Phillip Thienger
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Phillip Thienger has a total of 26 co-authors. Here are the top co-authors by number of shared publications:
- Mark A. Rubin
Department for BioMedical Research, University of Bern, Bern, Switzerland
18 shared publications - Alden King-Yung Leung
School of Life Sciences, The Chinese University of Hong Kong, Hong Kong, China
16 shared publications - Alina Naveed
University of Bern 1 Department for Biomedical Research Bern, Switzerland
16 shared publications - Andrej Benjak
Department for BioMedical Research (DBMR), University of Bern, Bern, Switzerland
16 shared publications - Bence Daniel
Department of Proteomic and Genomic Technologies, Genentech, South San Francisco, USA
16 shared publications - Charlotte Kiu Yan Ng
IRCCS Humanitas Research Hospital, Rozzano, Milan, Italy; Department of Biomedical Sciences, Humanitas University, Pieve Emanuele, Milan, Italy
16 shared publications
Latest Publications
- Open Access
- 2 April 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Figure S5 from A Double-Negative Prostate Cancer Subtype Is Vulnerable to SWI/SNF-Targeting Degrader Molecules
A947-treatment consistently modulates lineage-defining CRPCWNT signature and master TFs
- 2 April 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure S5 from A Double-Negative Prostate Cancer Subtype Is Vulnerable to SWI/SNF-Targeting Degrader Molecules
A947-treatment consistently modulates lineage-defining CRPCWNT signature and master TFs
- Open Access
- 2 April 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Figure S7 from A Double-Negative Prostate Cancer Subtype Is Vulnerable to SWI/SNF-Targeting Degrader Molecules
A947-treatment leads to decreased chromatin accessibility in CRPC-WNT
- 2 April 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure S7 from A Double-Negative Prostate Cancer Subtype Is Vulnerable to SWI/SNF-Targeting Degrader Molecules
A947-treatment leads to decreased chromatin accessibility in CRPC-WNT
- Open Access
- 2 April 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Figure S1 from A Double-Negative Prostate Cancer Subtype Is Vulnerable to SWI/SNF-Targeting Degrader Molecules
Drug screen with SMARCA2/4 degrader
- 2 April 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure S1 from A Double-Negative Prostate Cancer Subtype Is Vulnerable to SWI/SNF-Targeting Degrader Molecules
Drug screen with SMARCA2/4 degrader
- Open Access
- 2 April 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Figure S11 from A Double-Negative Prostate Cancer Subtype Is Vulnerable to SWI/SNF-Targeting Degrader Molecules
TCF7L2 chromatin binding is reduced upon treatment with A947 in CRPC-WNT
- 2 April 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure S11 from A Double-Negative Prostate Cancer Subtype Is Vulnerable to SWI/SNF-Targeting Degrader Molecules
TCF7L2 chromatin binding is reduced upon treatment with A947 in CRPC-WNT
- Open Access
- 2 April 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Figure S3 from A Double-Negative Prostate Cancer Subtype Is Vulnerable to SWI/SNF-Targeting Degrader Molecules
CRPC-WNT organoids are SMARCA4 but not SMARCA2 dependent
- 2 April 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure S3 from A Double-Negative Prostate Cancer Subtype Is Vulnerable to SWI/SNF-Targeting Degrader Molecules
CRPC-WNT organoids are SMARCA4 but not SMARCA2 dependent
- Open Access
- 2 April 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Figure S6 from A Double-Negative Prostate Cancer Subtype Is Vulnerable to SWI/SNF-Targeting Degrader Molecules
CRPC-WNT organoids become deregulated in multiple proliferative pathways upon SMARCA2/4 degradation
- 2 April 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure S6 from A Double-Negative Prostate Cancer Subtype Is Vulnerable to SWI/SNF-Targeting Degrader Molecules
CRPC-WNT organoids become deregulated in multiple proliferative pathways upon SMARCA2/4 degradation
- Open Access
- 2 April 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Figure S12 from A Double-Negative Prostate Cancer Subtype Is Vulnerable to SWI/SNF-Targeting Degrader Molecules
TCF7L2 regulates pro-proliferative pathways in CRPC-WNT
- 2 April 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure S12 from A Double-Negative Prostate Cancer Subtype Is Vulnerable to SWI/SNF-Targeting Degrader Molecules
TCF7L2 regulates pro-proliferative pathways in CRPC-WNT
- Open Access
- 2 April 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Figure S9 from A Double-Negative Prostate Cancer Subtype Is Vulnerable to SWI/SNF-Targeting Degrader Molecules
The TCF7L2 promoter interacts with an intragenic enhancer that is kept accessible by the SWI/SNF complex
- 2 April 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure S9 from A Double-Negative Prostate Cancer Subtype Is Vulnerable to SWI/SNF-Targeting Degrader Molecules
The TCF7L2 promoter interacts with an intragenic enhancer that is kept accessible by the SWI/SNF complex
- Open Access
- 2 April 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Figure S8 from A Double-Negative Prostate Cancer Subtype Is Vulnerable to SWI/SNF-Targeting Degrader Molecules
CRPC-WNT is dependent on TCF7L2
- 2 April 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure S8 from A Double-Negative Prostate Cancer Subtype Is Vulnerable to SWI/SNF-Targeting Degrader Molecules
CRPC-WNT is dependent on TCF7L2