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

1-5 of 5

Sort by

Sort Order Select

Journal Articles

Mutations At The FLT3 Activation Loop D835 Residue Confer Differential Resistance To Clinically Active FLT3 Inhibitors

Kimberly Lin, BS, Catherine C Smith, MD, Sara Salerno, PharmD, Neil P. Shah, MD, PhD

Blood (2013) 122 (21): 3929.

https://doi.org/10.1182/blood.V122.21.3929.3929

Published: 2013

Journal Articles

Preclinical and Clinical Resistance Mechanisms To The Investigational Selective FLT3 Inhibitor PLX3397 In FLT3-ITD+ Acute Myeloid Leukemia (AML)

Catherine C Smith, MD, Kimberly Lin, BS, Elisabeth Lasater, PhD, Whitney Stewart, BS, Lauren E Damon, Andrew Kasarskis, PhD, Ali Bashir, PhD, Matthew Pendleton, Robert Sebra, Alexander E Perl, MD, Mai H Le, MD, Chao Zhang, PhD, Brian West, Ph.D., Neil P. Shah, MD, PhD

Blood (2013) 122 (21): 3938.

https://doi.org/10.1182/blood.V122.21.3938.3938

Published: 2013

Journal Articles

Crenolanib (CP-868,596) Is a Potent and Selective Type I FLT3 Inhibitor That Retains Activity Against AC220 Resistance-Causing FLT3 Kinase Domain Mutants

Catherine C Smith, MD, Elisabeth Lasater, PhD, Melissa Mccreery, BS, Kimberly Lin, BS, Whitney Stewart, BS, Lauren E Damon, Alexander E Perl, MD, Grace R Jeschke, Mayumi Sugita, MD, Martin Carroll, MD, Scott C. Kogan, MD, Neil Shah, MD, PhD

Blood (2012) 120 (21): 141.

https://doi.org/10.1182/blood.V120.21.141.141

Published: 2012

Journal Articles

Constitutively Activating Mutations At the FLT3 Activation Loop Residue D835 Are Associated with Clinical Resistance to AC220

Catherine C Smith, MD, Jason Chin, PhD, Elisabeth Lasater, PhD, Amy L. Paguirigan, PhD, Kimberly Lin, BS, Whitney Stewart, BS, Sara Salerno, BS, Lauren E Damon, Mark J. Levis, MD, PhD, Alexander E Perl, MD, Kevin Travers, PhD, Andrew Kasarskis, PhD, Jerald P. Radich, MD, Neil Shah, MD, PhD

Blood (2012) 120 (21): 674.

https://doi.org/10.1182/blood.V120.21.674.674

Published: 2012

Journal Articles

Single Molecule Real Time (SMRT™) Sequencing Sensitively Detects the Evolution of Polyclonal and Compound BCR-ABL Mutations in Patients Who Relapse On Kinase Inhibitor Therapy

Catherine C Smith, MD, Michael Brown, PhD, Wendy T Parker, PhD, Kimberly Lin, BS, Kevin Travers, PhD, Susana Wang, Susan Branford, PhD, Neil Shah, MD, PhD

Blood (2012) 120 (21): 917.

https://doi.org/10.1182/blood.V120.21.917.917

Published: 2012

NARROW

Mutations At The FLT3 Activation Loop D835 Residue Confer Differential Resistance To Clinically Active FLT3 Inhibitors

Preclinical and Clinical Resistance Mechanisms To The Investigational Selective FLT3 Inhibitor PLX3397 In FLT3-ITD+ Acute Myeloid Leukemia (AML)

Crenolanib (CP-868,596) Is a Potent and Selective Type I FLT3 Inhibitor That Retains Activity Against AC220 Resistance-Causing FLT3 Kinase Domain Mutants

Constitutively Activating Mutations At the FLT3 Activation Loop Residue D835 Are Associated with Clinical Resistance to AC220

Single Molecule Real Time (SMRT™) Sequencing Sensitively Detects the Evolution of Polyclonal and Compound BCR-ABL Mutations in Patients Who Relapse On Kinase Inhibitor Therapy

Email alerts

ASH Publications

American Society of Hematology

Mutations At The FLT3 Activation Loop D835 Residue Confer Differential Resistance To Clinically Active FLT3 Inhibitors

Preclinical and Clinical Resistance Mechanisms To The Investigational Selective FLT3 Inhibitor PLX3397 In FLT3-ITD+ Acute Myeloid Leukemia (AML)

Crenolanib (CP-868,596) Is a Potent and Selective Type I FLT3 Inhibitor That Retains Activity Against AC220 Resistance-Causing FLT3 Kinase Domain Mutants

Constitutively Activating Mutations At the FLT3 Activation Loop Residue D835 Are Associated with Clinical Resistance to AC220

Single Molecule Real Time (SMRT™) Sequencing Sensitively Detects the Evolution of Polyclonal and Compound BCR-ABL Mutations in Patients Who Relapse On Kinase Inhibitor Therapy

Email alerts

ASH Publications

American Society of Hematology

This Feature Is Available To Subscribers Only