leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
We conclude that all human TEL/JAK2 fusion variants are oncoproteins in vitro that strongly activate STAT 5, and cause lethal myelo- and lymphoproliferative syndromes in murine bone marrow transplant models of leukemia.
|
9736611 |
1998 |
leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
In this study, we identified STAT5b as a new gene fused to RARA in leukaemia; this is the first human tumour bearing a structurally abnormal STAT gene.
|
10441338 |
1999 |
leukemia
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
These results indicate that constitutive activation of STAT5 is a secondary event in most leukemias.
|
10729993 |
2000 |
leukemia
|
0.100 |
AlteredExpression
|
disease |
LHGDN |
Infrequent rearrangement of the STAT5b locus in primary human hematologic malignancies.
|
12145702 |
2002 |
leukemia
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Our results indicated that (1) the expression of TEL-FGFR3 but not DeltaHLH-TEL-FGFR3 resulted in efficient focus formation in NIH/3T3 cells and conferred interleukin 3 independence to Ba/F3 cells by a constitutive tyrosine kinase activity probably through oligomerization by the HLH domain of TEL; (2) although effector proteins including classical mitogen-activated protein kinase (MAPK), p38 MAPK, phosphatidylinositol 3-kinase (PI3-K), mammalian target or rapamycin (mTOR), signal transducer and activator of transcription 3 (STAT-3) and STAT-5 were activated in TEL-FGFR3 transformants, the growth of the transformants was inhibited by SU5402 (concentration that inhibits 50% [IC5)]=5 microM) and the PI3-K inhibitor, LY294002 (IC5)=10 microM) and wortmannin (IC50=5 microM), but not by U0126, SB203580, or rapamycin; and (3) injection of TEL-FGFR3 transformants induced lethal leukemia into syngeneic mice.
|
15514005 |
2005 |
leukemia
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Aberrant activation of the JAK-STAT pathway has been implicated in tumor formation; for example, constitutive activation of JAK2 kinase or the enforced expression of STAT5 induces leukemia in mice.
|
15578097 |
2004 |
leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
In addition, Stat5 tetramers were found to accumulate in excess compared to dimers in various human leukemias.
|
15652752 |
2005 |
leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Because we also found preferential constitutive STAT5B activation after transformation of cells by a truncated form of the G-CSF-R that produces severe neutropenia (Kostmann syndrome) and favors leukemia in humans, we discuss the potential role of STAT5B in oncogenic transformation of hematopoietic cells.
|
15677477 |
2005 |
leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
STAT5 (signal transducers and activators of transcription) are suggested to play a role in the pathogenesis of leukaemia and lymphoma; however, their influence on the growth of cutaneous T-cell lymphoma cells is not clear enough.
|
16502315 |
2006 |
leukemia
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
One possible pathomechanism causing leukemia is that clones of cells harboring acquired CSF3R mutations have a growth advantage over wild type cells in vivo during granulocyte-colony stimulating factor treatment due to activation of STAT5 and ss-catenin, both known to be involved in leukemogenesis.
|
18536571 |
2008 |
leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Modeling the functional heterogeneity of leukemia stem cells: role of STAT5 in leukemia stem cell self-renewal.
|
19667399 |
2009 |
leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
STAT5 in B cell development and leukemia.
|
20227268 |
2010 |
leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Hence, interference with Stat5a serine phosphorylation might provide a new therapeutic option for leukemia and myeloid dysplasias without affecting major functions of Stat5 in normal hematopoiesis.
|
20508164 |
2010 |
leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
This study investigated the potential therapeutic effect of STAT5 decoy oligodeoxynucleotides (ODN) using leukemia K562 cells as a model.
|
21091189 |
2011 |
leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
It also suggests that STAT5 may serve as an attractive target to overcome imatinib resistance in BCR-ABL1(+) leukemia.
|
21220747 |
2011 |
leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Genotype analyses showed that two SNPs, namely rs17886724 and rs2293157 located in STAT3 and STAT5, respectively, were significantly associated with leukemia (p < 0.05 for all).
|
22126101 |
2012 |
leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Indeed, Stat5b Ser-193 was found constitutively phosphorylated in several lymphoid tumor cell lines as well as primary leukemia and lymphoma patient tumor cells.
|
22442148 |
2012 |
leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
To search for these molecules we aligned IL-2 regulated genes detected by Affymetrix gene expression microarrays with the STAT5 cistrome identified by chip-on-ChIP analysis in an IL-2-dependent human leukemia cell line, Kit225.
|
23451206 |
2013 |
leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Taken together, our results indicate that the inhibition of STAT5 by IL-1β may be a promising treatment strategy to eradicate leukemia stem cells in AML.
|
23564444 |
2013 |
leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
In experimental models of acute T-cell lymphoblastic leukemias, where activated STAT5 contributes to leukemia cell survival, Brd2 knockdown or JQ1 treatment shows strong synergy with tyrosine kinase inhibitors (TKI) in inducing apoptosis in leukemia cells.
|
24435449 |
2014 |
leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
We conclude that combining kinase inhibition with STAT5 inhibition represents a promising therapeutic approach in BCR-ABL1+ leukemias.
|
24813920 |
2015 |
leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
The constitutive activation of signal transducer and activator of transcription 5 (STAT5) occurs during the transformation of fusion genes in leukemia.
|
26384082 |
2016 |
leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
We show that mouse thymic stromal lymphopoietin does not stimulate the downstream pathways (JAK/STAT5 and PI3K/AKT/mTOR) activated by the human cytokine in primary high-risk leukemia with overexpression of the receptor component.
|
26611474 |
2016 |
leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Antagonism of B cell enhancer networks by STAT5 drives leukemia and poor patient survival.
|
28369050 |
2017 |
leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
The most frequent STAT5B mutation, Asp642His (N642H), has been found in over 90 leukemia and lymphoma patients.
|
29200404 |
2018 |