Transgenic mouse models and ex vivo tumoroids, characterized through single-cell RNA sequencing, faithfully recapitulate neuroblastoma cellular identity, offering a useful platform for investigating potential therapeutic strategies.

CLK1 drives intrahepatic cholangiocarcinoma initiation and progression by increasing YAP activity, suggesting that targeting YAP could be a potential strategy for treating and preventing CLK1-driven intrahepatic cholangiocarcinoma.

Characterization of the epigenomic landscape of pancreatic cancer to identify early drivers of tumorigenesis uncovered MICAL2 as a super-enhancer–associated gene critical for tumor progression that represents a potential pharmacologic target.

A hypoxic microenvironment and cancer cells cooperate to induce a senescent fibroblast subset that supports tumor stemness, suggesting that targeting this cancer-associated fibroblast subpopulation is a potential therapeutic strategy to overcome chemoresistance.

B-cell and CD4⁺ T follicular helper cell activation via BAFF/APRIL from abundant myeloid cells in the intracranial tumor microenvironment enables a combinatorial effect of CTLA4 and PD-1 blockade in brain metastases.

SNHG17 cooperates with NF-κB to induce expression of mitochondrial DNA and boost ATP production in breast cancer, suggesting that targeting SNHG17 could reverse metabolic reprogramming to suppress tumor progression.

MTHFD2 regulates cMYC O-GlcNAcylation to promote sunitinib resistance in renal cell carcinoma, highlighting the important role of one-carbon metabolism in sunitinib resistance and proposing therapeutic strategies to improve patient outcomes.

Treating high-mutation burden mice with immunotherapy prior to cancer onset significantly improves survival, raising the possibility of utilizing immune checkpoint blockade for cancer prevention, especially in individuals with increased risk.

Persister cancer cells that survive endocrine therapy exhibit increased energetic dependence upon mitochondria for survival and tumor regrowth potential, indicating that therapies targeting this metabolic dependency could help prevent disease recurrence.

Radiotherapy mediates tumor evolution by leading to the expansion of resistant subclonal cancer cell populations, indicating that developing approaches to target resistant subclones will be crucial to improve radiotherapy response.