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Abstract
STAT3 is important for transcriptional regulation in human acute myeloid leukemia (AML). STAT3 has thousands of potential DNA binding sites but usually shows cell type specific binding preferences to a limited number of these. Furthermore, AML is a very heterogeneous disease, and studies of the prognostic impact of STAT3 in human AML have also given conflicting results. A more detailed characterization of STAT3 functions and the expression of various isoforms in human AML will therefore be required before it is possible to design clinical studies of STAT3 inhibitors in this disease, and it will be especially important to investigate whether the functions of STAT3 differ between patients. Several other malignancies also show extensive biological heterogeneity, and the present discussion and the suggested scientific approaches may thus be relevant for other cancer patients.
Financial & competing interests disclosure
This work was supported by the Norwegian Cancer Society and the Solveig and Ove Lundes Foundation. The authors also receive financial support for their research from Helse-Vest and the University of Bergen. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.
No writing assistance was utilized in the production of this manuscript.
STAT3 has thousands of potential DNA-binding sites.
STAT3 shows cell type-specific preferences to a limited number of binding sites.
STAT3 is an important regulator of normal hematopoiesis.
The effect of STAT3 differs between different types of hematopoietic cells.
Acute myeloid leukemia (AML) is a very heterogeneous disease and it is not known whether the functional importance of STAT3 differs between patients.
Studies of the prognostic impact of STAT3 in AML patients receiving intensive chemotherapy show conflicting results.
Direct STAT3 inhibitors are now being tried in the treatment of several human malignancies.
The initial experiences suggest that the toxicity of direct STAT3 inhibition is acceptable.
Further biological studies of the function of STAT3 in heterogeneous AML patients will be needed before clinical studies can be designed and before it is possible to decide whether this therapeutic strategy should be further investigated in specific subsets of AML patients.
