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Involvement of interleukin-8, vascular endothelial growth factor, and basic fibroblast growth factor in tumor necrosis factor alpha-dependent angiogenesis
Angiogenesis by TNF-alpha appears to be modulated through various angiogenic factors, both in vitro and in vivo, and this pathway is controlled through paracrine and/or autocrine mechanisms. Expand
Interleukin-17 promotes angiogenesis and tumor growth.
A novel role for IL-17 is revealed as a CD4 T-cell-derived mediator of angiogenesis that stimulates vascular endothelial cell migration and cord formation and regulates production of a variety of proangiogenic factors. Expand
Induction of Vascular Endothelial Growth Factor by Tumor Necrosis Factor α in Human Glioma Cells
The chloramphenicol acetyltransferase assay with VEGF promoter deletion constructs demonstrated that four clusterized SP-1 binding sites in the proximal promoter were essential for the basal transcription and the TNF-α-dependent activation. Expand
A novel brain-specific p53-target gene, BAI1, containing thrombospondin type 1 repeats inhibits experimental angiogenesis
A novel p53-inducible gene that encodes a 1584-amino-acid product containing five thrombospondin type 1 (TSP-type 1) repeats and is specifically expressed in the brain is isolated, suggesting BAI1 plays a significant role in angiogenesis inhibition, as a mediator of p53. Expand
Effect of multidrug resistance-reversing agents on transporting activity of human canalicular multispecific organic anion transporter.
It is found that LLC/cMOAT-1 cells have increased resistance to vincristine (VCR), 7-ethyl-10-hydroxy-camptothecin, and cisplatin but not to etoposide, and it is demonstrated that cMOAT confers a novel drug-resistance phenotype. Expand
EGFR and MET receptor tyrosine kinase–altered microRNA expression induces tumorigenesis and gefitinib resistance in lung cancers
The involvement of the MET oncogene in de novo and acquired resistance of non-small cell lung cancers (NSCLCs) to tyrosine kinase inhibitors (TKIs) has previously been reported, but the preciseExpand
Loss of PTEN expression by blocking nuclear translocation of EGR1 in gefitinib-resistant lung cancer cells harboring epidermal growth factor receptor-activating mutations.
It is strongly suggested that loss of PTEN expression contributes to gefitinib and erlotinib resistance in NSCLC and the therapeutic importance ofPTEN expression in the treatment of NSCLc with EGFR-targeted drugs is reinforced. Expand
The Impact of EGFR T790M Mutations and BIM mRNA Expression on Outcome in Patients with EGFR-Mutant NSCLC Treated with Erlotinib or Chemotherapy in the Randomized Phase III EURTAC Trial
Low-level pretreatment T790M mutations can frequently be detected and can be used for customizing treatment with T790m-specific inhibitors and can potentially be used as a biomarker of survival in EGFR-mutant NSCLC and for synthetic lethality therapies. Expand
ZD1839 (Iressa) induces antiangiogenic effects through inhibition of epidermal growth factor receptor tyrosine kinase.
The antitumor effects of ZD1839 could, therefore, be mediated in part by the inhibition of tumor angiogenesis through direct effects on microvascular endothelial cells that express EGFR and also through reduced production of proangiogenic factors by tumor cells. Expand
Tumor growth suppression in pancreatic cancer by a putative metastasis suppressor gene Cap43/NDRG1/Drg-1 through modulation of angiogenesis.
Immunohistochemical analysis of specimens from 65 patients with pancreatic ductal adenocarcinoma showed a significant association between Cap43 expression and tumor microvascular density as well as depth of invasion, and overall survival rates for patients with Pancreatic cancer. Expand