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In This Issue

In the Spotlight

Cancer Hallmarks Review


Research Articles

Genetic coalterations in KEAP1, SMARCA4, and CDKN2A were revealed as major independent determinants of KRASG12C inhibitor clinical outcomes in advanced non–small cell lung cancer that together allow for patient segregation into prognostic subgroups.

A genomic investigation of 3,600 small cell lung cancer (SCLC) tumors reveals novel rare cohorts with potential therapeutic importance, biopsy site–specific heterogeneity, and new insights into SCLC histologic transformation.

Models of pediatric high-grade glioma reveal genotype–phenotype associations, differences in cell type composition, and sensitivity to targeted and combination therapy approaches, making preclinical evaluation of a precision therapy approach possible.

Metabolic rewiring of liver metabolism by extrahepatic tumors via innate immune cells occurs at the early disease stage, promoting tumor progression and cancer-related systemic manifestations, such as weight loss.

Continuous type I interferon signaling that is mediated by the transcriptional regulator EGR2 fuels CAR T-cell dysfunction and points to the EGR2–type I interferon axis as a therapeutic vulnerability to improve efficacy of CAR T-cell therapy.

Mitophagy modulators like MFN2 drive BH3-mimetic resistance in acute myeloid leukemia (AML), and genetic or pharmacologic inhibition of MFN2 improved leukemia cell elimination both in vitro and in preclinical AML patient-derived models.

The expression of splicing factor SRSF1 is tightly regulated to maintain pancreas homeostasis, and dysregulated SRSF1 induces pancreatitis and accelerates KRASG12D-mediated tumor progression through alternative splicing.

The epigenetic modifier PADI4, which has a role in the immune recognition of proteins, is not transactivated by several p53 hypomorphs, including the African-specific genetic variant Y107H, but plays a key role in tumor suppression by p53.

FLT3 mutations in acute myeloid leukemia drive an aggressive phenotype, but a critical vulnerability mediated by C/EBPα regulation of lipid metabolism offers new avenues for targeted therapies that leverage the synthetic lethality of ferroptosis induction and FLT3 inhibition.

News in Brief

Research Watch

Prostate Cancer
Disease Progression
Barrett Esophagus
Bladder Cancer
RNA Stability
Immune Evasion
Clinical Trial
Breast Cancer
Cell Plasticity


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