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New paper on Targeting STAT5B in T-Cell Neoplasia.

STAT5BN642H-driven proliferation in T-cell leukemia/lymphoma via common γ-chain (γc)-receptor signaling. STAT5BN642H is activated by Janus kinase (JAK) upon cytokine stimulation such as interleukin 2 (IL-2). Subsequently, phosphorylated STAT5BN642H translocates into the nucleus and initiates transcription. (1) STAT5BN642H exhibits prolonged activation and enhanced DNA binding leading to (2) increased transcription of STAT5 target genes and enhanced proliferation.

The somatic hot spot mutation in STAT5B was found in many T cell leukemia/lymphoma patients. The team of  Moriggl generated and analyzed a transgenic mouse model with hematopoietic STAT5BN642H expression that caused aggressive T-cell leukemia/lymphomas. Herein, we discuss the scientific merit of our model and its relevance for pre-clinical studies.

Now published in Molecular & Cellular Oncology Volume 5, 2018 - Issue 3