Notch Signaling in Myeloid Cells as a Regulator of Tumor Immune Responses
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Summary
The roles of Notch signaling in modulating tumor-infiltrating myeloid cells and implications for therapeutic strategies that modulate Notch signalling to enhance cancer immunotherapy are discussed.
- Type
- review
- Published
- 2018-06-04
- Cited by
- 43
- References
- 97
- Access
- Open access
- OpenAlex
- https://openalex.org/W2805146785
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:44131003
Keywords
Immunotherapy, Tumor microenvironment, Immune system, Cancer immunotherapy, Myeloid-derived Suppressor Cell
References
- Canonical and non-canonical Notch signaling in CD4⁺ T cells.
- Dendritic cells in antitumor immune responses. II. Dendritic cells grown from bone marrow precursors, but not mature DC from tumor-bearing mice, are effective antigen carriers in the therapy of established tumors.
- Decreased antigen presentation by dendritic cells in patients with breast cancer.
- Notch-1 Up-Regulation and Signaling following Macrophage Activation Modulates Gene Expression Patterns Known to Affect Antigen-Presenting Capacity and Cytotoxic Activity1
- Much More than M1 and M2 Macrophages, There are also CD169+ and TCR+ Macrophages
- Ligand independent mechanisms of Notch activity
- In Brief: Notch signalling in health and disease
- Notch Signaling Induces Multilineage Myeloid Differentiation and Up-Regulates PU.1 Expression1
- Myeloid-derived suppressor cells in the tumor microenvironment: expect the unexpected.
- The Notch signalling system: recent insights into the complexity of a conserved pathway
- TAM macrophages promote growth and metastasis within the cancer ecosystem
- Mammary Stem Cells and Breast Cancer—Role of Notch Signalling
- Selective induction of the Notch ligand Jagged‐1 in macrophages by soluble egg antigen from Schistosoma mansoni involves ERK signalling
- Adoptive cell transfer as personalized immunotherapy for human cancer
- Cancer immunotherapy: moving beyond current vaccines
- Identification and Characterization of Presenilin-independent Notch Signaling*
- Notch signaling is activated by TLR stimulation and regulates macrophage functions
- Non-Canonical Notch Signaling in Cancer and Immunity
- The Canonical Notch Signaling Pathway: Unfolding the Activation Mechanism
- Adipose tissue immunity and cancer
Cited by
- Notch Signaling Regulates Immune Responses in Atherosclerosis
- Notch signaling pathway suppresses CD8+ T cells activity in patients with lung adenocarcinoma
- Targeting gamma secretase: has progress moved up a Notch?
- Kloniranje liganda JAGGED1 i njegov utjecaj na proliferaciju limfocita
- Transcriptome analysis of fowl adenovirus serotype 4 infection in chickens
- The Notch pathway: a novel therapeutic target for cardiovascular diseases?
- Long Non-coding RNA in CNS Injuries: A New Target for Therapeutic Intervention
- Modulation of Immunosuppression by Oligonucleotide-Based Molecules and Small Molecules Targeting Myeloid-Derived Suppressor Cells
- Myeloid-Derived Suppressor Cells: Major Figures that Shape the Immunosuppressive and Angiogenic Network in Cancer
- Shaping of the Tumor Microenvironment by Notch Signaling.
- Tumor Microenvironment: Challenges and Opportunities in Targeting Metastasis of Triple Negative Breast Cancer.
- Reduction of myeloid derived suppressor cells by inhibiting Notch pathway prevents the progression of endometriosis in mice model.
- NF-κB1 Regulates Immune Environment and Outcome of Notch-Dependent T-Cell Acute Lymphoblastic Leukemia
- Roles of HMGB1 in regulating myeloid-derived suppressor cells in the tumor microenvironment
- Potential New Cancer Immunotherapy: Anti-CD47-SIRPα Antibodies
- The stability analysis of tumor-immune responses to chemotherapy system driven by Gaussian colored noises
- Notch Pathway: A Journey from Notching Phenotypes to Cancer Immunotherapy.
- Molecular Profiling of Exceptional Responders to Cancer Therapy.
- Targeting Notch in oncology: the path forward
- Metformin Induces Apoptosis and Inhibits Notch1 in Malignant Pleural Mesothelioma Cells
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