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In This Issue

In the Spotlight


Research Briefs

Colorectal cancer patients receiving KRASG12C and EGFR inhibitors develop resistance alterations that largely converge on ERK reactivation, with KRASG12C amplification standing out as a dominant mechanism that leads to oncogene-induced senescence off drug.

An allele-specific covalent small molecule was identified that selectively reacts with the mutant cysteine Y220C of p53 and leads to the rescue of wild-type thermal stability levels.

Human papillomavirus (HPV) 42 is a novel tumorigenic virus that drives a germ cell–like program conserved in all HPV-driven tumors that distinguishes HPV-driven from mutation-driven tumors and outperforms established clinical markers.

Cell competition triggers displacement of latent metastatic cells from the primary tumor that persist in distal organs and initiate metachronous metastasis.

Research Articles

Savolitinib plus osimertinib combination therapy has an acceptable safety profile and demonstrated antitumor activity in patients with MET-amplified, EGFR-mutated advanced NSCLC who experienced disease progression on prior EGFR tyrosine kinase inhibitor therapy.

This first report of repeatedly dosed intracranial B7-H3 chimeric antigen receptor (CAR) T cells for patients with DIPG includes preclinical efficacy, preliminary clinical tolerability, and serial correlative biospecimen analysis of circulating CAR T cells, cytokine production, and targeted mass spectrometry.

Cancer-specific neoantigens created in the form of a covalent drug conjugated to a fragment of an intracellular oncoprotein selectively mark drug-resistant cancer cells for killing with bispecific T-cell engagers.

Inhibition of Menin–MLL complexes allows tumor-suppressive MLL3/4–UTX chromatin-modifying complexes to bind target gene loci; reactivation of this program with CDK4/6 inhibitors can overcome intrinsic Menin inhibitor resistance.

Mutational scanning in base-edited IDH-mutant leukemia cells uncovered recurrent mutations that disable uncompetitive inhibition, which reveals a new class of pathogenic mutations and mechanisms for resistance to IDH-targeting therapies.

An in vivo screen of a human melanoma transcriptional signature identified a role for free cholesterol in activating an AP-1 metastasis program.

Extranodal B-cell lymphoma founder mutations induce the clonal expansion of a traceable B-cell population reminiscent of that driving autoimmune disorders, setting the stage for early detection and targeted interventions.

News in Brief

News in Depth

Research Watch

Intratumoral Heterogeneity
Clinical Trials
Cell Movement
Prostate Cancer
Gene Expression
Colorectal Cancer
Early Detection
Immune Evasion

Acknowledgment to Reviewers

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