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Alimonti and colleagues show that coordinated activation of the Akt/mTOR and MNK/eIF4E pathways rewires the prostate cancer translatome to secrete HGF, SPP1 and BGN and recruit suppressive myeloid cells, which can be therapeutically targeted.
Jia and colleagues profile human glioblastoma samples and identify a population of macrophages characterized by Siglec-9 that drives immune evasion and immunotherapy resistance via restriction of T-cell priming. Their therapeutic elimination synergizes with immunotherapy.
Mota et al. show that poor response to immune checkpoint blockade in mouse models of ALK-rearranged NSCLC can be overcome by vaccination with an immunogenic ALK peptide and identify immunogenic human ALK peptides for future translational study.
Using genetically engineered models, Genovese and colleagues study patterns of convergent evolution in renal cancer, and pinpoint dysregulation of interferon signaling as a means of adaptation to chromosomal instability in metastatic progression.
Sorger and colleagues present Orion, a technique to analyze H&E histology and multiplex immunofluorescence imaging data from the same cells, which they apply to human colorectal cancer samples to identify spatial biomarkers of disease progression.
Xiong et al. engineer CAR T cells to express the c-Kit D816V mutation, which enhances antigen-dependent proliferation and cytotoxicity, translates into extended survival in solid tumor models and is controllable by tyrosine kinase inhibitors.
Zhou et. al. report the interim results of the randomized phase III GEMSTONE-302 trial, showing the overall survival benefits of first-line treatment with the PD-L1 inhibitor sugemalimab versus placebo in combination with chemotherapy, in patients with NSCLC.
Sung et. al. identify genetic, molecular and clinical risk factors for immune-related adverse events in multicancer cohorts of patients treated with checkpoint inhibitors and develop predictive models that they validate in an independent cohort.
Adachi et al. describe a mechanism of adaptive resistance to KRAS G12C inhibitors which involves a Scribble mis-localization via palmitoylation and subsequent YAP and MRAS activation that leads to feedback reactivation of MAPK signaling.
Hagenbeek et al. identify a small-molecule pan-TEAD inhibitor that blocks the interaction between YAP/TAZ and TEAD proteins. They demonstrate that treatment with the inhibitor leads to antitumor activity and can synergize with KRAS G12C inhibition.
Malladi and colleagues show that inhibiting DRP1 limits mitochondrial plasticity, resulting in increased mitochondrial fusion, impaired fatty acid oxidation and reduced metastasis formation in breast cancer models.
Bousso and colleagues show that IFN-γ production is the dominant tumor elimination mechanism exerted by CD4+ CAR T cells and define tumor cell sensitivity to IFN-γ as a determinant of CD4+ CAR T efficacy.
Mitsiades and colleagues utilize functional genomics data in over 700 cancer cell lines, to identify genes with preferentially essential functions in multiple myeloma, which may represent targets for precision medicine strategies.
Joyce and colleagues use bulk and single-cell profiling of T cell phenotypes in human samples from primary brain tumors and brain metastases as a resource for understanding the biology and therapeutic relevance of the brain tumor microenvironment.
Merbl and colleagues demonstrate that high expression of the proteasome regulator PSME4 is associated with immune-cold lung tumors and reduced antitumor immune responses, by functioning to modulate the protein degradome and antigen diversity.
Watson et al. demonstrate that astrocyte mitochondria can be horizontally transferred to glioblastoma cells in a GAP43-dependent manner, leading to changes in mitochondrial respiration and metabolism that promote proliferation and tumor growth.
Culbertson et al. profile antisense RNAs using a newly developed computational pipeline and identify NQO1-AS as contributor to breast cancer progression and lung metastasis through regulation of the redox enzyme NQO1.
Ruscetti and colleagues show that the pancreatic cancer tumor microenvironment suppresses immune surveillance following therapy-induced senescence via repression of inflammatory gene expression through EZH2.