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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.
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.
Bodenmiller and colleagues pair imaging mass cytometry with data from the METABRIC cohort to define single-cell phenotypic and genomic features of breast cancer with spatial context, finding associations with breast cancer subtypes and prognosis.
Stewart et al. use circulating tumor cell-derived xenografts from patients with small-cell lung cancer to study tumor heterogeneity following the onset of therapeutic resistance.
Marais and colleagues report that checkpoint inhibitor treatment of patients with melanoma leads to dynamic changes in peripheral T cells and expansion of immune effector cells. This awakening of the immune system occurs early after treatment and could be exploited in the clinic.
Kupper and colleagues introduce the T-cell fraction as a molecular assessment of T-cell-mediated antitumor responses in primary melanomas that can predict metastatic recurrence.
Cong et al. show that MTSS1 suppresses breast cancer initiation by promoting ubiquitin-mediated suppression of the NF-κB pathway. Loss of this regulatory mechanism promotes the activation and expansion of tumor-initiating cells.
Diehn and colleagues report that assaying circulating DNA in patients receiving chemoradiation therapy for non-small-cell lung cancer could identify the patients most likely to benefit from consolidation immunotherapy.
Anagnostou et al. present an improved predictor of response to immune checkpoint blockade that integrates estimates of tumor mutational burden corrected for tumor purity, RTK genomic alterations, a smoking-related mutational signature and HLA status.
Ryan and colleagues analyze genomic features in tumors from African Americans and European Americans and find that homologous recombination deficiency is more prevalent in African Americans.
Iacobuzio-Donahue and colleagues use integrated transcriptomic, histologic and mutational data to analyze squamous features of pancreatic ductal adenocarcinoma (PDAC), further refining the understanding of heterogeneity and evolution in PDAC.
Ajona and colleagues report that short-term starvation synergizes with anti-PD-1 blockade to reduce lung tumor growth and metastasis. This antitumor effect is mediated through the reduction of plasma IGF-1 levels and IGF-1R levels on tumor cells.
The authors identify a population of L1CAM-positive cells that, following loss of epithelial integrity, promote intestinal tissue regeneration and mediate metastasis initiation and chemoresistance in colorectal cancer.
Ribas and colleagues report that inhibition of PAK4 improves response to anti-PD-1 immunotherapy by reducing Wnt pathway activation and increasing tumor infiltration by T cells.