Eri Arai

TL;DR: In this paper, the authors developed an in-vivo T-cell CRISPR screening platform and identified a key mechanism restraining TEFF biology through the ETS family TF, Fli1.

TL;DR: Using a CRISPR-based screen, this article identified the PAR-binding chromatin remodeller ALC1/CHD1L as a key determinant of PARPi toxicity in HR-deficient cells.

TL;DR: Using a CRISPR based screen, this work identifies the PAR-binding Snf2-like ATPase, ALC1/CHD1L, as a key determinant of PARPi toxicity in HR-deficient cells, and establishes PAR-dependent chromatin remodeling as a mechanistically distinct aspect ofPARPi responses, implicating A LC1 inhibition as a new approach to overcome therapeutic resistance in HR -deficient cancers.

TL;DR: In melanoma, transient fluctuations in the molecular state of tumor cells mark the formation of rare cells primed to survive BRAF inhibition and reprogram into a stably drug-resistant fate as discussed by the authors.

TL;DR: This method takes advantage of the heterogeneous in-frame alleles produced following Cas9-mediated DNA cleavage to generate rare alleles that confer resistance to the growth-arrest caused by chemical inhibitors and identifies novel resistance alleles of two lysine methyltransferases, DOT1L and EZH2, which are each essential for the growth of MLL-fusion leukemia cells.