Mutations in the STAT family of genes in cancer

Abstract

In recent years, it has become clear that members of the signal transducer and activator of transcription (STAT) family of genes play an important role in cancer. The STAT family consists of six genes, STAT1-4, STAT5A/ STAT5B and STAT6, that are involved in regulating cellular proliferation, apoptosis, angiogenesis and the immune system response. Constitutive activation of STAT3, via mutational changes, has been shown to be important in oncogenesis in both solid and hematopoietic cancers. In the case of hematopoietic neoplasms, STAT3 driver mutations have been described in T-cell large granular lymphocytic leukemia (T-LGL) and chronic natural killer lymphoproliferative disorders (CLPD-NK) and are seen in 30-40% of T-LGL patients. STAT5B is also mutated in T-LGL and CLPD-NK, but in a much smaller proportion. Here we review past and current research on STAT genes, with the emphasis on STAT3 and STAT5B, and their roles in the pathogenesis of hematopoietic and solid cancers with emphasis on hematopoietic malignancies, particularly T-LGL and CLPD-NK.

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