Peihua Zhao
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Peihua Zhao has a total of 53 co-authors. Here are the top co-authors by number of shared publications:
- Alexis Battle
Department of Biomedical Engineering, Johns Hopkins University, Baltimore, MD, USA
13 shared publications - Amaia Arruabarrena-Aristorena
Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, New York
13 shared publications - Candice Stoudmann
Swiss Institute for Experimental Cancer Research (ISREC), School of Life Sciences, EPFL, Lausanne, Switzerland
13 shared publications - Christina S. Leslie
Computational and Systems Biology Program, Memorial Sloan Kettering Cancer Center, New York, USA
13 shared publications - Emiliano Cocco
Sylvester Comprehensive Cancer Center, University of Miami Miller School of Medicine, Miami, USA
13 shared publications - Eneda Toska
Department of Oncology, Sidney Kimmel Comprehensive Cancer Center, Baltimore, USA
13 shared publications
Latest Publications
- Open Access
- 2 March 2026
- Published by American Association for Cancer Research (AACR)
Figure S9 from The Histone Methyltransferase KMT2D Is a Critical Mediator of Lineage Plasticity and Therapeutic Response in Castration-Resistant Prostate Cancer
Immunohistochemical staining of CRPC-SCL models
- 2 March 2026
- Published by American Association for Cancer Research (AACR)
Open AccessFigure S9 from The Histone Methyltransferase KMT2D Is a Critical Mediator of Lineage Plasticity and Therapeutic Response in Castration-Resistant Prostate Cancer
Immunohistochemical staining of CRPC-SCL models
- Open Access
- 2 March 2026
- Published by American Association for Cancer Research (AACR)
Figure S2 from The Histone Methyltransferase KMT2D Is a Critical Mediator of Lineage Plasticity and Therapeutic Response in Castration-Resistant Prostate Cancer
KMT2D regulates AR response in AR-high patient derived organoid models and clinical samples from patient cohorts
- 2 March 2026
- Published by American Association for Cancer Research (AACR)
Open AccessFigure S2 from The Histone Methyltransferase KMT2D Is a Critical Mediator of Lineage Plasticity and Therapeutic Response in Castration-Resistant Prostate Cancer
KMT2D regulates AR response in AR-high patient derived organoid models and clinical samples from patient cohorts
- Open Access
- 2 March 2026
- Published by American Association for Cancer Research (AACR)
Figure S5 from The Histone Methyltransferase KMT2D Is a Critical Mediator of Lineage Plasticity and Therapeutic Response in Castration-Resistant Prostate Cancer
AR-low prostate cancer models exhibit loss of AP-1/YAP TAZ binding and a decrease in AR gene expression upon KMT2D knockdown
- 2 March 2026
- Published by American Association for Cancer Research (AACR)
Open AccessFigure S5 from The Histone Methyltransferase KMT2D Is a Critical Mediator of Lineage Plasticity and Therapeutic Response in Castration-Resistant Prostate Cancer
AR-low prostate cancer models exhibit loss of AP-1/YAP TAZ binding and a decrease in AR gene expression upon KMT2D knockdown
- Open Access
- 2 March 2026
- Published by American Association for Cancer Research (AACR)
Figure S6 from The Histone Methyltransferase KMT2D Is a Critical Mediator of Lineage Plasticity and Therapeutic Response in Castration-Resistant Prostate Cancer
Mapping single cell transcriptional signatures regulated by KMT2D in AR-low prostate cancer
- 2 March 2026
- Published by American Association for Cancer Research (AACR)
Open AccessFigure S6 from The Histone Methyltransferase KMT2D Is a Critical Mediator of Lineage Plasticity and Therapeutic Response in Castration-Resistant Prostate Cancer
Mapping single cell transcriptional signatures regulated by KMT2D in AR-low prostate cancer
- Open Access
- 2 March 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Data 2 from The Histone Methyltransferase KMT2D Is a Critical Mediator of Lineage Plasticity and Therapeutic Response in Castration-Resistant Prostate Cancer
Top enriched pathways upon DHT treatment, PI3K inhibition and the combination with KMT2D knockdown in LNCaP AR-high cells
- 2 March 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Data 2 from The Histone Methyltransferase KMT2D Is a Critical Mediator of Lineage Plasticity and Therapeutic Response in Castration-Resistant Prostate Cancer
Top enriched pathways upon DHT treatment, PI3K inhibition and the combination with KMT2D knockdown in LNCaP AR-high cells
- Open Access
- 2 March 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Data 1 from The Histone Methyltransferase KMT2D Is a Critical Mediator of Lineage Plasticity and Therapeutic Response in Castration-Resistant Prostate Cancer
Top enriched pathways upon DHT treatment and PI3K inhibition in LNCaP AR-high cells
- 2 March 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Data 1 from The Histone Methyltransferase KMT2D Is a Critical Mediator of Lineage Plasticity and Therapeutic Response in Castration-Resistant Prostate Cancer
Top enriched pathways upon DHT treatment and PI3K inhibition in LNCaP AR-high cells
- Open Access
- 2 March 2026
- Published by American Association for Cancer Research (AACR)
Figure S4 from The Histone Methyltransferase KMT2D Is a Critical Mediator of Lineage Plasticity and Therapeutic Response in Castration-Resistant Prostate Cancer
AR-low prostate cancer models display loss of AP-1/YAP TAZ binding profiles and downregulation of AR gene expression profiles with KMT2D knockdown
- 2 March 2026
- Published by American Association for Cancer Research (AACR)
Open AccessFigure S4 from The Histone Methyltransferase KMT2D Is a Critical Mediator of Lineage Plasticity and Therapeutic Response in Castration-Resistant Prostate Cancer
AR-low prostate cancer models display loss of AP-1/YAP TAZ binding profiles and downregulation of AR gene expression profiles with KMT2D knockdown
- Open Access
- 2 March 2026
- Published by American Association for Cancer Research (AACR)
Figure S7 from The Histone Methyltransferase KMT2D Is a Critical Mediator of Lineage Plasticity and Therapeutic Response in Castration-Resistant Prostate Cancer
CRPC-SCL models exhibit heterogeneity in lineage marker expression
- 2 March 2026
- Published by American Association for Cancer Research (AACR)
Open AccessFigure S7 from The Histone Methyltransferase KMT2D Is a Critical Mediator of Lineage Plasticity and Therapeutic Response in Castration-Resistant Prostate Cancer
CRPC-SCL models exhibit heterogeneity in lineage marker expression
- Open Access
- 2 March 2026
- Published by American Association for Cancer Research (AACR)
Figure S8 from The Histone Methyltransferase KMT2D Is a Critical Mediator of Lineage Plasticity and Therapeutic Response in Castration-Resistant Prostate Cancer
Multiplex Immunofluorescence staining in CRPC-SCL models
- 2 March 2026
- Published by American Association for Cancer Research (AACR)
Open AccessFigure S8 from The Histone Methyltransferase KMT2D Is a Critical Mediator of Lineage Plasticity and Therapeutic Response in Castration-Resistant Prostate Cancer
Multiplex Immunofluorescence staining in CRPC-SCL models
- Open Access
- 2 March 2026
- Published by American Association for Cancer Research (AACR)
Figure S10 from The Histone Methyltransferase KMT2D Is a Critical Mediator of Lineage Plasticity and Therapeutic Response in Castration-Resistant Prostate Cancer
KMT2D regulates luminal and stem cell like identity in AR-low prostate cancer
- 2 March 2026
- Published by American Association for Cancer Research (AACR)
Open AccessFigure S10 from The Histone Methyltransferase KMT2D Is a Critical Mediator of Lineage Plasticity and Therapeutic Response in Castration-Resistant Prostate Cancer
KMT2D regulates luminal and stem cell like identity in AR-low prostate cancer