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Journal Articles

Selection of RARA-Positive Newly Diagnosed Unfit AML Patients with Elevated RARA Gene Expression Enriches for Features Associated with Primary Resistance to Venetoclax and Clinical Response to SY-1425, a Potent and Selective RARα Agonist, Plus Azacitidine

Christopher Fiore, PhD, Michael J. Kelly, MD MPH, MS, Angela Volkert, Li Zhou, PhD, Kate Madigan, MD, Matthew Eaton, PhD, Graeme Hodgson, PhD, David A. Roth, MD, Qing Kang-Fortner, PhD

Blood (2020) 136 (Supplement 1): 15–16.

https://doi.org/10.1182/blood-2020-137323

Published: 2020

Journal Articles

Sy-1365, a Potent and Selective CDK7 Inhibitor, Exhibits Anti-Tumor Activity in Preclinical Models of Hematologic Malignancies, and Demonstrates Interactions with the BCL-XL/BCL2 Mitochondrial Apoptosis Signaling Pathway in Leukemia

Graeme Hodgson, PhD, Liv Johannessen, PhD, Nisha Rajagopal, PhD, Shanhu Hu, PhD, David Orlando, PhD, Matthew Eaton, PhD, Michael McKeown, PhD, Jeffrey W. Tyner, PhD, Stephen E Kurtz, PhD, Kevin Sprott, PhD, Christian Fritz, PhD, Emmanuelle Di Tomaso, PhD

Blood (2017) 130 (Supplement 1): 2651.

https://doi.org/10.1182/blood.V130.Suppl_1.2651.2651

Published: 2017

Journal Articles

Analysis of the Sub-Clonal Origins of Compound Mutations in Patients with Refractory Ph+ Malignancies Treated with Ponatinib

Justin R. Pritchard, PhD, Michael W. Schmitt, MD PhD, J. Graeme Hodgson, PhD, Stephanie Lustgarten, PhD, Shijie Tang, PhD, Lawrence A. Loeb, MD PhD, Jerald P. Radich, MD, Victor M. Rivera, PhD

Blood (2016) 128 (22): 1061.

https://doi.org/10.1182/blood.V128.22.1061.1061

Published: 2016

Journal Articles

Emergence of Sub-Clonal Drug Resistance Mutations during CML Therapy

Michael W. Schmitt, MD PhD, Justin R. Pritchard, PhD, Graeme Hodgson, PhD, Victor M. Rivera, PhD, Bella I. Aminov, Lan Beppu, Lawrence A. Loeb, MD PhD, Jerald P. Radich

Blood (2015) 126 (23): 478.

https://doi.org/10.1182/blood.V126.23.478.478

Published: 2015

Journal Articles

Comparative TKI Profiling Analyses to Explore Potential Mechanisms of Ponatinib-Associated Arterial Thrombotic Events

Victor M. Rivera, PhD, Justin R. Pritchard, PhD, Francois Gonzalvez, PhD, Theresa Baker, Joseph M. Gozgit, PhD, Graeme Hodgson, PhD

Blood (2014) 124 (21): 1783.

https://doi.org/10.1182/blood.V124.21.1783.1783

Published: 2014

Journal Articles

Additional BCR-ABL1 Mutations Identified By Sensitive Mass Spectrometry In Chronic Phase CML Patients With T315I Treated With Ponatinib Are Associated With Relatively Inferior Responses and Outcome

Wendy T Parker, PhD, Alexandra L Yeoman, BSc, Haley Altamura, BSc, Nicola Roberts, BSc, David T Yeung, BSc, MBBS, FRACP, FRCPA, Bronte A Jamison, BSc, Chani Field, BSc, Stephanie Lustgarten, PhD, Graeme Hodgson, PhD, Victor M. Rivera, PhD, Timothy P. Hughes, MD, MBBS, Susan Branford, PhD

Blood (2013) 122 (21): 651.

https://doi.org/10.1182/blood.V122.21.651.651

Published: 2013

Journal Articles

Impact Of Baseline (BL) Mutations, Including Low-Level and Compound Mutations, On Ponatinib Response and End Of Treatment (EOT) Mutation Analysis In Patients (Pts) With Chronic Phase Chronic Myeloid Leukemia (CP-CML)

Blood (2013) 122 (21): 652.

https://doi.org/10.1182/blood.V122.21.652.652

Published: 2013

NARROW

Selection of RARA-Positive Newly Diagnosed Unfit AML Patients with Elevated RARA Gene Expression Enriches for Features Associated with Primary Resistance to Venetoclax and Clinical Response to SY-1425, a Potent and Selective RARα Agonist, Plus Azacitidine

Sy-1365, a Potent and Selective CDK7 Inhibitor, Exhibits Anti-Tumor Activity in Preclinical Models of Hematologic Malignancies, and Demonstrates Interactions with the BCL-XL/BCL2 Mitochondrial Apoptosis Signaling Pathway in Leukemia

Analysis of the Sub-Clonal Origins of Compound Mutations in Patients with Refractory Ph+ Malignancies Treated with Ponatinib

Emergence of Sub-Clonal Drug Resistance Mutations during CML Therapy

Comparative TKI Profiling Analyses to Explore Potential Mechanisms of Ponatinib-Associated Arterial Thrombotic Events

Additional BCR-ABL1 Mutations Identified By Sensitive Mass Spectrometry In Chronic Phase CML Patients With T315I Treated With Ponatinib Are Associated With Relatively Inferior Responses and Outcome

Impact Of Baseline (BL) Mutations, Including Low-Level and Compound Mutations, On Ponatinib Response and End Of Treatment (EOT) Mutation Analysis In Patients (Pts) With Chronic Phase Chronic Myeloid Leukemia (CP-CML)

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ASH Publications

American Society of Hematology

Selection of RARA-Positive Newly Diagnosed Unfit AML Patients with Elevated RARA Gene Expression Enriches for Features Associated with Primary Resistance to Venetoclax and Clinical Response to SY-1425, a Potent and Selective RARα Agonist, Plus Azacitidine

Sy-1365, a Potent and Selective CDK7 Inhibitor, Exhibits Anti-Tumor Activity in Preclinical Models of Hematologic Malignancies, and Demonstrates Interactions with the BCL-XL/BCL2 Mitochondrial Apoptosis Signaling Pathway in Leukemia

Analysis of the Sub-Clonal Origins of Compound Mutations in Patients with Refractory Ph+ Malignancies Treated with Ponatinib

Emergence of Sub-Clonal Drug Resistance Mutations during CML Therapy

Comparative TKI Profiling Analyses to Explore Potential Mechanisms of Ponatinib-Associated Arterial Thrombotic Events

Additional BCR-ABL1 Mutations Identified By Sensitive Mass Spectrometry In Chronic Phase CML Patients With T315I Treated With Ponatinib Are Associated With Relatively Inferior Responses and Outcome

Impact Of Baseline (BL) Mutations, Including Low-Level and Compound Mutations, On Ponatinib Response and End Of Treatment (EOT) Mutation Analysis In Patients (Pts) With Chronic Phase Chronic Myeloid Leukemia (CP-CML)

Email alerts

ASH Publications

American Society of Hematology

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