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A druggable genome CRISPR-Cas9 screen followed by functional validation in preclinical lung cancer models uncovers Slc33a1 as a Keap1-mutant-specific targetable dependency.
Zhang and colleagues report that multicellular clusters of circulating tumor cells are more resistant to killing by natural killer (NK) cells through altered NK ligand expression, resulting in polyclonal metastases.
Gui et al. report that tumor-cell-derived factors induce p38a activation in lung fibroblasts, leading to inactivation of type I interferon signaling, matrix remodeling and neutrophil infiltration, thereby generating a metastasis-permissive niche.
Ghorani et al. use a multiomics approach to characterize the effect of tumour mutational burden on the differentiation of CD4 and CD8 T cell subpopulations in non-small cell lung cancer.
Li et al. report that c-Rel, a member of the NF-κB transcription factor family, acts as a checkpoint for antitumor immunity as it promotes the generation of myeloid-derived suppressor cells and its inhibition in myeloid cells suppresses tumor growth.
Aparicio and colleagues identify gene expression changes in breast cancer datasets putatively associated with age-related endocrine effects, suggesting that patient age may influence the prognostic potential of certain biomarkers.
O’Donnell and colleagues report that activation of the integrated stress response in non-small cell lung cancer cells by impairing heme production leads to enhanced PD-L1 translation in an eIF5B-dependent manner.
Reya and colleagues use in vivo CRISPR screens to identify the Stau2 RNA-binding protein as a key regulator of myeloid leukemia growth and progression.
Marra and colleagues describe POG570, a pan-cancer, whole-genome, transcriptome and clinical dataset stressing the molecular interactions in advanced and post-therapy cancer patients.
Simpson et al. present a living biobank of 38 small cell lung cancer circulating-tumor-cell-derived explants and use them to study tumor heterogeneity. These models can be used further to study SCLC biology, progression and therapy responses.
Habib and colleagues show that type 1 IFN signaling is triggered by EGFR inhibition in nonsmall cell lung cancer models and propose EGFR inhibition and IFN-neutralizing antibody as a potential combination therapy approach.
Chandarlapaty and colleagues use longitudinal ctDNA samples to identify genomic alterations in PTEN and ESR1 associated with resistance in a phase I/II trial of a PI3K inhibitor and aromatase inhibition for hormone receptor–positive metastatic breast cancer.
Tran et al. show that environmental glutamine restriction promotes Wnt signaling and intestinal tumorigenesis, whereas supplementation of the metabolite α-ketoglutarate has the reverse effect, reducing tumor growth and extending survival.
Two papers by Schumacher and colleagues and Bousso and colleagues show that sensing of IFN-γ by a small number of tumor cells leads to propagation of IFN-γ sensing and response across a larger fraction of the tumor.
Autry et al. combine genome-wide genomic, epigenetic and transcriptomic analyses in an integrated polygenomic approach to identify mechanisms of glucocorticoid resistance in acute lymphoblastic leukemia.
Two papers by Schumacher and colleagues and Bousso and colleagues show that sensing of IFN-γ by a small number of tumor cells leads to propagation of IFN-γ sensing and response across a larger fraction of the tumor.
Poirier and colleagues have developed a system for in vivo genome editing of patient-derived xenografts using inducible CRISPR-Cas9 and demonstrate applications for modeling gene dependencies and drug resistance.
Amgalan et al. identify BAX as a therapeutic target to prevent chemotherapy-induced cardiotoxicity without affecting the antitumor properties of doxorubicin.
Li and colleagues report that extracellular cGAMP produced by cancer cells acts as an immunotransmitter that, when combined with ionizing radiation, can reduce tumor volume.