Issues

Pharmacologic inhibition of Kras^G12D in therapy-refractory models of pancreatic ductal adenocarcinoma promotes deep tumor regressions with alterations in the tumor microenvironment.

Microsatellite instability–high endometrial cancers can be classified by the underlying mechanism of mismatch-repair deficiency, revealing two distinct modes of response to PD-1 immunotherapy.

Ribomethylome profiling of primary acute myeloid leukemia cells uncovered a specific and dynamic rRNA 2′-O-methylation pattern that influences protein translation and thus leukemia stem cell phenotypes and disease progression.

Genomic biomarker profiling of circulating tumor cells enabled by the MinimuMM-seq assay could be used clinically for early diagnosis, monitoring, and management of patients with multiple myeloma with a simple peripheral blood sample.

Development of human bone marrow organoids that capture key cellular, molecular, and architectural features of hematopoietic tissue enables disease modeling and target screening using primary cells from patients with myeloid and lymphoid blood cancers.

OncoLoop is a novel, transcriptomic-based experimental and computational framework for rapid-turnaround coclinical studies to identify and validate drugs for individual patients and their adaptation to clinical practice.

Therapy-induced senescence renders cancer cells highly immunogenic, making them very efficient in triggering protective CD8-dependent antitumor immune responses.

Tumor cells triggered to senesce alter how they send and receive microenvironmental signals, leading to tissue remodeling, immune cell recruitment, hypersensitization to environmental IFNγ, and improved antitumor immunity.

Lysosomal autophagy inhibition (LAI) in cancer induces lipid remodeling that resists cell death associated with lysosomal membrane permeabilization, which can be abrogated by targeting UDP-glucose ceramide glucosyltransferase in the face of LAI.

NG2⁺ mesenchymal stem cells provoke early-stage bone colonization by interacting with tumor cells via N-cadherin–based adhesion, which was strengthened by osteogenesis, thereby linking bone remodeling to metastasis.

Synthetic lethality and mass spectrometry were used to identify novel metabolic vulnerabilities in cancers with IDH1, but not IDH2, mutations that are targetable in the setting of ivosidenib resistance.