Xinyu Guo
Xinyu Guo has a total of 83 co-authors. Here are the top co-authors by number of shared publications:
- Eneda Toska
Department of Oncology, Sidney Kimmel Comprehensive Cancer Center, Baltimore, USA
36 shared publications - Alejandro V. Villarino
Department of Microbiology and Immunology, Miller School of Medicine, University of Miami, Miami, USA
22 shared publications - Anna Bianchi
University of Miami, Miami, FL
22 shared publications - Austin R. Dosch
Division of Colon & Rectal Surgery, Department of Surgery, University of Miami Miller School of Medicine, Miami, Florida; Sylvester Comprehensive Cancer Center, University of Miami, Miami, Florida
22 shared publications - Ben Z. Stanger
Department of Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA
22 shared publications - Carina Shiau
Massachusetts General Hospital 1 Center for Systems Biology Harvard Medical School, Boston, Massachusetts
22 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