Abstract
Recurrent chromosomal aberrations are the main hallmark of multiple myeloma (MM). A recent large scale genome-wide analysis has unveiled that the co-occurrence of 17p13(del) and 1q21(amp) lesions constitute a novel high-risk disease group. Within 17p13, lies TP53 that maintains the genomic integrity by keeping the double stranded DNA damage (DSB) pathway in check. On the other hand, ADAR1 is a critical gene within 1q21 and we have recently reported that its direct RNA editing mechanism on NEIL1 (base-excision repair (BER) gene) caused defective single stranded DNA breaks (SSB) repair, resulting in CHK1 activation.
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