Pembrolizumab activates innate immune metabolism and function in primary human non-small cell lung cancer, whereas Pembrolizumab and beta-glucan synergize in enhancing immune metabolism and tumoridical action in brain-metastasized lung cancer.

Cancer cell antigen presentation, a requirement for immune-mediated tumor rejection, is induced by dihydroorotate dehydrogenase-inhibitor-mediated cancer cell pyrimidine nucleotide depletion via P-TEFb-dependent transcriptional upregulation of MHC-I and related genes.

The peptidoglycan hydrolase activity of Enterococcus faecium secreted antigen A is crucial for cell wall remodeling during bacterial cell separation and generates muropeptides that stimulate host immunity to enhance immune checkpoint inhibitor anti-cancer 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.

DUX4 expression is a common feature of metastatic tumors, where it is significantly associated with immune cell exclusion, decreased objective response to immune checkpoint blockade, and reduced patient survival.

Tim-3 promotes the ubiquitination and degradation of NF90, a novel virus sensor, and negatively regulates the NF90-SG pathway-mediated antiviral innate immunity.

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.

In metastatic NSCLC patients, CHIP showed minimal impact on immunotherapy response but was more prevalent and associated with inflammatory pathways in myeloid cells, particularly in lung squamous cell carcinoma.

Immune checkpoint inhibition therapy for cancer paradoxically activates tuberculosis infection, and advanced human cell culture modelling demonstrates excess TNF-α section is the primary driver.

Tumor stiffness blocks T cell migration in tumors.