Abstract：
:The AT-rich interaction domain 1A (ARID1A, also known as BAF250a) is a chromatin remodeling gene, which frequently mutates across a broad spectrum of cancers with loss expression of the ARID1A protein. Recently, the association between ARID1A deficiency and immune checkpoint blockade (ICB) therapy has been reported. ARID1A deficiency contributes to the high microsatellite instability phenotype, increases tumor mutation burden, elevates expression of programmed cell death ligand 1 (PD-L1), and modulates the immune microenvironment, supporting the view that ARID1A loss might serve as a predictive biomarker for ICB. Furthermore, the therapeutic targeting strategies, which show "synthetic lethality" with ARID1A deficiency, exhibit potential synergy with ICB. We collectively reviewed the mechanisms underlying the correlation between ARID1A deficiency and ICB, the predictive function of ARID1A deficiency for ICB, and potential combined strategies of targeting agents, vulnerable for ARID1A deficiency, with ICB in cancer treatment.
journal_name
Cancer Lettjournal_title
Cancer lettersauthors
Hu G,Tu W,Yang L,Peng G,Yang Ldoi
10.1016/j.canlet.2020.01.001subject
Has Abstractpub_date
2020-03-31 00:00:00pages
148-155eissn
0304-3835issn
1872-7980pii
S0304-3835(20)30001-Xjournal_volume
473pub_type
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