Targeting the mechanisms of tumoral immune tolerance with small-molecule inhibitors. - Wikidata - awgldk - TriplyDB

Targeting the mechanisms of tumoral immune tolerance with small-molecule inhibitors.

Targeting the mechanisms of tumoral immune tolerance with small-molecule inhibitors.

http://www.wikidata.org/entity/Q34550440

about

Expression, purification, assay, and crystal structure of perdeuterated human arginase I Tumour progression and metastasis CpG Oligonucleotides as Cancer Vaccine Adjuvants In vitro models of cancer stem cells and clinical applications Effects of various phytochemicals on indoleamine 2,3-dioxygenase 1 activity: galanal is a novel, competitive inhibitor of the enzyme Mathematical modeling of Interleukin-35 promoting tumor growth and angiogenesis Nanomedicine and cancer immunotherapy: focus on indoleamine 2,3-dioxygenase inhibitors Principles of cancer therapy: oncogene and non-oncogene addiction Cancer immunotherapy comes of age Modulators of arginine metabolism support cancer immunosurveillance.Blocking TLR2 activity attenuates pulmonary metastases of tumor.T-cell/histiocyte-rich large B-cell lymphoma shows transcriptional features suggestive of a tolerogenic host immune response.Combination of physical activity, nutrition, or other metabolic factors and vaccine response Towards a genetic definition of cancer-associated inflammation: role of the IDO pathway BAR the door: cancer suppression by amphiphysin-like genes Preoperative treatment with a non-steroidal anti-inflammatory drug (NSAID) increases tumor tissue infiltration of seemingly activated immune cells in colorectal cancer.IDO is a nodal pathogenic driver of lung cancer and metastasis development.Non-hematopoietic expression of IDO is integrally required for inflammatory tumor promotion IDO2 is a critical mediator of autoantibody production and inflammatory pathogenesis in a mouse model of autoimmune arthritis.Indoleamine 2,3-dioxygenase pathways of pathogenic inflammation and immune escape in cancer Effect of TLR agonists on the differentiation and function of human monocytic myeloid-derived suppressor cells Big opportunities for small molecules in immuno-oncology.O-alkylhydroxylamines as rationally-designed mechanism-based inhibitors of indoleamine 2,3-dioxygenase-1.1-Methyl-tryptophan synergizes with methotrexate to alleviate arthritis in a mouse model of arthritis.Inhibitors of indoleamine 2,3-dioxygenase: a review of novel patented lead compounds.Indoleamine 2,3-dioxygenase is the anticancer target for a novel series of potent naphthoquinone-based inhibitors.Indoleamine 2,3-dioxygenase in T-cell tolerance and tumoral immune escape.Chronic inflammation that facilitates tumor progression creates local immune suppression by inducing indoleamine 2,3 dioxygenase.Structure based development of phenylimidazole-derived inhibitors of indoleamine 2,3-dioxygenase.Classification of current anticancer immunotherapies Immunotherapeutic suppression of indoleamine 2,3-dioxygenase and tumor growth with ethyl pyruvate.Indoleamine 2,3-dioxygenase as a modifier of pathogenic inflammation in cancer and other inflammation-associated diseases.Intratumoral injection of CpG oligonucleotides induces the differentiation and reduces the immunosuppressive activity of myeloid-derived suppressor cells Development of a Sox2 reporter system modeling cellular heterogeneity in glioma.Cardiac and gastrointestinal liabilities caused by deficiency in the immune modulatory enzyme indoleamine 2,3-dioxygenase Ligand migration in human indoleamine-2,3 dioxygenase.Altered tryptophan metabolism as a paradigm for good and bad aspects of immune privilege in chronic inflammatory diseases.Tumor-infiltrating lymphocytes in melanoma.4-1BB regulates NKG2D costimulation in human cord blood CD8+ T cells Oligodeoxynucleotides expressing polyguanosine motifs promote antitumor activity through the upregulation of IL-2.

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Targeting the mechanisms of tumoral immune tolerance with small-molecule inhibitors.

http://www.wikidata.org/entity/Q34550440

description

2006 nî lūn-bûn

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2006 թուականի Օգոստոսին հրատարակուած գիտական յօդուած

@hyw

2006 թվականի օգոստոսին հրատարակված գիտական հոդված

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2006年の論文

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2006年論文

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2006年論文

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2006年論文

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2006年論文

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2006年論文

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2006年论文

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name

Targeting the mechanisms of tumoral immune tolerance with small-molecule inhibitors.

@ast

Targeting the mechanisms of tumoral immune tolerance with small-molecule inhibitors.

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Targeting the mechanisms of tumoral immune tolerance with small-molecule inhibitors.

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type

label

Targeting the mechanisms of tumoral immune tolerance with small-molecule inhibitors.

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Targeting the mechanisms of tumoral immune tolerance with small-molecule inhibitors.

@en

Targeting the mechanisms of tumoral immune tolerance with small-molecule inhibitors.

@nl

prefLabel

Targeting the mechanisms of tumoral immune tolerance with small-molecule inhibitors.

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Targeting the mechanisms of tumoral immune tolerance with small-molecule inhibitors.

@en

Targeting the mechanisms of tumoral immune tolerance with small-molecule inhibitors.

@nl

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Nature Reviews Cancer

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Targeting the mechanisms of tumoral immune tolerance with small-molecule inhibitors

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Peggy A Scherle

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P2860

Safeguarding patients in clinical trials with high mortality rates

Induction of antitumor immunity by indomethacin

Prostaglandin E2 up-regulates macrophage-derived chemokine production but suppresses IFN-inducible protein-10 production by APC.

Antigen-specific inhibition of CD8+ T cell response by immature myeloid cells in cancer is mediated by reactive oxygen species.

Stat3 activity in melanoma cells affects migration of immune effector cells and nitric oxide-mediated antitumor effects.

Cutting edge: CpG oligonucleotides induce splenic CD19+ dendritic cells to acquire potent indoleamine 2,3-dioxygenase-dependent T cell regulatory functions via IFN Type 1 signaling.

Discovery and pharmacological characterization of a novel rodent-active CCR2 antagonist, INCB3344.

Activation of dendritic cells via inhibition of Jak2/STAT3 signaling.

Prostaglandin E2 induces FOXP3 gene expression and T regulatory cell function in human CD4+ T cells.

Reduction of myeloid-derived suppressor cells and induction of M1 macrophages facilitate the rejection of established metastatic disease.

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613-625

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10.1038/NRC1929

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Alexander J Muller

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1005270932

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