Key result
Deletion of the RNA-editing enzyme ADAR1 sensitizes tumors to PD-1 immune checkpoint blockade by promoting interferon-associated innate immune responses.
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ADAR1 is identified as an attractive target to improve treatment response in ICB-resistant patients.
In a recent study in Nature , Ishizuka et al. 1 proposed a new strategy to restore sensitivity to immune checkpoint blockades (ICBs) through the loss of RNA-editing enzyme ADAR1 (adenine deaminase acting on RNA 1). This finding identifies ADAR1 as an attractive target to improve the treatment response in ICB-resistant patient.
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Wang et al. (2019) conducted an editorial in Cancer (Immune Checkpoint Blockade Resistance). ADAR1 deletion was evaluated. Deletion of the RNA-editing enzyme ADAR1 sensitizes tumors to PD-1 immune checkpoint blockade by promoting interferon-associated innate immune responses.
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