Artificial intelligence agents may have a transformative effect on how biological research is performed.

Acetate accumulation and metastasis of hepatocarcinoma cells is driven by a metabolic interaction involving HCC-derived lactate and acetate secretion from tumour-associated macrophages.

Cheung et al. describe efficient T cell control of nascent neoantigen+ and nearby neoantigen-negative sarcoma cells, underlying a ∼50% reduction in tumor penetrance. This otherwise imperceptible immunoediting process is revealed by time-resolved profiling of autochthonously arising, muscle-derived sarcoma cells expressing fluorescent reporter-embedded model T cell antigens within the native tissue environment.

Clonal hematopoiesis (CH), an expansion of hematopoietic clones harboring somatic mutations, is common in patients with solid tumors and associates with poor outcomes. In this issue of Cancer Cell, a study shows that, in response to immunotherapy, TET2-mutant CH enhances macrophage antigen presentation and CD8⁺ T cell activation, thereby improving therapeutic efficacy.

Randomly acquired mutations face strong negative selection, except on certain cancer-promoting backgrounds.

A natural experiment found that herpes zoster vaccination reduced the occurrence of mild cognitive impairment and deaths due to dementia, indicating that the vaccine may slow the progression of dementia throughout its clinical disease course.

Artificial intelligence promises rapid and polite feedback on papers — but we must first review the reviewer.

MiTEs are myeloid-targeted immunocytokine prodrugs that block TREM2+ tumor-associated macrophages while activating cytotoxic lymphocytes via TME-specific IL-2 activity, eliciting strong anti-tumor efficacy in preclinical models with minimal systemic toxicity.

Immunosuppressive monocyte-derived macrophages are key targets in cancer therapy; however, the mechanisms of their replenishment and functional plasticity remain elusive. In a recent issue of Nature, Hedge et al. challenge the conventional view that immunosuppressive macrophages are acquired exclusively through tumor microenvironment reprogramming; instead, their study demonstrates that the developmental fate of these macrophages is predisposed in the bone marrow.

Triple-negative breast cancer (TNBC) is characterized by high risks of relapse or metastatic disease. Mattavelli et al. identify a chemokine axis that recruits immunosuppressive monocytes to tumor-dra...

Bi et al. describe cell-type-specific transcriptional signatures of interferon (IFN) signaling in renal cell carcinoma (RCC) tumors and examine effects on immunotherapy outcomes. They find that myeloid IFNγ signaling, but not tumor IFNγ signaling, predicts poor outcomes in clinical trial cohorts, pointing to myeloid cells as mediators of IFN-driven immunotherapy resistance in RCC.

Tu et al. present a systematic analysis of the tumor microenvironment across 14,837 breast cancers, identifying distinct cellular patterns that predict disease-specific survival independently of genomic and intrinsic subtypes. Characterizing microenvironment composition may provide critical prognostic markers that can complement current molecular classification for treatment selection and preventing recurrence.

Triple-negative breast cancer (TNBC) is characterized by high risks of relapse or metastatic disease. Mattavelli et al. identify a chemokine axis that recruits immunosuppressive monocytes to tumor-draining lymph nodes. By co-targeting this recruitment, the TNBC response to immune checkpoint blockade is augmented and metastasis to the lung is reduced.

Lamkanfi, Shirasaki, Izawa and colleagues show that IL-1β release in human monocytes stimulated with lipopolysaccharide or carrying NLRP3 activatory mutations is mostly restricted to cells undergoing…

By sidestepping Cas9 immunogenicity, the StealTHY CRISPR platform enables immune-compatible in vivo genetic screens, directly translatable to humanized cancer models. Using this immune-stealth strategy allows for the discovery of metastatic drivers and reveals the AMH-AMHR2 axis as a clinically actionable pathway for dampening carcinoma metastasis.