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Nabbi et. al. analyze immunohistochemistry, comprehensive genomic profiling, RNA-sequencing, and TCR-sequencing data from 66 pediatric patients with cancer from a phase 1–2 clinical trial (iMATRIX-atezo) to nominate biomarkers associated with response to immunotherapy in pediatric cancer.
Beltran and colleagues examine the underlying mechanisms behind the observed heterogeneous expression of the prostate cancer drug target and biomarker, PSMA, in castration-resistant prostate cancer, involving regulatory roles of both HOXB13 and AR.
Sun et al. identify the deubiquitinase USP15 as a regulator of PARP1 stability in triple-negative breast cancer and show that the hormone receptors ER, PR and HER2 inhibit USP15-mediated PARP1 stabilization, modulating base excision repair.
Schellenberger and colleagues engineer masked, conditionally active T-cell engagers targeting tumor antigens and CD3 and show potent, protease-dependent antitumor activity in mouse models, as well as safety in non-human primates.
Su et al. find that BACH1 specifically interacts with the p53 (R175H) hotspot mutant. This has double oncogenic effects, leading to increased expression of the pro-metastatic targets of BACH1 as well as blockage of its capacity to activate ferroptosis.
Park et al. show that in the process of metastasis, dying tumor cells enhance the outgrowth of their surviving counterparts via nuclear expulsion, resulting in an extracellular DNA–protein complex that activates RAGE receptors on tumor cells.
Using single-cell and high-dimensional profiling of the immune microenvironment, Vignali and colleagues uncover distinct cell subsets and interactions in human invasive ductal and lobular breast carcinoma, with potential prognostic and therapeutic relevance.
Shi et al. report a sulfonation-dependent vulnerability of liver tumors expressing the sulfotransferase SULT1A1 by showing their sensitivity to the small molecule YC-1 and identifying structurally related compounds that can be modified by SULT1A1.
Turrell et al. show that, in young mice, low-level PDGF-C expression maintains dormancy of disseminated tumor cells, but, in aged or fibrotic lungs, the PDGF-C-high environment promotes proliferation, which can be counteracted with inhibition of PDGFRα or PDGF-C blockade.
Wu et al. report that IFNγ induces the phase separation of KAT8 and IRF1 into condensates that promote PD-L1 upregulation. They further identify a peptide that blocks KAT8–IRF1 condensates, reducing PD-L1 levels and increasing antitumor immunity.
Adler et al. identify granulocyte-derived lipocalin-2 as a mediator of inflammatory astrocyte activation, which in turn facilitates brain metastasis in breast cancer and melanoma.
Coppé and colleagues define a resistance mechanism to combination BRAF- and EGFR-targeted therapy in BRAFV600E colorectal cancers that could be overcome in vitro and in vivo by repurposing COX2 inhibitors.
Fendt and colleagues find that pre-metastatic niche formation and a high-fat diet increase palmitate availability in future organs of metastases and show that breast cancer cells use palmitate to generate acetyl-CoA, acetylate the NF-κB subunit p65 and induce pro-metastatic signaling.
Iavarone and colleagues develop a computational approach called SPINKS to identify master kinases for functional subtypes of human glioblastoma defined using integrated multi-omics data, which show potential as subtype-specific therapeutic targets.
Jäger and colleagues analyze single-base substitution and indel mutational signatures across 27 pediatric cancer types, revealing marked differences in mutational patterns compared with adult cancers and insights into underlying molecular mechanisms.
Lau and colleagues show that the dietary addition of the sugar l-fucose enhances immunotherapy response in melanoma models. This is mediated via the fucosylation and cell surface enrichment of HLA-DRB1 and induction of anti-tumor immunity.
Qiu et al. show that chronic interferon (IFN) stimulation establishes an epigenetic signature of inflammatory memory in tumor cells, resulting in elevated levels of IFN-stimulated genes that sustain immune cell dysfunction when IFN is low.