|
Acute Promyelocytic Leukemia
|
0.570 |
Biomarker
|
disease |
BEFREE |
In addition, STAT5b-RARalpha and other APL fusion proteins may contribute to leukemogenesis by interaction with the STAT3 oncogene pathway.
|
11929748 |
2002 |
|
Acute Promyelocytic Leukemia
|
0.570 |
Biomarker
|
disease |
BEFREE |
In acute promyelocytic leukemia (APL) cells with rearrangement of retinoic acid receptor a (RAR alpha) (including: PML-RAR alpha, PLZF-RAR alpha, NPM-RAR alpha, NuMA- RAR alpha or STAT5b-RAR alpha) as a result of chromosomal translocations, the RA signal pathway is disrupted and myeloid differentiation is arrested at the promyelocytic stage.
|
11022230 |
2000 |
|
Acute Promyelocytic Leukemia
|
0.570 |
AlteredExpression
|
disease |
BEFREE |
The RAR alpha gene fuses to variable partners (PML, PLZF, NPM, NuMA and STAT5B: X genes) leading to the expression of APL-specific fusion proteins with identical RAR alpha moieties.
|
16331271 |
2006 |
|
Acute Promyelocytic Leukemia
|
0.570 |
Biomarker
|
disease |
BEFREE |
With RT-PCR and karyotype, Case A is diagnosed with STAT5b-RARα-positive APL.Case B, C are diagnosed with PLZF-RARα-positive APL.
|
31083206 |
2019 |
|
Acute Promyelocytic Leukemia
|
0.570 |
Biomarker
|
disease |
BEFREE |
Some APL cases also involve rearrangements that fuse RAR to partner genes other than PML, including nucleophosmin (NPM), promyelocytic leukemia zinc finger (PLZF), nuclear mitotic apparatus (NUMA), and Stat5b, but the clinical characteristics of APL without PML-RAR have not been fully clarified.
|
17988991 |
2007 |
|
Acute Promyelocytic Leukemia
|
0.570 |
GeneticVariation
|
disease |
BEFREE |
To the best of our knowledge, we report here only the sixth APL patient in the world with the STAT5b-RARα fusion transcript.
|
22749039 |
2012 |
|
Acute Promyelocytic Leukemia
|
0.570 |
Biomarker
|
disease |
BEFREE |
Clinical characteristics of APL with STAT5B-RARA are also discussed.
|
18221386 |
2008 |
|
T-Cell Large Granular Lymphocyte Leukemia
|
0.530 |
Biomarker
|
disease |
BEFREE |
Here we review past and current research on STAT genes in hematopoietic and solid cancers with emphasis on STAT3 and STAT5B and their roles in the pathogenesis of hematopoietic malignancies, particularly T-LGL leukemia and CLPD-NK.
|
29417693 |
2018 |
|
T-Cell Large Granular Lymphocyte Leukemia
|
0.530 |
GeneticVariation
|
disease |
BEFREE |
Uncovering the pathogenesis of large granular lymphocytic leukemia-novel STAT3 and STAT5b mutations.
|
24512550 |
2014 |
|
T-Cell Large Granular Lymphocyte Leukemia
|
0.530 |
GeneticVariation
|
disease |
BEFREE |
Discovery of somatic STAT5b mutations in large granular lymphocytic leukemia.
|
23596048 |
2013 |
|
Lymphoma, T-Cell, Cutaneous
|
0.350 |
AlteredExpression
|
disease |
BEFREE |
Jak3, STAT3, and STAT5 inhibit expression of miR-22, a novel tumor suppressor microRNA, in cutaneous T-Cell lymphoma.
|
26244872 |
2015 |
|
Lymphoma, T-Cell, Cutaneous
|
0.350 |
AlteredExpression
|
disease |
BEFREE |
STAT5 induces miR-21 expression in cutaneous T cell lymphoma.
|
27329723 |
2016 |
|
Lymphoma, T-Cell, Cutaneous
|
0.350 |
AlteredExpression
|
disease |
BEFREE |
Furthermore, the results indicate that SHP2 may not be involved in the activation of Stat3 or Stat5 in CTCL cells.
|
12543077 |
2002 |
|
Lymphoma, T-Cell, Cutaneous
|
0.350 |
AlteredExpression
|
disease |
BEFREE |
STAT5-mediated expression of oncogenic miR-155 in cutaneous T-cell lymphoma.
|
23676217 |
2013 |
|
Lymphoma, T-Cell, Cutaneous
|
0.350 |
Biomarker
|
disease |
BEFREE |
The influence of STAT5 antisense oligodeoxynucleotides on the proliferation and apoptosis of selected human cutaneous T-cell lymphoma cell lines.
|
16502315 |
2006 |
|
Leukemia, Large Granular Lymphocytic
|
0.330 |
GeneticVariation
|
disease |
BEFREE |
This is the first time somatic STAT5 mutations are discovered in human cancer and further emphasizes the role of STAT family genes in the pathogenesis of LGL leukemia.
|
23596048 |
2013 |
|
Leukemia, Large Granular Lymphocytic
|
0.330 |
GeneticVariation
|
disease |
BEFREE |
We observed activating STAT5B mutations (1/5) and hypermethylation of HACE1 (3/4) in ANKL cases, suggesting that these aberrations may contribute to ANKL pathogenesis.
|
26975038 |
2016 |
|
Leukemia, Large Granular Lymphocytic
|
0.330 |
GeneticVariation
|
disease |
BEFREE |
STAT3 and STAT5b mutations can be used as molecular markers for LGL leukemia diagnostics, and they present novel therapeutic targets for STAT3 and STAT5b inhibitors, which currently are in development for treatment of cancer and autoimmune disorders.
|
24512550 |
2014 |
|
Precursor T-Cell Lymphoblastic Leukemia-Lymphoma
|
0.330 |
AlteredExpression
|
disease |
BEFREE |
STAT5 chromatin immunoprecipitation sequencing and RNA sequencing reveal a diverse IL-7-driven STAT5-dependent transcriptional program in T-ALL cells, which includes <i>BCL6</i> inactivation by alternative transcription and upregulation of the oncogenic serine/threonine kinase <i>PIM1</i> Pharmacological inhibition of PIM1 abrogates IL-7-mediated proliferation on T-ALL cells, indicating that strategies involving the use of PIM kinase small-molecule inhibitors may have therapeutic potential against a majority of leukemias that rely on IL-7 receptor (IL-7R) signaling.
|
30185437 |
2018 |
|
Precursor T-Cell Lymphoblastic Leukemia-Lymphoma
|
0.330 |
Biomarker
|
disease |
BEFREE |
Taken together, we demonstrated that IL7 mediates an intrinsic and physiologic mechanism of GC resistance in normal thymocyte development that is retained during leukemogenesis in a subset of T-ALLs and is reversible with targeted inhibition of the IL7R/JAK/STAT5/BCL-2 axis.
|
31687977 |
2020 |
|
Precursor T-Cell Lymphoblastic Leukemia-Lymphoma
|
0.330 |
AlteredExpression
|
disease |
BEFREE |
Lacking comma: Chromosomal deletion of the STAT5 binding site in LOUCY cells reduced protein levels of STAT5 in some MEF2C-positve T-ALL cell lines, and the presence of inhibitory IL7-JAK-STAT5 signaling highlighted the repressive impact of this factor in MEF2C regulation.
|
21261500 |
2011 |
|
T-Cell Prolymphocytic Leukemia
|
0.330 |
AlteredExpression
|
disease |
BEFREE |
Overall, considering such losses of negative regulators and the GOF mutations in <i>JAK</i> and <i>STAT</i> genes, a total of 89.8% of T-PLL revealed a genomic aberration potentially explaining enhanced STAT5B activity.
|
31766351 |
2019 |
|
T-Cell Prolymphocytic Leukemia
|
0.330 |
GeneticVariation
|
disease |
BEFREE |
Mutated STAT3 is mainly associated with large granular lymphocytic T-cell leukemia, whereas mutated STAT5B is associated with T-cell prolymphocytic leukemia, T-cell acute lymphoblastic leukemia and γδ T-cell-derived lymphomas.
|
31817042 |
2019 |
|
T-Cell Prolymphocytic Leukemia
|
0.330 |
Biomarker
|
disease |
BEFREE |
These results for the first time provide a portrait of the mutational landscape of T-PLL and implicate deregulation of DNA repair and epigenetic modulators as well as high-frequency mutational activation of the IL2RG-JAK1-JAK3-STAT5B axis in the pathogenesis of T-PLL.
|
24825865 |
2014 |
|
T-Cell Lymphoma
|
0.320 |
GeneticVariation
|
disease |
BEFREE |
STAT5B N642H is particularly frequent in all forms of γδ-T-cell lymphomas.
|
25586472 |
2015 |