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Dysfunctional homologous recombination mediates genomic instability and progression in myeloma.

Abstract：

:A prominent feature of most if not all cancers is a striking genetic instability, leading to ongoing accrual of mutational changes, some of which underlie tumor progression, including acquisition of invasiveness, drug resistance, and metastasis. Thus, the molecular basis for the generation of this genetic diversity in cancer cells has important implications in understanding cancer progression. Here we report that homologous recombination (HR) activity is elevated in multiple myeloma (MM) cells and leads to an increased rate of mutation and progressive accumulation of genetic variation over time. We demonstrate that the inhibition of HR activity in MM cells by small inhibitory RNA (siRNAs) targeting recombinase leads to significant reduction in the acquisition of new genetic changes in the genome and, conversely, the induction of HR activity leads to significant elevation in the number of new mutations over time and development of drug resistance in MM cells. These data identify dysregulated HR activity as a key mediator of DNA instability and progression of MM, with potential as a therapeutic target.

journal_name

Blood

journal_title

Blood

authors

Shammas MA,Shmookler Reis RJ,Koley H,Batchu RB,Li C,Munshi NC

doi

10.1182/blood-2007-05-089193

subject

Has Abstract

pub_date

2009-03-05 00:00:00

pages

2290-7

issue

10

eissn

0006-4971

issn

1528-0020

pii

blood-2007-05-089193

journal_volume

113

pub_type

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