p53-dependent chemokine production by senescent tumor cells supports NKG2D-dependent tumor elimination by natural killer cells - Wikidata - wikimedia - TriplyDB

p53-dependent chemokine production by senescent tumor cells supports NKG2D-dependent tumor elimination by natural killer cells

p53-dependent chemokine production by senescent tumor cells supports NKG2D-dependent tumor elimination by natural killer cells

http://www.wikidata.org/entity/Q37194949

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Radiotherapy combination opportunities leveraging immunity for the next oncology practice Tumor-intrinsic oncogene pathways mediating immune avoidance Cellular senescence impact on immune cell fate and function Chloroquine and hydroxychloroquine for cancer therapy Autophagy in malignant transformation and cancer progression NK cell receptor imbalance and NK cell dysfunction in HBV infection and hepatocellular carcinoma Immune surveillance of unhealthy cells by natural killer cells Of flies, mice, and men: evolutionarily conserved tissue damage responses and aging Recent advances in understanding antitumor immunity Immunomodulatory Function of the Tumor Suppressor p53 in Host Immune Response and the Tumor Microenvironment "Adherent" versus Other Isolation Strategies for Expanding Purified, Potent, and Activated Human NK Cells for Cancer Immunotherapy Immunosurveillance of senescent cancer cells by natural killer cells Iscador Qu inhibits doxorubicin-induced senescence of MCF7 cells Type 1 interferons contribute to the clearance of senescent cell.Recognition of tumors by the innate immune system and natural killer cells.Balancing the innate immune system in tumor development.New insights into cancer immunoediting and its three component phases--elimination, equilibrium and escape Primed for cancer: Li Fraumeni Syndrome and the pre-cancerous niche Tumor and Host Factors Controlling Antitumor Immunity and Efficacy of Cancer Immunotherapy.Combining an Aurora Kinase Inhibitor and a Death Receptor Ligand/Agonist Antibody Triggers Apoptosis in Melanoma Cells and Prevents Tumor Growth in Preclinical Mouse Models Combined CSL and p53 downregulation promotes cancer-associated fibroblast activation NKG2D ligands mediate immunosurveillance of senescent cells.Metronomic topotecan impedes tumor growth of MYCN-amplified neuroblastoma cells in vitro and in vivo by therapy induced senescence.Antitumor immunity. A shed NKG2D ligand that promotes natural killer cell activation and tumor rejection.Context-dependent effects of cellular senescence in cancer development.Stromal senescence establishes an immunosuppressive microenvironment that drives tumorigenesis.Dynamic alterations of bone marrow cytokine landscape of myelodysplastic syndromes patients treated with 5-azacytidine.CBP/p300 acetyltransferases regulate the expression of NKG2D ligands on tumor cells Emerging roles of p53 and other tumour-suppressor genes in immune regulation Advances in NKG2D ligand recognition and responses by NK cells.Cellular senescence and its effector programs.NKG2D signaling in cancer immunosurveillance.Molecular Bases for the Regulation of NKG2D Ligands in Cancer.Physiological and pathological consequences of cellular senescence.New perspective on targeting the tumor suppressor p53 pathway in the tumor microenvironment to enhance the efficacy of immunotherapy.DDR-mediated crosstalk between DNA-damaged cells and their microenvironment.Senescence and cancer: An evolving inflammatory paradox.Melanocytic nevi and melanoma: unraveling a complex relationship.Molecular Pathways: Oncologic Pathways and Their Role in T-cell Exclusion and Immune Evasion-A New Role for the AXL Receptor Tyrosine Kinase.BRD4 Connects Enhancer Remodeling to Senescence Immune Surveillance.

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p53-dependent chemokine production by senescent tumor cells supports NKG2D-dependent tumor elimination by natural killer cells

http://www.wikidata.org/entity/Q37194949

description

article científic

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article scientifique

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articolo scientifico

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artigo científico

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bilimsel makale

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scientific article published on 16 September 2013

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vedecký článok

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vetenskaplig artikel

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videnskabelig artikel

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vědecký článek

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name

p53-dependent chemokine produc ...... nation by natural killer cells

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p53-dependent chemokine produc ...... ation by natural killer cells.

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type

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p53-dependent chemokine produc ...... nation by natural killer cells

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p53-dependent chemokine produc ...... ation by natural killer cells.

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p53-dependent chemokine produc ...... nation by natural killer cells

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p53-dependent chemokine produc ...... ation by natural killer cells.

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Journal of Experimental Medicine

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p53-dependent chemokine produc ...... nation by natural killer cells

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P2093

Alexandre Iannello

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Michele Ardolino

http://www.w3.org/2001/XMLSchema#string

Scott W Lowe

http://www.w3.org/2001/XMLSchema#string

Thornton W Thompson

http://www.w3.org/2001/XMLSchema#string

P2860

Oncogene-Induced Senescence: Putting the Brakes on Tumor Development

Expression and role of MICA and MICB in human hepatocellular carcinomas and their regulation by retinoic acid

The DNA damage pathway regulates innate immune system ligands of the NKG2D receptor

Oncogenic ras provokes premature cell senescence associated with accumulation of p53 and p16INK4a

Senescence of activated stellate cells limits liver fibrosis

Oncogene-induced senescence relayed by an interleukin-dependent inflammatory network.

Chemokine signaling via the CXCR2 receptor reinforces senescence

A novel ligand for the NKG2D receptor activates NK cells and macrophages and induces tumor immunity

Innate or adaptive immunity? The example of natural killer cells

Senescence-associated secretory phenotypes reveal cell-nonautonomous functions of oncogenic RAS and the p53 tumor suppressor

P304

2057-2069

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scholarly article

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10.1084/JEM.20130783

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P407

P433

10

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210

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David H. Raulet

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2013-09-16T00:00:00Z

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256666572

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24043758

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3782044

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