JAK/STAT, Raf/MEK/ERK, PI3K/Akt and BCR-ABL in cell cycle progression and leukemogenesis

By Linda S. Steelman, S. Pohnert, J. G. Shelton, R. Franklin, F. E. Bertrand, J. McCubrey. Leukemia, 2004

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Roles of the Raf/MEK/ERK pathway in cell growth, malignant transformation and drug resistance. (2007, background): “ERK can also phosphorylate and activate the 90 kDa ribosomal S6 kinase (p90Rsk), which then leads to the activation of the transcription factor CREB [1] (see Fig.”
Dasatinib (BMS-354825) targets an earlier progenitor population than imatinib in primary CML but does not eliminate the quiescent fraction. (2006, methodology): “17,49 To compare the antiproliferative properties of IM with those of dasatinib and to assess the net effect of these drugs alone and in combination on total and CFSEmax cells, 6 test conditions were assayed: (1) no drug control, (2) IM alone for 6 days (5 M), (3) dasatinib alone for 6 days (150 nM)”
The role of IL-6 and STAT3 in inflammation and cancer. (2005, background): “Interleukin (IL)-6 is a potent, pleiotropic, inflammatory cytokine that mediates a plethora of physiological functions, including the developmental differentiation of lymphocytes, cell proliferation, and cell survival and amelioration of apoptotic signals [18–20].”