Haoxuan Ying
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Haoxuan Ying has a total of 15 co-authors. Here are the top co-authors by number of shared publications:
- Amanda Day
Center for Advanced Preclinical Research, Center for Cancer Research, Frederick National Laboratory for Cancer Research, Frederick, MD 21701, USA
1 shared publication - Anish Thomas
Developmental Therapeutics Branch, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, MD 20892, USA
1 shared publication - Azam Ghafoor
Division of Hematology/Oncology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, Clinical and Translational Research Center, New York, New York
1 shared publication - Devon Atkinson
Frederick National Laboratory for Cancer Research 6 Center for Advanced Preclinical Research Frederick, Maryland
1 shared publication - Kanak Parmar
National Cancer Institute 9 Developmental Therapeutics Branch, Center for Cancer Research , Bethesda, Maryland
1 shared publication - Katherine Rainsford Calvo
National Institutes of Health 7 Department of Laboratory Medicine, Clinical Center Bethesda, Maryland
1 shared publication
Latest Publications
- 26 June 2026
- Published by American Association for Cancer Research (AACR) in Molecular Cancer Therapeutics
- Vol. 25 (10) , OF1-OF14
HDAC Inhibition Unlocks Tumor Plasticity and Enhances Immunotherapy Response in Myc-Driven Small Cell Lung Cancer
Small cell lung cancer (SCLC) is a highly aggressive malignancy, accounting for approximately 15% of all lung cancer cases. Characterized by low immunogenicity, SCLC may utilize epigenetic mechanisms to evade immune detection. In this study, we demonstrate that entinostat, a class I histone deacetylase inhibitor, upregulates immune-related genes in human SCLC cells. In vivo, we confirmed that entinostat treatment increased the expression of immune checkpoint ligands and antigen presentation machinery in Myc-driven tumors in a Rb1/Trp53/MycT58A (RPM) SCLC mouse model while shifting tumors from a neuroendocrine (NE)-high phenotype to a NE-low phenotype and was associated with increased T-cell infiltration. Notably, combining entinostat with anti–PD-1 immunotherapy suppresses tumor growth and significantly prolongs survival in RPM allograft models. These findings underscore the potential of entinostat to reprogram the NE status of SCLC, enhance immune checkpoint blockade efficacy, and improve therapeutic outcomes.
- 26 June 2026
- Published by American Association for Cancer Research (AACR) in Molecular Cancer Therapeutics
- Vol. 25 (10) , OF1-OF14
HDAC Inhibition Unlocks Tumor Plasticity and Enhances Immunotherapy Response in Myc-Driven Small Cell Lung Cancer
Small cell lung cancer (SCLC) is a highly aggressive malignancy, accounting for approximately 15% of all lung cancer cases. Characterized by low immunogenicity, SCLC may utilize epigenetic mechanisms to evade immune detection. In this study, we demonstrate that entinostat, a class I histone deacetylase inhibitor, upregulates immune-related genes in human SCLC cells. In vivo, we confirmed that entinostat treatment increased the expression of immune checkpoint ligands and antigen presentation machinery in Myc-driven tumors in a Rb1/Trp53/MycT58A (RPM) SCLC mouse model while shifting tumors from a neuroendocrine (NE)-high phenotype to a NE-low phenotype and was associated with increased T-cell infiltration. Notably, combining entinostat with anti–PD-1 immunotherapy suppresses tumor growth and significantly prolongs survival in RPM allograft models. These findings underscore the potential of entinostat to reprogram the NE status of SCLC, enhance immune checkpoint blockade efficacy, and improve therapeutic outcomes.