In this week's Nature, a team led by scientists from the National Cancer Institute reports on the discovery of genes that are required for certain cancer immunotherapies to be effective and which contribute to drug-resistant tumors. Using a genome-scale CRISPR/Cas9 screen, the team profiled genes whose loss in tumor cells impaired the effector function of CD8-positive T cells (EFT). They uncovered both well-established and novel genes in cancer cells that regulate EFT, and the findings "may serve as a functional blueprint to study the emergence of tumor resistance to T cell-based cancer therapies," they write. GenomeWeb has more on this study, here.
Also in Nature, a Broad Institute-led team describes a novel genome-scale CRISPR/Cas9 activation screen designed to overcome the challenges facing the identification of functional long, noncoding RNA loci. Using the screen — which targeted more than 10,000 lncRNA transcriptional start sites in order to identify noncoding loci that influence a phenotype of interest — the investigators uncovered 11 loci that involved in melanoma resistance to BRAF inhibitors. The work provides "a CRISPR toolkit with which to systematically discover the functions of noncoding loci and elucidate their diverse roles in gene regulation and cellular function," the researchers say.