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.

Driving melanoma differentiation through G protein-coupled estrogen receptor signaling decreases proliferative capacity, decreases expression of the oncodriver and stem cell marker c-Myc, and increases the effectiveness of immunotherapy.

Tumor immunogenicity is quantified with a novel method, and the resulting tumor immunogenicity score is an effective tumor-inherent biomarker for prediction of response to immune checkpoint inhibitors.

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

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.

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.

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.

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.