An active mediator of cytokine signaling in solid and hematologic malignancies is the JAK-STAT (Janus Kinase and Signal Transducer and Activator of Transcription) pathway. The latent cytoplasmic transcription factors make up the STAT family which has seven mammalian members. A network with activation interwoven with phosphorylation activates the STAT family. Eventually, it leads to cell proliferation. One or more STAT factors are phosphorylated by an active kinase enzyme as it travels to the nucleus to manage gene expression. Therefore, cell survival is promoted. In recent times, mutations in somatic STAT3 have been recorded in aplastic anemia, lymphocytic leukemia, and myelodysplastic syndrome. In addition, there is a need to explore the association between STAT3 and BCL6 in diffuse large B-cell lymphomas, especially on the subtype of activated B-cell.
Presently, the exploration for therapeutic STAT3 inhibitors that nullify the JAK-STAT pathway is being carried out. The STAT pathway appears to be critical in tumorigenesis. Hence, targeting it is promising for multiple malignancies, which include leukemia and lymphoma.
Link:theoncologist.onlinelibrary.wiley.com/doi/10.1634/theoncologist.2013-0407
