Genomic Instability in Multiple Myeloma.

Autor:	Alagpulinsa DA; Vaccine and Immunotherapy Center, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02129, USA. Electronic address: davida_alagpulinsa@dfci.harvard.edu., Szalat RE; Department of Medical Oncology, Dana Farber Cancer Institute and Harvard Medical School, Boston, MA 02215, USA; Department of Medical Oncology, Boston University School of Medicine, Boston, MA 02118, USA., Poznansky MC; Vaccine and Immunotherapy Center, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02129, USA., Shmookler Reis RJ; Central Arkansas Veterans Healthcare Service, Little Rock, AR 72205, USA; Department of Geriatrics, Reynolds Institute on Aging, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA.
Jazyk:	angličtina
Zdroj:	Trends in cancer [Trends Cancer] 2020 Oct; Vol. 6 (10), pp. 858-873. Date of Electronic Publication: 2020 May 30.
DOI:	10.1016/j.trecan.2020.05.006
Abstrakt:	Genomic instability (GIN), an increased tendency to acquire genomic alterations, is a cancer hallmark. However, its frequency, underlying causes, and disease relevance vary across different cancers. Multiple myeloma (MM), a plasma cell malignancy, evolves through premalignant phases characterized by genomic abnormalities. Next-generation sequencing (NGS) methods are deconstructing the genomic landscape of MM across the continuum of its development, inextricably linking malignant transformation and disease progression with increasing acquisition of genomic alterations, and illuminating the mechanisms that generate these alterations. Although GIN drives disease evolution, it also creates vulnerabilities such as dependencies on 'superfluous' repair mechanisms and the induction of tumor-specific antigens that can be targeted. We review the mechanisms of GIN in MM, the associated vulnerabilities, and therapeutic targeting strategies. (Copyright © 2020 Elsevier Inc. All rights reserved.)
Databáze:	MEDLINE
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