Immune cells in cancer

This study shows paclitaxel induces MenaINV in breast cancer cells by repolarizing tumor-associated macrophages, enhancing metastasis.

This study shows that inhibiting glutamine metabolism with JHU083 reduces tumor progression by altering macrophage polarization in immunocompetent mouse models.

This study shows that dermal macrophages can maintain functional diversity without monocyte replenishment, but require monocytes during bacterial infections.

The paper uses single-cell RNA sequencing to study myeloid cell repopulation after chemotherapy in mice, identifying a neutrophil-like monocyte subset with immunosuppressive and pro-tumor activities.

This study shows tumor-associated macrophages promote tumor innervation and spinal cord repair through neural growth and mTORC2 signaling.

This study identifies a signaling pathway in macrophages where ionizing radiation induces mitochondrial fragmentation and cGAS activation, leading to proinflammatory activation, which is modulated by the P2Y2 purinergic receptor.

This study shows eosinophils inhibit CRC metastasis by blocking SPP1+ macrophage differentiation, using transcriptomics and a murine model.

This study identifies a SOX2-CCL2-IL1 pathway that drives immune suppression in precancerous epithelial dysplasia, promoting malignant transformation.

The paper identifies CD226high macrophages derived from MDP monocytes as a new myeloid cell type involved in lipid metabolism regulation across tissues.

The paper uses multi-omics analysis to show macrophages in breast tumors correlate with better treatment response but worse survival, driven by immune suppression mechanisms.

This study identifies SPP1+ tumor-associated macrophages as a key driver of radioresistance in nasopharyngeal carcinoma through interactions with the tumor microenvironment.

The paper identifies a novel Cdkn2a-positive tumor-associated macrophage population in brain tumors using scRNA-seq data, linking it to poor prognosis in glioblastoma.

The paper uses ensemble machine learning on metabolomic data to identify fatty acid metabolites associated with macrophage polarization into anti-tumor M1 or pro-tumor M2 states.

This study uses single-cell RNA sequencing to show that Dicer1 deficiency in macrophages reprograms tumor-associated macrophages to an immunostimulatory state, enhancing antiangiogenic immunotherapy response in mouse models.

This study develops an in vitro platform to investigate macrophage recruitment to breast cancer spheroids and their impact on spheroid behavior.

This study shows that macrophages transfer intact cancer cell surface proteins to their own surface after phagocytosis, which may affect their function and metabolism.

This study shows that ablating hematopoietic stem cell-derived adipocytes reduces tumor burden in mouse models of high-grade serous carcinoma through metabolic and immune mechanisms.

The paper identifies a subpopulation of bone marrow macrophages that support AML growth by inhibiting T cells and are enriched in patients with early relapse.

This study shows that blocking IL-27 reduces CD39 expression in tumor cells and enhances anti-PD-L1 therapy effectiveness.

This study establishes an in vitro model using Raw 264.7 macrophage cells to simulate resolving macrophage polarisation, showing sequential shifts from M1-like to M2-like to Mres-like phenotypes.

This study identifies BST2 as a driver of vascular smooth muscle cell plasticity and macrophage-like phenotype switching in tumors, with implications for immunosuppression and therapy.

The paper identifies a cellular network involving neutrophils and M2 macrophages in obese breast cancer patients that promotes tumor growth through bacterial LPS and S100A8.

This study identifies high-motility tumor-associated monocytes (TAMos) that drive macrophage infiltration and cancer cell proliferation via IL-6 and MAPK pathways, suggesting IL-6 as a therapeutic target.

This study identifies NOTCH2-JAG1 juxtacrine signaling as a target to reverse macrophage-mediated taxane resistance in ovarian cancer by sensitizing tumors to paclitaxel.

This study shows that macrophages in Drosophila tumors promote heterogeneity and malignancy by activating innate immune signaling through the Toll pathway.

The paper identifies HTR2B on MDSCs as a target to enhance immune checkpoint inhibitors in breast-to-brain metastasis using clozapine and anti-PD-1 therapy.

This study shows that the cell of origin in lung adenocarcinoma affects the immunosuppressive state of the tumor microenvironment, with AT1-derived tumors showing an anti-tumor immune profile and AT2-derived tumors showing immunosuppressive features.

This study identifies IL-8 as a key factor instructing macrophage identity in glioblastoma, showing IL-8 is necessary for generating CD32+ M_IL-8 macrophages in tumors contacting the lateral ventricle.