Fig. 1 | Nature Communications

Fig. 1

From: Structural and functional consequences of the STAT5BN642H driver mutation

Fig. 1

STAT5B is overexpressed and mutated at hot-spot residues in hematopoietic cancers. a Schematic depicting mutations found within the SH2 and C-terminal domains of human STAT5B in patients with various hematological malignancies. Each dot is representative of one patient. Numbers in brackets denote the number of patients reported to harbor any of the STAT5B mutations shown, for each disease entity. b Box plots showing human hematopoietic cancers with significant upregulation of STAT5B mRNA in tumor cells, compared with tissue-matched normal control cells. Data were extracted from the Oncomine database, from the following studies: 1 Haslinger Leukemia (chronic lymphocytic leukemia, CLL); 2 Andersson Leukemia (T-cell acute lymphoblastic leukemia, T-ALL; B-cell ALL); 3 Zhang Leukemia (Childhood T-ALL); 4 Choi Leukemia (chronic adult T-cell leukemia/lymphoma, ATLL); 5 Haferlach Leukemia (T-ALL). Representation: boxes as interquartile range, horizontal line as the mean, whiskers as lower and upper limits

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