Concept

ABL (gene)

Publications associées (55)

Mechanisms of resistance to BCR-ABL and other kinase inhibitors

Oliver Hantschel, Allan Joaquim Lamontanara, Emel Basak Gencer Akçok, Orest Kuzyk

In this article, we are reviewing the molecular mechanisms that lead to kinase inhibitor resistance. As the oncogenic BCR-ABL kinase is the target of the first approved small-molecule kinase inhibitor imatinib, we will first focus on the structural and mec ...

Elsevier Science Bv2013

Dissection of the BCR-ABL signaling network using highly specific monobody inhibitors to the SHP2 SH2 domains

Sandrine Madeleine Suzanne Georgeon, Oliver Hantschel, Emel Basak Gencer Akçok

The dysregulated tyrosine kinase BCR-ABL causes chronic myelogenous leukemia in humans and forms a large multiprotein complex that includes the Src-homology 2 (SH2) domain-containing phosphatase 2 (SHP2). The expression of SHP2 is necessary for BCR-ABL-dep ...

National Academy of Sciences2013

A Control Flow Prototype for a Dose Recommending Device for Chronic Myeloid Leukemia Patients

Giovanni De Micheli, Alena Simalatsar, Wenqi You Dubout, Dechao Sun

In this paper we present a prototype of a control flow for an a posteriori drug dose adaptation for Chronic Myelogenous Leukemia (CML) patients. The control flow is modeled using Timed Automata extended with Tasks (TAT) model. The feedback loop of the cont ...

2013

The Growing Arsenal of ATP-Competitive and Allosteric Inhibitors of BCR-ABL

Oliver Hantschel

The BCR-ABL fusion kinase is the driving mutation of chronic myelogenous leukemias and is also expressed in a subset of acute lymphoblastic leukemias. Recent advances in elucidating the structure, regulation, and signaling of BCR-ABL have led to the identi ...

Amer Assoc Cancer Research2012

Structure, regulation, signaling, and targeting of abl kinases in cancer

Oliver Hantschel

Abl kinases are prototypic cytoplasmic tyrosine kinases and are involved in a variety of chromosomal aberrations in different cancers. This causes the expression of Abl fusion proteins, such as Bcr-Abl, that are constitutively activated and drivers of tumo ...

2012

Nilotinib as frontline and second-line therapy in chronic myeloid leukemia: open questions

Oliver Hantschel

Nilotinib is a second generation ABL tyrosine kinase inhibitor (TKI) that exerts major anti-leukemic effects in newly diagnosed patients with chronic myeloid leukemia (CML) as well as in most patients with imatinib-resistant CML. In freshly diagnosed patie ...

2012

Mig6 is a sensor of EGF receptor inactivation that directly activates c-Abl to induce apoptosis during epithelial homeostasis

Oliver Hantschel

A fundamental aspect of epithelial homeostasis is the dependence on specific growth factors for cell survival, yet the underlying mechanisms remain obscure. We found an "inverse" mode of receptor tyrosine kinase signaling that directly links ErbB receptor ...

2012

BCR-ABL uncouples canonical JAK2-STAT5 signaling in chronic myeloid leukemia

Oliver Hantschel

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 STAT5-activating kinase JAK2 have been discussed as a treatment option fo ...

Nature Publishing Group2012

Targeting the SH2-Kinase Interface in Bcr-Abl Inhibits Leukemogenesis

Oliver Hantschel

Chronic myelogenous leukemia (CML) is caused by the constitutively active tyrosine kinase Bcr-Abl and treated with the tyrosine kinase inhibitor (TKI) imatinib. However, emerging TKI resistance prevents complete cure. Therefore, alternative strategies targ ...

2011

The SCF-FBXW5 E3-ubiquitin ligase is regulated by PLK4 and targets HsSAS-6 to control centrosome duplication

Pierre Gönczy, Debora Keller

Deregulated centrosome duplication can result in genetic instability and contribute to tumorigenesis(1,2). Here, we show that centrosome duplication is regulated by the activity of an E3-ubiquitin ligase that employs the F-box protein FBXW5 (ref. 3) as its ...

Nature Publishing Group2011

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