Associated Papers
JAK/STAT in human diseases: a common axis in immunodeficiencies and hematological disorders.
Djidjik R et al.
Frontiers in Immunology, 2025
41438753 (PubMed )
Supplement: Table1.pdf
Pro-inflammatory cells sustain leukemic clonal expansion in T-cell large granular lymphocyte leukemia.
Vicenzetto C et al.
Haematologica, 2024
37439335 (PubMed )
Supplement: 2022_282306_VICENZETTO_SUPPL.pdf
Identification of novel STAT5B mutations and characterization of TCRβ signatures in CD4+ T-cell large granular lymphocyte leukemia.
Bhattacharya D et al.
Blood Cancer Journal, 2022
STAT5b: A master regulator of key biological pathways.
Smith MR et al.
Frontiers in Immunology, 2022
STAT3 and STAT5B mutations have unique distribution in T-cell large granular lymphocyte proliferations and advanced myeloid neoplasms.
Qu S et al.
Leukemia & Lymphoma, 2021
Twins with different personalities: STAT5B-but not STAT5A-has a key role in BCR/ABL-induced leukemia.
Kollmann S et al.
Leukemia, 2019
Nonclassical GH Insensitivity: Characterization of Mild Abnormalities of GH Action.
Storr HL et al.
Endocrine Reviews, 2019
High incidence of activating STAT5B mutations in CD4-positive T-cell large granular lymphocyte leukemia.
Andersson EI et al.
Blood, 2016
Signal transducer and activator of transcription (STAT)5 activation by BCR/ABL is dependent on intact Src homology (SH)3 and SH2 domains of BCR/ABL and is required for leukemogenesis.
Nieborowska-Skorska M et al.
The Journal of Experimental Medicine, 1999
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