Abstract
Genomic instability, a hallmark of almost all cancers, originates from the combined effects of a deregulated DNA damage response, DNA repair defects, and a failure of cell-cycle checkpoints before the damaged DNA is propagated to daughter cells [1]. Alterations in this network of genomic integrity-preserving pathways lead to the accumulation of mutations, aneuploidy, and chromosomal alterations, the main causes of cancer. Multiple myeloma (MM) is a clonal malignancy of terminally differentiated plasma cells that reside and expand in the bone marrow. MM cells are characterized by a high aneuploidy incidence and recurrent structural chromosomal alterations, features that reflect these cells' underlying genomic instability [2].
Original language | English (US) |
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Pages (from-to) | 73-74 |
Number of pages | 2 |
Journal | Oncoscience |
Volume | 4 |
Issue number | 7-8 |
DOIs | |
State | Published - 2017 |
Keywords
- DNA damage
- Genomic instability
- Multiple myeloma
- RNA-binding proteins
ASJC Scopus subject areas
- Oncology
- Cancer Research