Single-cell RNA sequencing of biopsy samples from advanced-stage lung cancer reveals tumor and immune cell features associated with response to immune checkpoint therapy.

Tumor stiffness blocks T cell migration in tumors.

Targeted therapies induce an aberrant fucosylation of complex tumor secretomes stimulating the expansion of minority drug-resistant clones and promoting therapy resistance.

Downregulation of mitochondrial activity by immunosuppressive tumor-derived soluble factors leads to systemic unresponsiveness to the PD-1 blockade therapy.

A mechanistic mathematical model informed by standard‐of‐care imaging and pathology predicts tumor responses to immunotherapy a priori on a per-patient basis.

Aberrant phosphorylation of tyrosine 78 on Atoh1 via Jak2 is responsible for sonic hedgehog type medulloblastoma growths in vivo.

Bacterial therapy can be impeded by nutrition deprivation in the tumor microenvironment, and enhancing bacteria resistance to iron sequestration enhances its antitumoral activity for therapeutic purposes.

Tregs form an "immunosuppressive ring" around solid tumors that is broken down during adoptive cell therapy and cyclophosphamide combination immunotherapy.

Integrated molecular analysis demonstrated that colorectal cancer can be classified into four molecular subtypes (proliferative, immunomodulatory, immunosuppressed, and immune-excluded subtypes), providing valuable insight into the intricate relationship between tumor microenvironment heterogeneity and various clinical phenotypes.

Analyses of genetically engineered mouse models reveal the androgen receptor-independent properties of a luminal stem/progenitor cell in the prostate epithelium, and its ability to serve as a cell of origin for castration-resistant prostate cancer.