MDM4 Is Targeted by 1q Gain and Drives Disease in Burkitt Lymphoma.
Animals
Apoptosis
Burkitt Lymphoma
/ genetics
Cell Cycle Checkpoints
Cell Cycle Proteins
/ genetics
Cell Proliferation
Chromosome Aberrations
Chromosomes, Human, Pair 1
/ genetics
Gene Expression Regulation, Neoplastic
Humans
Mice
Mutation
Proto-Oncogene Proteins
/ genetics
Tumor Cells, Cultured
Tumor Suppressor Protein p53
/ genetics
Xenograft Model Antitumor Assays
Journal
Cancer research
ISSN: 1538-7445
Titre abrégé: Cancer Res
Pays: United States
ID NLM: 2984705R
Informations de publication
Date de publication:
15 06 2019
15 06 2019
Historique:
received:
06
11
2018
revised:
11
03
2019
accepted:
15
04
2019
pubmed:
20
4
2019
medline:
12
3
2020
entrez:
20
4
2019
Statut:
ppublish
Résumé
Oncogenic MYC activation promotes proliferation in Burkitt lymphoma, but also induces cell-cycle arrest and apoptosis mediated by p53, a tumor suppressor that is mutated in 40% of Burkitt lymphoma cases. To identify molecular dependencies in Burkitt lymphoma, we performed RNAi-based, loss-of-function screening in eight Burkitt lymphoma cell lines and integrated non-Burkitt lymphoma RNAi screens and genetic data. We identified 76 genes essential to Burkitt lymphoma, including genes associated with hematopoietic cell differentiation (
Identifiants
pubmed: 31000522
pii: 0008-5472.CAN-18-3438
doi: 10.1158/0008-5472.CAN-18-3438
doi:
Substances chimiques
Cell Cycle Proteins
0
MDM4 protein, human
0
Proto-Oncogene Proteins
0
TP53 protein, human
0
Tumor Suppressor Protein p53
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
3125-3138Informations de copyright
©2019 American Association for Cancer Research.