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.

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