Lysosomal sequestration of sunitinib: a novel mechanism of drug resistance. - Wikidata - awgldk - TriplyDB

Lysosomal sequestration of sunitinib: a novel mechanism of drug resistance.

Lysosomal sequestration of sunitinib: a novel mechanism of drug resistance.

http://www.wikidata.org/entity/Q35703000

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Resistance to receptor tyrosine kinase inhibitors in solid tumors: can we improve the cancer fighting strategy by blocking autophagy?Nanoparticle-mediated drug delivery for treating melanoma Combining radiotherapy with sunitinib: lessons (to be) learned Giant Lysosomes as a Chemotherapy Resistance Mechanism in Hepatocellular Carcinoma Cells Photoactivation of lysosomally sequestered sunitinib after angiostatic treatment causes vascular occlusion and enhances tumor growth inhibition.Sunitinib: the antiangiogenic effects and beyond Sunitinib-induced morpho-functional changes and drug effectiveness in malignant solitary fibrous tumours Mechanisms of Acquired Resistance to Tyrosine Kinase Inhibitors in Clear - Cell Renal Cell Carcinoma (ccRCC)Response-predictive gene expression profiling of glioma progenitor cells in vitro.Acquired tumor cell resistance to sunitinib causes resistance in a HT-29 human colon cancer xenograft mouse model without affecting sunitinib biodistribution or the tumor microvasculature.Sunitinib dose escalation overcomes transient resistance in clear cell renal cell carcinoma and is associated with epigenetic modifications.The relevance of testing the efficacy of anti-angiogenesis treatments on cells derived from primary tumors: a new method for the personalized treatment of renal cell carcinoma.Role of IL13RA2 in Sunitinib Resistance in Clear Cell Renal Cell Carcinoma Limited Tumor Tissue Drug Penetration Contributes to Primary Resistance against Angiogenesis Inhibitors Activation of alternate prosurvival pathways accounts for acquired sunitinib resistance in U87MG glioma xenografts.p21-activated kinase 1 determines stem-like phenotype and sunitinib resistance via NF-κB/IL-6 activation in renal cell carcinoma.Modulation of Akt/mTOR signaling overcomes sunitinib resistance in renal and prostate cancer cells Resistance to sunitinib in renal clear cell carcinoma results from sequestration in lysosomes and inhibition of the autophagic flux pH-Responsive Triblock Copolymeric Micelles Decorated with a Cell-Penetrating Peptide Provide Efficient Doxorubicin Delivery Autophagy Modulation in Disease Therapy: Where Do We Stand?Evaluation of a tyrosine kinase peptide microarray for tyrosine kinase inhibitor therapy selection in cancer.Controlling escape from angiogenesis inhibitors.Strategies for improving the clinical benefit of antiangiogenic drug based therapies for breast cancer.Somatic alterations as the basis for resistance to targeted therapies.Intratumor heterogeneity and its impact on drug distribution and sensitivity.Resistance to antiangiogenic therapies.The emerging quest for the optimal angiostatic combination therapy.Physicochemical properties of novel protein kinase inhibitors in relation to their substrate specificity for drug transporters.Protein trafficking in colorectal carcinogenesis-targeting and bypassing resistance to currently applied treatments.Sunitinib activates Axl signaling in renal cell cancer.Targeting the lysosome in cancer.Autophagy, a double-edged sword in anti-angiogenesis therapy.LDL cholesterol counteracts the antitumour effect of tyrosine kinase inhibitors against renal cell carcinoma.Actin filament-associated protein 1 (AFAP-1) is a key mediator in inflammatory signaling-induced rapid attenuation of intrinsic P-gp function in human brain capillary endothelial cells.Inhibition of breast cancer metastasis by paclitaxel-loaded pH responsive poly(β-amino ester) copolymer micelles.Postsurgical adjuvant or metastatic renal cell carcinoma therapy models reveal potent antitumor activity of metronomic oral topotecan with pazopanib.Optimal treatment scheduling of ionizing radiation and sunitinib improves the antitumor activity and allows dose reduction Lysosomal sequestration of hydrophobic weak base chemotherapeutics triggers lysosomal biogenesis and lysosome-dependent cancer multidrug resistance.Resistance to Targeted Therapies in Renal Cancer: The Importance of Changing the Mechanism of Action.Can individualized sunitinib dose and schedule changes optimize outcomes for kidney cancer patients?

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P2860

Lysosomal sequestration of sunitinib: a novel mechanism of drug resistance.

http://www.wikidata.org/entity/Q35703000

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Lysosomal sequestration of sunitinib: a novel mechanism of drug resistance.

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Lysosomal sequestration of sunitinib: a novel mechanism of drug resistance

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Gerrit Jansen

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Godefridus J Peters

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Henk J Broxterman

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Henk M W Verheul

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Kristy J Gotink

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Laurens V Beerepoot

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Mariette Labots

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Michelle A Rudek

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René J Musters

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P2860

The lipid phosphatase activity of PTEN is critical for its tumor supressor function

Cell signaling by receptor tyrosine kinases

Modes of resistance to anti-angiogenic therapy

Overall survival and updated results for sunitinib compared with interferon alfa in patients with metastatic renal cell carcinoma

A quantitative analysis of kinase inhibitor selectivity

A small molecule-kinase interaction map for clinical kinase inhibitors

Bafilomycins: a class of inhibitors of membrane ATPases from microorganisms, animal cells, and plant cells.

Anti-angiogenic tyrosine kinase inhibitors: what is their mechanism of action?

Sunitinib malate for the treatment of pancreatic neuroendocrine tumors.

Fluorescence probe measurement of the intralysosomal pH in living cells and the perturbation of pH by various agents.

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