TMPRSS2-ERG Controls Luminal Epithelial Lineage and Antiandrogen Sensitivity in PTEN and TP53-Mutated Prostate Cancer
Abstract
Purpose: Deletions or mutations in PTEN and TP53 tumor suppressor genes have been linked to lineage plasticity in therapy-resistant prostate cancer. Fusion-driven overexpression of the oncogenic transcription factor ERG is observed in approximately 50% of all prostate cancers, many of which also harbor PTEN and TP53 alterations. However, the role of ERG in lineage plasticity of PTEN/TP53–altered tumors is unclear. Understanding the collective effect of multiple mutations within one tumor is essential to combat plasticity-driven therapy resistance.
Document Details
- Document Type
- Pub Defense Publication
- Publication Date
- Sep 14, 2018
- Source ID
- 10.1158/1078-0432.ccr-18-0653
Entities
People
- Alexandra M. Blee
- Emily Kuehn
- Haojie Huang
- Joseph Dugdale
- Liguo Wang
- Manish Kohli
- Rafael Jimenez
- Tao Ma
- Wanhai Xu
- Yinhui Yang
- Yu Chen
- Yundong He
- Yunqian Pan
- Yuqian Yan
- Zhenqing Ye
Organizations
- Harbin Medical University
- Mayo Clinic
- Mayo Clinic Graduate School of Biomedical Sciences
- Mayo Medical School
- Memorial Sloan Kettering Cancer Center
- National Institutes of Health
- United States Department of Defense