Inducible knock-out of BCL6 in lymphoma cells results in tumor stasis.
BCL6
DLBCL
in vivo xenograft
inducible CRISPR/Cas9
lymphoma
Journal
Oncotarget
ISSN: 1949-2553
Titre abrégé: Oncotarget
Pays: United States
ID NLM: 101532965
Informations de publication
Date de publication:
03 Mar 2020
03 Mar 2020
Historique:
received:
24
05
2019
accepted:
08
02
2020
entrez:
18
3
2020
pubmed:
18
3
2020
medline:
18
3
2020
Statut:
epublish
Résumé
Diffuse large B-cell lymphoma (DLBCL) is the most common type of non-Hodgkin lymphomas worldwide and is characterized by a high diversity of genetic and molecular alterations. Chromosomal translocations and mutations leading to deregulated expression of the transcriptional repressor BCL6 occur in a significant fraction of DLBCL patients. An oncogenic role of BCL6 in the initiation of DLBCL has been shown as the constitutive expression of BCL6 in mice recapitulates the pathogenesis of human DLBCL. However, the role of BCL6 in tumor maintenance remains poorly investigated due to the absence of suitable genetic models and limitations of pharmacological inhibitors. Here, we have utilized tetracycline-inducible CRISPR/Cas9 mutagenesis to study the consequences of BCL6 deletion in established DLBCL models in culture and
Identifiants
pubmed: 32180900
doi: 10.18632/oncotarget.27506
pii: 27506
pmc: PMC7061739
doi:
Types de publication
Journal Article
Langues
eng
Pagination
875-890Déclaration de conflit d'intérêts
CONFLICTS OF INTEREST All authors except A. Ebert, A. Traunbauer, J. Jude, M. Hinterndorfer, M. Minnich and J. Zuber are employees of Boehringer Ingelheim. The main sponsor of the IMP is Boehringer Ingelheim. S.M. Blake was an employee of Boehringer Ingelheim now working for Astra Zeneca. No potential conflicts of interest were disclosed by the other authors.
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