Publication

Notch Signaling - a Booster of Chronic Lymphocytic Leukemia During Initiation and Disease Progression

Related publications (43)

Unpaired extracellular cysteine mutations of CSF3R mediate gain or loss of function

Oliver Hantschel, Tim Kükenshöner

Exclusive of membrane-proximal mutations seen commonly in chronic neutrophilic leukemia (e.g. T618I), functionally defective mutations in the extracellular domain of the granulocyte colony-stimulating factor receptor (CSF3R) have been reported only in seve ...
American Association for Cancer Research2017

Targeting macrophages sensitizes chronic lymphocytic leukemia to apoptosis and inhibits disease progression

Michele De Palma

The role of monocytes/macrophages in the development and progression of chronic lymphocytic leukemia (CLL) is poorly understood. Transcriptomic analyses show that monocytes/macrophages and leukemic cells cross talk during CLL progression. Macrophage deplet ...
Elsevier2016

Identification and functional characterization of protein kinases that modulate Notch signaling under physiological conditions and in cancer

Chhavi Jain

The Notch signaling pathway is a key regulator of cell fate decisions in embryonic development and in adult tissue homeostasis. Mounting evidence suggests that Notch signaling is frequently deregulated in human neoplasms, where depending upon the cellular ...
EPFL2016

Identification and Characterization of Tyrosine Kinase Nonreceptor 2 Mutations in Leukemia through Integration of Kinase Inhibitor Screening and Genomic Analysis

Oliver Hantschel, Sina Maren Reckel

The amount of genomic information about leukemia cells currently far exceeds our overall understanding of the precise genetic events that ultimately drive disease development and progression. Effective implementation of personalized medicine will require t ...
American Association for Cancer Research2016

The chromatin remodeller Chd7 and the calcium ATPase Serca2 - adding new facets to the role of Notch in Hematopoiesis and T-ALL

Monique Coersmeyer

Project I: Chd7 Deficiency does not affect N1-driven T-ALL Induction and Maintenance nor impair Hematopoiesis Notch1 has been shown to be a key driver in pediatric T-cell acute lymphobastic leukemia (T-ALL). Previous work in the lab identified the chromati ...
EPFL2015

Functional Perturbation of the Gab2 Multiprotein Complex by High-affinity SH2-binding Monobodies in Chronic Myelogenous Leukemia

Emel Basak Gencer Akçok

Chronic myeloid leukemia is characterized by a reciprocal chromosomal translocation between chromosome 9 and 22, resulting in the expression of the Bcr-Abl oncoprotein. Despite the great improvement in patient survival using tyrosine kinase inhibitors (TKI ...
EPFL2015

Mechanisms underlying cell-fate determination in the mammary gland development

Duje Buric

Notch signaling pathway is an important developmental pathway and has been implicated in both mammary gland development and tumorigenesis. Several studies investigating Notch signaling in mouse mammary gland implied that Notch signaling is an important fac ...
EPFL2015

Assessing the role of Hes1 and identification of target genes in human and murine T-ALL

Silvia Wirth

The Notch signalling pathway is an ancient cell signalling mechanism that enables short-range communications between cells and controls a broad spectrum of cell fates and developmental processes. In the haematopoietic system Notch signalling has been linke ...
EPFL2014

MicroRNA 21 is a novel oncogene in Notch1-driven acute lymphoblastic T cell leukemia

Fabian Junker

Notch signaling is a conserved cell-to-cell communication pathway essential in the development and maintenance of various tissues. Upon ligand binding, Notch receptors on the cell surface are proteolytically cleaved, generating the intracellular domain of ...
EPFL2014

NUP214-ABL1 mediated cell proliferation in T-cell acute lymphoblastic leukemia is dependent on the LCK kinase and various interacting proteins

Oliver Hantschel

The NUP214-ABL1 fusion protein is a constitutively active protein tyrosine kinase that is found in 6% of patients with T-cell acute lymphoblastic leukemia and that promotes proliferation and survival of T-lymphoblasts. Although NUP214-ABL1 is sensitive to ...
Pensiero Scientifico / Ferrata Storti Foundation2014

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