Activation of Akt as a mechanism for tumor immune evasion. - Wikidata - wikimedia - TriplyDB

Activation of Akt as a mechanism for tumor immune evasion.

Activation of Akt as a mechanism for tumor immune evasion.

http://www.wikidata.org/entity/Q33713327

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The effect of chemotherapy on programmed cell death 1/programmed cell death 1 ligand axis: some chemotherapeutical drugs may finally work through immune response The phosphoinositide 3-kinase pathway and therapy resistance in cancer A multi-targeted approach to suppress tumor-promoting inflammation Novel PI3K/Akt inhibitors screened by the cytoprotective function of human immunodeficiency virus type 1 Tat Pleckstrin homology domain of Akt kinase: a proof of principle for highly specific and effective non-enzymatic anti-cancer target Synaptonemal complex protein 3 is a prognostic marker in cervical cancer.Ectopic expression of X-linked lymphocyte-regulated protein pM1 renders tumor cells resistant to antitumor immunity.Chemical compounds from anthropogenic environment and immune evasion mechanisms: potential interactions DNA microarray-based analysis of voluntary resistance wheel running reveals novel transcriptome leading robust hippocampal plasticity.Gain of HIF-1α under normoxia in cancer mediates immune adaptation through the AKT/ERK and VEGFA axes.API5 confers tumoral immune escape through FGF2-dependent cell survival pathway.Reprogramming the tumor microenvironment: tumor-induced immunosuppressive factors paralyze T cells.The role of the PI3K/Akt/mTOR signalling pathway in human cancers induced by infection with human papillomaviruses.Cancer vaccination drives Nanog-dependent evolution of tumor cells toward an immune-resistant and stem-like phenotype.A matched couple: Combining kinase inhibitors with immunotherapy for cancer treatment Nanog signaling in cancer promotes stem-like phenotype and immune evasion Synaptonemal complex protein 3 as a novel prognostic marker in early stage non-small cell lung cancer.Concomitant targeting of tumor cells and induction of T-cell response synergizes to effectively inhibit trastuzumab-resistant breast cancer.API5 confers cancer stem cell-like properties through the FGF2-NANOG axis.PI3K and Akt as molecular targets for cancer therapy: current clinical outcomes.PI3K functions in cancer progression, anticancer immunity and immune evasion by tumors.Combining immunotherapy and targeted therapies in cancer treatment.Strategies for enhancing vaccine-induced CTL antitumor immune responses.Cellular and molecular mechanisms in cancer immune escape: a comprehensive review.Immune consequences of kinase inhibitors in development, undergoing clinical trials and in current use in melanoma treatment.Signaling pathways in HPV-associated cancers and therapeutic implications.Integrated Akt/PKB signaling in immunomodulation and its potential role in cancer immunotherapy.Advancing Immunotherapy in Metastatic Breast Cancer.Beyond the antigen receptor: editing the genome of T-cells for cancer adoptive cellular therapies.API5 induces cisplatin resistance through FGFR signaling in human cancer cells.Harness the synergy between targeted therapy and immunotherapy: what have we learned and where are we headed?A Multicenter Phase I Study Evaluating Dual PI3K and BRAF Inhibition with PX-866 and Vemurafenib in Patients with Advanced BRAF V600-Mutant Solid Tumors.Tumor-targeted delivery of sunitinib base enhances vaccine therapy for advanced melanoma by remodeling the tumor microenvironment.Genomic Landscapes of EBV-Associated Nasopharyngeal Carcinoma vs. HPV-Associated Head and Neck Cancer Mitochondrial reprogramming via ATP5H loss promotes multimodal cancer therapy resistance

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P2860

Activation of Akt as a mechanism for tumor immune evasion.

http://www.wikidata.org/entity/Q33713327

description

2008 nî lūn-bûn

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2008 թուականի Դեկտեմբերին հրատարակուած գիտական յօդուած

@hyw

2008 թվականի դեկտեմբերին հրատարակված գիտական հոդված

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2008年の論文

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2008年論文

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2008年論文

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2008年論文

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2008年論文

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2008年論文

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2008年论文

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name

Activation of Akt as a mechanism for tumor immune evasion.

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Activation of Akt as a mechanism for tumor immune evasion.

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Activation of Akt as a mechanism for tumor immune evasion.

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Activation of Akt as a mechanism for tumor immune evasion.

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Activation of Akt as a mechanism for tumor immune evasion.

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Activation of Akt as a mechanism for tumor immune evasion.

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Molecular Therapy

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Activation of Akt as a mechanism for tumor immune evasion.

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P2093

Chien-Fu Hung

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

Jin Hee Kim

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

Ken Y Lin

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

Kyung Hee Noh

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Sara I Pai

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T-C Wu

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Tae Heung Kang

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Tae Woo Kim

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P2860

Expression of a constitutively active Akt Ser/Thr kinase in 3T3-L1 adipocytes stimulates glucose uptake and glucose transporter 4 translocation

Cancer immunotherapy: moving beyond current vaccines

The role of vascular cell adhesion molecule-1 in tumor immune evasion

Engineering an intracellular pathway for major histocompatibility complex class II presentation of antigens.

Akt/protein kinase B signaling inhibitor-2, a selective small molecule inhibitor of Akt signaling with antitumor activity in cancer cells overexpressing Akt.

Activation of the PI3K/Akt pathway and chemotherapeutic resistance.

Ectopic expression of vascular cell adhesion molecule-1 as a new mechanism for tumor immune evasion.

Cancer immunotherapy using a DNA vaccine encoding a single-chain trimer of MHC class I linked to an HPV-16 E6 immunodominant CTL epitope

Tumor-specific immunity and antiangiogenesis generated by a DNA vaccine encoding calreticulin linked to a tumor antigen.

The Akt/PKB pathway: molecular target for cancer drug discovery.

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10.1038/MT.2008.255

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3

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17

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23688790

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19107122

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2835083

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