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HDAC6 inhibitor ACY-1215 enhances STAT1 acetylation to block PD-L1 for colorectal cancer immunotherapy.
Cancer Immunol Immunother
January 2024
Cancer Research Institute, School of Basic Medical Science, Central South University, Changsha, Hunan, China.
The search for effective combination therapy with immune checkpoint inhibitors (ICI) has become important for cancer patients who do not respond to the ICI well. Histone deacetylases (HDACs) inhibitors have attracted wide attention as anti-tumor agents. ACY-1215 is a selective inhibitor of HDAC6, which can inhibit the growth of a variety of tumor.
View Article and Find Full Text PDFReply to: Ricolinostat is not a highly selective HDAC6 inhibitor.
Nat Cancer
June 2023
Department of Hematology and Medical Oncology, Emory University School of Medicine, Atlanta, GA, USA.
Ricolinostat is not a highly selective HDAC6 inhibitor.
Nat Cancer
June 2023
Yale University School of Medicine, New Haven, CT, USA.
First-in-Class Selective HDAC6 Inhibitor (ACY-1215) Has a Highly Favorable Safety Profile in Patients with Relapsed and Refractory Lymphoma.
Oncologist
March 2021
Division of Hematology and Oncology, Columbia University Irving Medical Center, New York, New York, USA.
Lessons Learned: Oral selective HDAC6 inhibitors could allow for decreased toxicity compared to pan-class inhibitors, and increased ease of use. ACY-1215 is well tolerated and led to disease stabilization in 50% of patients treated on a twice-daily dosing schedule. Rational drug combinations with ACY-1215 improve efficacy in patients with lymphoma.
View Article and Find Full Text PDFHDAC6 Inhibition Alleviates CLL-Induced T-Cell Dysfunction and Enhances Immune Checkpoint Blockade Efficacy in the Eμ-TCL1 Model.
Front Immunol
July 2021
Department of Immunology, H. Lee Moffitt Cancer Center & Research Institute, Tampa, FL, United States.
Development of chronic lymphocytic leukemia (CLL) is associated with severe immune dysfunction. T-cell exhaustion, immune checkpoint upregulation, and increase of regulatory T cells contribute to an immunosuppressive tumor microenvironment. As a result, CLL patients are severely susceptible to infectious complications that increase morbidity and mortality.
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