Further strengthening its suppressive role in MM pathobiology, analysis of publicly available genome-scale, pooled CRISPR-Cas9 loss-of viability screens (DepMap portal 23Q2 release) showed that TENT5C ablation results in an extremely significant, MM-specific proliferative advantage ( Figure 1B ).
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TENT5C/FAM46C modulation <i>in vivo</i> reveals a trade-off between antibody secretion and tumor growth in multiple myeloma.
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