Chronic myeloid leukemia (CML) is caused by the acquisition of the tyrosine kinase BCR-
ABL1 in a hemopoietic stem cell, transforming it into a leukemic stem cell (LSC) that self …

Diverse cellular processes are regulated by tyrosyl phosphorylation, which is controlled by
protein-tyrosine kinases (PTKs) and protein-tyrosine phosphatases (PTPs). De-regulated …

The transcription factor STAT5 is an essential mediator of the pathogenesis of chronic
myelogenous leukemia (CML). In CML, the BCR/ABL fusion kinase causes the constitutive …

Tumourigenesis caused by the Bcr/Abl oncoprotein is a multi‐step process proceeding from
initial to tumour‐maintaining events and finally results in a complex tumour‐supporting …

Tyrosyl phosphorylation, which is controlled by protein-tyrosine kinases (PTKs) and protein-
tyrosine phosphatases (PTPs), regulates numerous cellular processes. Altered expression …

Constitutive activation of STAT5 is critical for the maintenance of chronic myeloid leukemia
(CML) characterized by the BCR-ABL oncoprotein. Tyrosine kinase inhibitors (TKIs) for the …

Mutations in the metabolic enzymes isocitrate dehydrogenase 1 (IDH1) and 2 (IDH2) are
frequently found in glioma, acute myeloid leukemia (AML), melanoma, thyroid cancer, and …

The protein tyrosine phosphatase Shp2 is a positive regulator of growth factor signaling.
Gain-of-function mutations in several types of leukemia define Shp2 as a bona fide …

STAT5 proteins are constitutively activated in malignant cells from many patients with
leukemia, including the myeloproliferative neoplasms (MPNs) chronic myeloid leukemia …

Since their discovery a little more than a decade ago, the docking proteins of the Gab/DOS
family have emerged as important signalling elements in metazoans. Gab/DOS proteins …