Identifying the Molecular Mechanisms of Prostate Tumorigenesis Associated with Multigenic 3p13-14 Locus Loss Using a Novel CRISPR-Organoid Platform
Abstract
Human prostate cancers can feature chromosome-scale alterations, but it remains challenging to determine the causal relationship between these alterations and cancer formation. We established a mouse primary prostate organoid platform to model the large 3p13-14 locus deletion, which typically spans six genes and occurs in 15~20 of prostate cancer patients. We performed multi-omics analysis to study the role of Foxp1, a putative tumor suppressor from this region. To model the loss of the entire locus, we developed a CRISPR editing approach to efficiently generate the large deletions through a single step. We are continuing the analysis of the multi-omics data and the in vivo transplantation of the organoids carrying the desired deletions. Together, our study will provide both mechanistic insight and a comprehensive view about the putative tumor suppressor locus and serve as a paradigm for studying other frequent chromosomal alterations in prostate cancer.
Document Details
- Document Type
- Technical Report
- Publication Date
- Jul 01, 2020
- Accession Number
- AD1108305
Entities
People
- Weiran Feng
Organizations
- Sloan-Kettering Institute