Abstract
Multiple myeloma is the second most common hematological malignancy and remains incurable despite recent advances in treatments. A comprehensive understanding of survival signaling pathways that sustain myeloma cells is lacking, partly due to the substantial heterogeneity found within this disease. Among the host of mutations identified in myeloma, oncogenic mutations of KRAS and NRAS are the most common and are associated with inferior patient outcomes. To understand how oncogenic RAS mutations function in the context of myeloma biology, we have employed quantitative mass spectrometry in tandem with genome-wide CRISPR-Cas9 screens in several myeloma lines to discover novel and essential RAS interaction partners.
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