles. Possibly because of the prevalence of genetic alterations activating canonical NF-κB activity, a role for oncogenic lesions that activate the alternative NF-κB pathway in DLBCL has remained elusive. Here, we show that deletion/mutation of TRAF3, a negative regulator of the alternative NF-κB pathway, occurs in ~15% of DLBCLs and that it often coexistswith BCL6 translocation, which prevents terminalBcell differentiation. Accordingly, in a mouse modelconstitutive activation of the alternative NF-κB pathway cooperates with BCL6 deregulation in DLBCL development. This work demonstrates a key oncogenic role for the alternative NF-κB pathway in DLBCL development.

UR - http://www.scopus.com/inward/record.url?scp=84933678552&partnerID=8YFLogxK

U2 - 10.1016/j.celrep.2015.03.059

DO - 10.1016/j.celrep.2015.03.059

M3 - Article

C2 - 25921526

AN - SCOPUS:84933678552

SN - 2211-1247

VL - 11

SP - 715

EP - 726

JO - Cell Reports

JF - Cell Reports

IS - 5

ER -

An Oncogenic Role for Alternative NF-κB Signaling in DLBCL Revealed upon Deregulated BCL6 Expression

Abstract

Zugriff auf Dokument

Andere Dateien und Links

Fingerprint

Dieses zitieren