Abstract
Improved clinical outcomes for MM in the last 2 decades have been driven by therapeutics which have limited activity in non-MM neoplasias; do not target specific oncogenic mutations in MM cells, but rather pathways which are critical for plasma cells (PCs), yet dispensable for normal or malignant cells of most other lineages. We performed genome-scale CRISPR gene-editing studies to systematically characterize the molecular vulnerabilities of 19 MM cell lines and define which genes are more pronounced and/or recurrent dependencies for MM vs.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.