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Stat3 Isoforms in Hematopoietic Neoplasms

One of the key pathways in cancer development is the Janus kinase (JAK) – signal transducer and activator of transcription (STAT) signaling pathway. One component of this pathway, STAT3 has been proposed as an oncogene, but recently it was also demonstrated as a tumor suppressor in different tumor models. In hematologic malignancies persistent STAT3 activation has frequently been detected suggesting an important role therein. Stat3 produces two isoforms (STAT3α and β) by alternative splicing that exhibit overlapping but distinct transcriptional activity. Interestingly, differential expression of STAT3 isoforms was detected in the bone marrow of patients with acute myeloid leukemia (AML) and in AML cell lines. Thus it is likely that the balance of the two isoforms may impact on leukemia development. 
We are investigating the contribution of STAT3 isoforms to hematopoietic neoplasms using various in vivo and in vitro models.

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