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STAT5A and STAT5B—Twins with Different Personalities in Hematopoiesis and Leukemia

Institute of Pharmacology and Toxicology, University of Veterinary Medicine, 1210 Vienna, Austria
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Author to whom correspondence should be addressed.
Equal first author contribution.
Cancers 2019, 11(11), 1726; https://doi.org/10.3390/cancers11111726
Received: 30 September 2019 / Revised: 25 October 2019 / Accepted: 1 November 2019 / Published: 4 November 2019
(This article belongs to the Special Issue JAK-STAT Signalling Pathway in Cancer)
The transcription factors STAT5A and STAT5B have essential roles in survival and proliferation of hematopoietic cells—which have been considered largely redundant. Mutations of upstream kinases, copy number gains, or activating mutations in STAT5A, or more frequently in STAT5B, cause altered hematopoiesis and cancer. Interfering with their activity by pharmacological intervention is an up-and-coming therapeutic avenue. Precision medicine requests detailed knowledge of STAT5A’s and STAT5B’s individual functions. Recent evidence highlights the privileged role for STAT5B over STAT5A in normal and malignant hematopoiesis. Here, we provide an overview on their individual functions within the hematopoietic system.
Keywords: STAT5A; STAT5B; hematopoietic stem cells; STAT5BN642H; STAT5 mouse models; BCR–ABL; leukemia; hematopoiesis STAT5A; STAT5B; hematopoietic stem cells; STAT5BN642H; STAT5 mouse models; BCR–ABL; leukemia; hematopoiesis
MDPI and ACS Style

Maurer, B.; Kollmann, S.; Pickem, J.; Hoelbl-Kovacic, A.; Sexl, V. STAT5A and STAT5B—Twins with Different Personalities in Hematopoiesis and Leukemia. Cancers 2019, 11, 1726.

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