Twins with different personalities: STAT5B-but not STAT5A-has a key role in BCR/ABL-induced leukemia.
Animals
Antineoplastic Agents
/ pharmacology
Cell Proliferation
Cell Transformation, Neoplastic
/ drug effects
Fusion Proteins, bcr-abl
/ genetics
Humans
Interferons
/ pharmacology
Leukemia, Large Granular Lymphocytic
/ drug therapy
Leukemia, Myelogenous, Chronic, BCR-ABL Positive
/ drug therapy
Mice
Mice, Inbred NOD
Mice, Knockout
Mice, SCID
Mutation
STAT5 Transcription Factor
/ genetics
Survival Rate
Tumor Suppressor Proteins
/ genetics
Xenograft Model Antitumor Assays
Journal
Leukemia
ISSN: 1476-5551
Titre abrégé: Leukemia
Pays: England
ID NLM: 8704895
Informations de publication
Date de publication:
07 2019
07 2019
Historique:
received:
05
06
2018
accepted:
03
12
2018
revised:
03
10
2018
pubmed:
27
1
2019
medline:
13
11
2019
entrez:
26
1
2019
Statut:
ppublish
Résumé
Deregulation of the Janus kinase/signal transducers and activators of transcription (JAK/STAT) signaling pathway is found in cancer with STAT5A/B controlling leukemic cell survival and disease progression. As mutations in STAT5B, but not STAT5A, have been frequently described in hematopoietic tumors, we used BCR/ABL as model systems to investigate the contribution of STAT5A or STAT5B for leukemogenesis. The absence of STAT5A decreased cell survival and colony formation. Even more drastic effects were observed in the absence of STAT5B. STAT5B-deficient cells formed BCR/ABL
Identifiants
pubmed: 30679796
doi: 10.1038/s41375-018-0369-5
pii: 10.1038/s41375-018-0369-5
pmc: PMC6755975
doi:
Substances chimiques
Antineoplastic Agents
0
STAT5 Transcription Factor
0
STAT5A protein, human
0
STAT5B protein, human
0
Tumor Suppressor Proteins
0
Interferons
9008-11-1
Fusion Proteins, bcr-abl
EC 2.7.10.2
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1583-1597Références
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