Table 1. Molecular alterations resulting in the enhanced activation of STAT3 signaling.

Components and mechanisms	Cells and phenotypes	References
v-src, activated oncogenic version of the tyrosine kinase c-src	Fibroblast transformation	8 and 9
JAK2 (V617F), activating mutation in the tyrosine kinase domain	Myeloproliferative neoplasms	10, 11 and 12
gp 130, activating deletion of the ligand binding site in the IL-6 coreceptor	Inflammatory hepatocellular adenoma	13
STAT3 (Y640F and D661V), activating mutations in the dimerization domain	Hepatocellular adenoma, T cell large granular lymphocytic leukemia	14 and 15
G-CSF receptor activation through increased JAK2 expression	Hematopoietic cell transformation	16
Sphingosine 1 phosphate receptor overexpression, auxilliary in IL-6 dependent STAT3 activation	B16 mouse melanoma cells, human breast cancer	17
EGF receptor, mutation in the kinase domain, induces IL-6 secretion	Human lung adenocarcinomas	20
Ras, oncogenic mutation induces IL-6 secretion	Pancreatic cancer	19
IL-6, autoregulation, autocrine induction of IL-6 secretion	Lung adenocarcinoma cells	22