Immune cells in cancer

This study shows that dabrafenib inhibits PMN-MDSC differentiation via GCN2 activation, altering their function and reducing their suppressive activity in tumors.

This study compares agent-based and equation-based models of macrophage polarization to understand their activation dynamics under pro- and anti-inflammatory stimuli.

This study shows EGFR-mutant lung adenocarcinomas exploit alveolar macrophage metabolism via GM-CSF--PPARγ signaling to support tumor growth and EGFR signaling, suggesting new therapeutic strategies combining statins and PPARγ inhibition.

This study shows that TRAIL+ cancer cells use noncanonical TRAIL signaling in MDSCs to promote their abundance and tumor progression in cholangiocarcinoma.

This study modifies myeloid cells to elicit tumor-specific cytotoxicity using chimeric receptors that signal through IgM and bind tumor antigens.

This study identifies hysteresis genes in macrophage polarization and shows that AP-1 and CTCF regulate chromatin state changes during de/repolarization.

This study shows that weight loss in formerly obese mice reduces mammary gland inflammation and fibrosis but does not fully resolve collagen deposition in tumors, suggesting partial microenvironmental recovery.

This paper develops a vascularized tumor model to study TAM recruitment and evaluates a multispecific antibody's effect on monocyte migration and TAM repolarization.

This study uses single-cell RNA sequencing to analyze TAM subtypes and their interactions with T cells in GBM, revealing new ligand-receptor interactions and communication patterns.

This study identifies subtype-specific phenotypic and signaling changes in circulating neutrophils from early breast cancer patients compared to healthy volunteers.

The paper identifies LGALS1 as an immunomodulating target in glioblastoma by analyzing GAM-GBM interactions using single-cell RNA sequencing and zebrafish models.

This study shows that increased myeloid-derived suppressor cells (MDSCs) in mice with renal injury or aging worsen lung inflammation caused by viral pneumonia.

The paper uses a Drosophila model to study tumor-associated macrophages via single-cell RNA-sequencing, identifying distinct hemocyte clusters and their differential gene expression in tumor versus wild-type larvae.

This study shows that targeting ACOD1 enhances the pro-inflammatory state and anti-tumor activity of human CAR-iMACs in solid tumors.

This study shows leucine reduces cytokine storm syndrome in mice by promoting M2 macrophage polarization via the mTORC1/LXRα signaling pathway.

The paper uses ensemble-based genome-scale modeling to predict metabolic differences between M1 and M2 macrophage subtypes in colorectal cancer and identifies metabolic perturbations that shift M2 metabolism toward M1.

This study identifies Cystatin C as a glucocorticoid-responsive factor that recruits Trem2+ macrophages and predicts immunotherapy failure in cancer.

The paper identifies a 338-gene signature of macrophage reactivity and tolerance that predicts disease outcomes across diverse conditions and species.

This study shows that gremlin 1 promotes M2-like polarization of macrophages in response to Th2 cytokines.

This study identifies functionally and metabolically distinct melanoma-associated macrophages originating from common bone-marrow precursors, with implications for targeted therapy.

This study shows RBP-J regulates blood Ly6Clo monocytes and their derived lung macrophages by controlling CCR2 expression.

The paper develops an agent-based model to simulate monocyte differentiation into nurse-like cells in chronic lymphocytic leukemia and identifies patient-specific macrophage phenotypes linked to cancer survival.

The paper develops a computational model of macrophage signaling to predict activation responses to cytokine combinations, revealing a second axis of activation distinct from the M1-M2 polarization.

This study maps the distribution of macrophages in mouse mammary glands across developmental stages using 3D imaging, revealing stage-specific variations and sexual dimorphism.