S. K. Knutson

发表

Durable tumor regression in genetically altered malignant rhabdoid tumors by inhibition of methyltransferase EZH2

Tim J. Wigle, R. Copeland, R. Pollock, 2013, Proceedings of the National Academy of Sciences.

The Y641C mutation of EZH2 alters substrate specificity for histone H3 lysine 27 methylation states

Tim J. Wigle, Lei Jin, R. Copeland, 2011, FEBS letters.

Histone Deacetylase 3 Depletion in Osteo/Chondroprogenitor Cells Decreases Bone Density and Increases Marrow Fat

M. McGee-Lawrence, J. Westendorf, S. Hiebert, 2010, PloS one.

Preclinical Evidence of Anti-Tumor Activity Induced by EZH2 Inhibition in Human Models of Synovial Sarcoma

Yonghong Xiao, R. Copeland, A. Grassian, 2016, PloS one.

EPZ011989, A Potent, Orally-Available EZH2 Inhibitor with Robust in Vivo Activity

Tim J. Wigle, R. Copeland, N. Waters, 2015, ACS medicinal chemistry letters.

Reply to "Uveal melanoma cells are resistant to EZH2 inhibition regardless of BAP1 status"

S. Armstrong, N. Kelleher, E. Stanchina, 2016, Nature Medicine.

Loss of BAP1 function leads to EZH2-dependent transformation

S. Armstrong, N. Kelleher, O. Abdel-Wahab, 2015, Nature Medicine.

A selective inhibitor of EZH2 blocks H3K27 methylation and kills mutant lymphoma cells.

Tim J. Wigle, E. Olhava, Lei Jin, 2012, Nature chemical biology.

277 The discovery and pre-clinical development of the first clinical stage EZH2-inhibitor, EPZ-6438 (E7438)

Tim J. Wigle, R. Copeland, R. Pollock, 2014 .

EZH2 Inhibitor EPZ-6438 Synergizes With Anti-Lymphoma Therapies In Preclinical Models

Tim J. Wigle, R. Copeland, R. Pollock, 2013 .

Liver‐specific deletion of histone deacetylase 3 disrupts metabolic transcriptional networks

S. Hiebert, S. Huppert, S. K. Knutson, 2008, The EMBO journal.

Selective Inhibition of EZH2 by EPZ-6438 Leads to Potent Antitumor Activity in EZH2-Mutant Non-Hodgkin Lymphoma

Tim J. Wigle, Yonghong Xiao, R. Copeland, 2014, Molecular Cancer Therapeutics.

The Importance of Being Me: Magic Methyls, Methyltransferase Inhibitors, and the Discovery of Tazemetostat.

R. Copeland, R. Pollock, V. Richon, 2016, Journal of medicinal chemistry.

A687V EZH2 is a gain‐of‐function mutation found in lymphoma patients

Lei Jin, R. Copeland, V. Richon, 2012, FEBS letters.

Coordinated activities of wild-type plus mutant EZH2 drive tumor-associated hypertrimethylation of lysine 27 on histone H3 (H3K27) in human B-cell lymphomas

R. Copeland, R. Pollock, V. Richon, 2010, Proceedings of the National Academy of Sciences.

Deletion of histone deacetylase 3 reveals critical roles in S phase progression and DNA damage control.

D. Cortez, S. Hiebert, Zu-Wen Sun, 2008, Molecular cell.

Reaction coupling between wild-type and disease-associated mutant EZH2.

Lei Jin, R. Copeland, R. Pollock, 2014, ACS chemical biology.

Hdac3 is essential for the maintenance of chromatin structure and genome stability.

Andrew J. Wilson, Christina E. Wells, Zhongming Zhao, 2010, Cancer cell.

Mutant Non-Hodgkin Lymphoma EZH 2 Activity in Selective Inhibition of EZH 2 by EPZ-6438 Leads to Potent Antitumor

Yonghong Xiao, R. Copeland, N. Waters, 2014 .

Selective Killing of SMARCA2- and SMARCA4-deficient Small Cell Carcinoma of the Ovary, Hypercalcemic Type Cells by Inhibition of EZH2: In Vitro and In Vivo Preclinical Models

I. Feldman, R. Copeland, A. Grassian, 2017, Molecular Cancer Therapeutics.

Synergistic Anti-Tumor Activity of EZH2 Inhibitors and Glucocorticoid Receptor Agonists in Models of Germinal Center Non-Hodgkin Lymphomas

R. Copeland, R. Pollock, B. Littlefield, 2014, PloS one.

Méthodes de traitement du cancer

S. K. Knutson, Heike Keilhack, Natalie Warholic, 2013 .

A Medium-Throughput Single Cell CRISPR-Cas9 Assay to Assess Gene Essentiality

J. Moore, R. Copeland, A. Grassian, 2015, Biological Procedures Online.

EZH2 Inhibition by Tazemetostat Results in Altered Dependency on B-cell Activation Signaling in DLBCL

I. Feldman, R. Copeland, A. Raimondi, 2017, Molecular Cancer Therapeutics.

A selective inhibitor of EZH2 blocks H3K27 methylation and kills mutant lymphoma cells.

E. Olhava, Lei Jin, R. Copeland, 2012, Nature chemical biology.

Durable tumor regression in genetically altered malignant rhabdoid tumors by inhibition of methyltransferase EZH2

R. Copeland, R. Pollock, V. Richon, 2013, Proceedings of the National Academy of Sciences.

Deletion of histone deacetylase 3 reveals critical roles in S phase progression and DNA damage control.

D. Cortez, S. Hiebert, Zu-Wen Sun, 2008, Molecular cell.

Hdac3 is essential for the maintenance of chromatin structure and genome stability.

Andrew J. Wilson, Christina E. Wells, M. Washington, 2010, Cancer cell.

Liver‐specific deletion of histone deacetylase 3 disrupts metabolic transcriptional networks

S. Hiebert, S. Huppert, S. K. Knutson, 2008, The EMBO journal.

Selective Inhibition of EZH2 by EPZ-6438 Leads to Potent Antitumor Activity in EZH2-Mutant Non-Hodgkin Lymphoma

Yonghong Xiao, R. Copeland, N. Waters, 2014, Molecular Cancer Therapeutics.

The Importance of Being Me: Magic Methyls, Methyltransferase Inhibitors, and the Discovery of Tazemetostat.

R. Copeland, R. Pollock, V. Richon, 2016, Journal of medicinal chemistry.

Preclinical Characterization of E7438, a Potent, Selective Inhibitor of Protein Methyltransferase EZH2 with Robust Antitumor Activity Against EZH2 Mutated Non-Hodgkin Lymphoma Xenografts in Mice

R. Copeland, R. Pollock, V. Richon, 2012 .