Reversible epithelial to mesenchymal transition and acquired resistance to sunitinib in patients with renal cell carcinoma: evidence from a xenograft study - Wikidata - wikimedia - TriplyDB

Reversible epithelial to mesenchymal transition and acquired resistance to sunitinib in patients with renal cell carcinoma: evidence from a xenograft study

Reversible epithelial to mesenchymal transition and acquired resistance to sunitinib in patients with renal cell carcinoma: evidence from a xenograft study

http://www.wikidata.org/entity/Q34629011

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Patient-derived tumour xenografts as models for oncology drug development Sequence of treatment in locally advanced and metastatic renal cell carcinoma One mouse, one patient paradigm: New avatars of personalized cancer therapy The future of patient-derived tumor xenografts in cancer treatment.Combination of the histone deacetylase inhibitor vorinostat with bevacizumab in patients with clear-cell renal cell carcinoma: a multicentre, single-arm phase I/II clinical trial.Gold nanoparticles attenuate metastasis by tumor vasculature normalization and epithelial-mesenchymal transition inhibition.Anti-angiogenic therapy for cancer: current progress, unresolved questions and future directions.Resistance of renal cell carcinoma to sorafenib is mediated by potentially reversible gene expression.Mechanisms of Acquired Resistance to Tyrosine Kinase Inhibitors in Clear - Cell Renal Cell Carcinoma (ccRCC)Development of a resistance-like phenotype to sorafenib by human hepatocellular carcinoma cells is reversible and can be delayed by metronomic UFT chemotherapy.KML001 displays vascular disrupting properties and irinotecan combined antitumor activities in a murine tumor model.Tailoring tyrosine kinase inhibitors to fit the lung cancer genome.Combination strategy targeting VEGF and HGF/c-met in human renal cell carcinoma models 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.New insights into the biology of renal cell carcinoma Dll4 blockade potentiates the anti-tumor effects of VEGF inhibition in renal cell carcinoma patient-derived xenografts The role of the cell-cell interactions in cancer progression.Tyrosine kinase inhibitors in the treatment of advanced renal cell carcinoma: focus on pazopanib.Role of IL13RA2 in Sunitinib Resistance in Clear Cell Renal Cell Carcinoma Effects of preset sequential administrations of sunitinib and everolimus on tumour differentiation in Caki-1 renal cell carcinoma Sunitinib re-challenge in advanced renal-cell carcinoma.Lysosomal sequestration of sunitinib: a novel mechanism of drug resistance.SOX9 was involved in TKIs resistance in renal cell carcinoma via Raf/MEK/ERK signaling pathway.Antiangiogenic therapy: impact on invasion, disease progression, and metastasis.Drug rechallenge and treatment beyond progression--implications for drug resistance.Von Hippel-Lindau disease (VHL): a need for a murine model with retinal hemangioblastoma Prognostic value of CC-chemokine receptor seven expression in patients with metastatic renal cell carcinoma treated with tyrosine kinase inhibitor.The Role of Hypoxia and Cancer Stem Cells in Renal Cell Carcinoma Pathogenesis.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 Targeting carcinoma-associated fibroblasts within the tumor stroma with a fibroblast activation protein-activated prodrug.Cox-2 inhibition enhances the activity of sunitinib in human renal cell carcinoma xenografts.Adjuvant sunitinib or sorafenib for high-risk, non-metastatic renal-cell carcinoma (ECOG-ACRIN E2805): a double-blind, placebo-controlled, randomised, phase 3 trial.Histologic subtype impacts cancer-specific survival in patients with sarcomatoid-variant renal cell carcinoma treated surgically.Vascular disruption in combination with mTOR inhibition in renal cell carcinoma.Co-option of Liver Vessels and Not Sprouting Angiogenesis Drives Acquired Sorafenib Resistance in Hepatocellular Carcinoma Everolimus affects vasculogenic mimicry in renal carcinoma resistant to sunitinib.Sunitinib Treatment Enhances Metastasis of Innately Drug-Resistant Breast Tumors.

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Reversible epithelial to mesenchymal transition and acquired resistance to sunitinib in patients with renal cell carcinoma: evidence from a xenograft study

http://www.wikidata.org/entity/Q34629011

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2010 nî lūn-bûn

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2010年の論文

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Reversible epithelial to mesen ...... vidence from a xenograft study

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Reversible epithelial to mesen ...... vidence from a xenograft study

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Molecular Cancer Therapeutics

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Reversible epithelial to mesen ...... vidence from a xenograft study

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Brenda Salumbides

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George Netto

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Hans J Hammers

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Henk M Verheul

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Janneke Jaspers

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Karl Dykema

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Li Shen

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Michelle Rudek

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P2860

Bioconductor: open software development for computational biology and bioinformatics

The tumour suppressor protein VHL targets hypoxia-inducible factors for oxygen-dependent proteolysis

Activation of vascular endothelial growth factor gene transcription by hypoxia-inducible factor 1

Evolving gene/transcript definitions significantly alter the interpretation of GeneChip data.

Modes of resistance to anti-angiogenic therapy

Gene expression programs in response to hypoxia: cell type specificity and prognostic significance in human cancers

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

Oncogenic pathway signatures in human cancers as a guide to targeted therapies

A small molecule-kinase interaction map for clinical kinase inhibitors

Detection of DNA copy number changes and oncogenic signaling abnormalities from gene expression data reveals MYC activation in high-grade papillary renal cell carcinoma.

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