Co-operating STAT5 and AKT signaling pathways in chronic myeloid leukemia and mastocytosis: possible new targets of therapy

• Published in: Haematologica (Roma) Vol. 99; no. 3; pp. 417 - 429
• Main Authors: Bibi, S., Arslanhan, M. D., Langenfeld, F., Jeanningros, S., Cerny-Reiterer, S., Hadzijusufovic, E., Tchertanov, L., Moriggl, R., Valent, P., Arock, M.
• Format: Journal Article
• Language: English
• Published: Italy Ferrata Storti Foundation 01.03.2014
• Subjects: Animals; Fusion Proteins, bcr-abl - genetics; Fusion Proteins, bcr-abl - metabolism; Humans; Janus Kinases - metabolism; Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy; Leukemia, Myelogenous, Chronic, BCR-ABL Positive - etiology; Leukemia, Myelogenous, Chronic, BCR-ABL Positive - metabolism; Life Sciences; Mast Cells - metabolism; Mast Cells - pathology; Mastocytosis - drug therapy; Mastocytosis - etiology; Mastocytosis - metabolism; Molecular Targeted Therapy; Mutation; Phosphatidylinositol 3-Kinases - metabolism; Proto-Oncogene Proteins c-akt - antagonists & inhibitors; Proto-Oncogene Proteins c-akt - metabolism; Proto-Oncogene Proteins c-kit - genetics; Proto-Oncogene Proteins c-kit - metabolism; Review; Signal Transduction - drug effects; STAT5 Transcription Factor - antagonists & inhibitors; STAT5 Transcription Factor - metabolism

Chronic myeloid leukemia and systemic mastocytosis are myeloid neoplasms sharing a number of pathogenetic and clinical features. In both conditions, an aberrantly activated oncoprotein with tyrosine kinase activity, namely BCR-ABL1 in chronic myeloid leukemia, and mutant KIT, mostly KIT D816V, in sy...