Page 1 | Search Results | Blood | American Society of Hematology

1-9 of 9

Sort by

Sort Order Select

Journal Articles

Expression and Function of the P-Glycoprotein (P-gp) In Myelodysplastic Syndromes (MDS) Treated with Azacytidine (AZA)

Marie Sebert, Elodie Lainey, PAscale Lepelley, Sylvain Thepot, Maximilien Tailler, Claude Gardin, MD, Guido Kroemer, MD, PhD, Simone Boehrer, Lionel Ades, Pierre Fenaux, MD, PhD

Blood (2011) 118 (21): 5028.

https://doi.org/10.1182/blood.V118.21.5028.5028

Published: 2011

Journal Articles

Potentiation of Apoptosis in MDS/AML by Combination of Azacitidine and the EGFR-Tyrosine Kinase Inhibitor (TKI) erlotinib

Elodie Lainey, Marie Sebert, Cyrielle Bouteloup, Carole Leroy, Sylvain Thepot, Maximilien Tailler, Lionel Ades, Claude Gardin, MD, Guido Kroemer, MD, PhD, Pierre Fenaux, MD, PhD, Simone Boehrer, MD, PhD

Blood (2011) 118 (21): 2790.

https://doi.org/10.1182/blood.V118.21.2790.2790

Published: 2011

Journal Articles

Erlotinib Antagonizes Efflux Via ABC Transporters and Decreases P-Gp Cell Surface Expression by Inhibiting SRC Kinase and mTOR Pathways in Acute Myeloid Leukemia (AML)

Blood (2011) 118 (21): 2564.

https://doi.org/10.1182/blood.V118.21.2564.2564

Published: 2011

Journal Articles

Increased Proliferation Induced by Constitutive Activation of the Src-Kinase Lyn and Aberrant mTOR Signaling in AML Is Abrogated by the EGFR-Inhibitor Erlotinib.

Simone Boehrer, MD, PhD, Lorenzo Galluzzi, phD, Lionel Ades, MD, Celine Fouassier, Claude Gardin, MD, Pierre Fenaux, MD, PhD, Guido Kroemer, MD, PhD

Blood (2009) 114 (22): 3813.

https://doi.org/10.1182/blood.V114.22.3813.3813

Published: 2009

Journal Articles

The EGFR-Inhibitor Erlotinib Induces Differentiation, Cell Cycle Arrest and Apoptosis in EGFR-Negative Cells of MDS and AML.

Simone Boehrer, MD, Lionel Ades, MD, Thorsten Braun, MD, Lorenzo Galluzzi, Jennifer Grosjean, Claire Fabre, MD, Genevieve Le Roux, Claude Gardin, MD, Antoine Martin, MD, Stephane de Botton, MD, Pierre Fenaux, MD, PhD, Guido Kroemer, MD, PhD

Blood (2007) 110 (11): 399.

https://doi.org/10.1182/blood.V110.11.399.399

Published: 2007

Journal Articles

Flt3 Receptor Inhibition Abolishes Constitutive NFκB Activation in High-Risk Myelodysplastic Syndrome and Acute Myeloid Leukemia.

Jennifer Grosjean, PhD, Lionel Ades, MD, Simone Bohrer, MD, PhD, Pierre Fenaux, MD, PhD, Guido Kroemer, MD, PhD

Blood (2007) 110 (11): 2434.

https://doi.org/10.1182/blood.V110.11.2434.2434

Published: 2007

Journal Articles

Further Evidence That MDS and AML Cells Exhibit a Differential Capacity To Activate the DNA-Damage Response (DDR) Pathways.

Simone Boehrer, MD, Lionel Ades, MD, Lorenzo Galluzzi, Ken Olaussen, PhD, Thorsten Braun, MD, Jennifer Grosjean, PhD, Claire Fabre, MD, Stephane de Botton, MD, Pierre Fenaux, MD, PhD, Guido Kroemer, MD, PhD

Blood (2007) 110 (11): 2438.

https://doi.org/10.1182/blood.V110.11.2438.2438

Published: 2007

Journal Articles

Abrogation of the DNA-Damage Response in De Novo AML Versus MDS Cell Lines.

Simone Boehrer, MD, PhD, Lionel Ades, MD, Claire Fabre, MD, Pierre Fenaux, MD, PhD, Guido Kroemer, MD, PhD

Blood (2006) 108 (11): 2649.

https://doi.org/10.1182/blood.V108.11.2649.2649

Published: 2006

Journal Articles

The EGFR-Inhibitor Erlotinib Induces Apoptosis in Neoplastic Cells of Myelodysplastic Syndrome (MDS) and Acute Myeloid Leukemia (AML), an Effect Determined by the Expression Level of Nucleophosmin (NPM).

Simone Boehrer, MD, PhD, Lionel Ades, MD, Claire Fabre, MD, Pierre Fenaux, MD, PhD, Guido Kroemer, MD, PhD

Blood (2006) 108 (11): 856.

https://doi.org/10.1182/blood.V108.11.856.856

Published: 2006

Update search

NARROW

Publications

Format

Article Type

Topics

Date

Availability

Expression and Function of the P-Glycoprotein (P-gp) In Myelodysplastic Syndromes (MDS) Treated with Azacytidine (AZA)

Potentiation of Apoptosis in MDS/AML by Combination of Azacitidine and the EGFR-Tyrosine Kinase Inhibitor (TKI) erlotinib

Erlotinib Antagonizes Efflux Via ABC Transporters and Decreases P-Gp Cell Surface Expression by Inhibiting SRC Kinase and mTOR Pathways in Acute Myeloid Leukemia (AML)

Increased Proliferation Induced by Constitutive Activation of the Src-Kinase Lyn and Aberrant mTOR Signaling in AML Is Abrogated by the EGFR-Inhibitor Erlotinib.

The EGFR-Inhibitor Erlotinib Induces Differentiation, Cell Cycle Arrest and Apoptosis in EGFR-Negative Cells of MDS and AML.

Flt3 Receptor Inhibition Abolishes Constitutive NFκB Activation in High-Risk Myelodysplastic Syndrome and Acute Myeloid Leukemia.

Further Evidence That MDS and AML Cells Exhibit a Differential Capacity To Activate the DNA-Damage Response (DDR) Pathways.

Abrogation of the DNA-Damage Response in De Novo AML Versus MDS Cell Lines.

The EGFR-Inhibitor Erlotinib Induces Apoptosis in Neoplastic Cells of Myelodysplastic Syndrome (MDS) and Acute Myeloid Leukemia (AML), an Effect Determined by the Expression Level of Nucleophosmin (NPM).

Email alerts

ASH Publications

American Society of Hematology

Update search

Email alerts

ASH Publications

American Society of Hematology

This Feature Is Available To Subscribers Only