High-definition CpG methylation of novel genes in gastric carcinogenesis identified by next-generation sequencing.
New York City, United States. In Mod Pathol, Feb 2016
Overall, 13 genes had significantly increased CpG methylation in gastric cancer vs non-metaplastic mucosa (BRINP1, CDH11, CHFR, EPHA5, EPHA7, FGF2, FLI1, GALR1, HS3ST2, PDGFRA, SEZ6L, SGCE, and SNRPN).
Lenvatinib: Role in thyroid cancer and other solid tumors.
Houston, United States. In Cancer Treat Rev, Jan 2016
Lenvatinib targets vascular endothelial growth factor receptors 1-3 (VEGFR1-3), fibroblast growth factor receptors 1-4 (FGFR-1-4), RET, c-kit, and platelet-derived growth factor receptor α (PDGFRα).
Identification of an oncogenic RAB protein.
New York City, United States. In Science, Nov 2015
Furthermore, oncogenic RAB35 is sufficient to drive platelet-derived growth factor receptor α to LAMP2-positive endomembranes in the absence of ligand, suggesting that there may be latent oncogenic potential in dysregulated endomembrane trafficking.
Lenvatinib versus placebo in radioiodine-refractory thyroid cancer.
Aş Şanamayn, Syria. In N Engl J Med, Mar 2015
BACKGROUND: Lenvatinib, an oral inhibitor of vascular endothelial growth factor receptors 1, 2, and 3, fibroblast growth factor receptors 1 through 4, platelet-derived growth factor receptor α, RET, and KIT, showed clinical activity in a phase 2 study involving patients with differentiated thyroid cancer that was refractory to radioiodine (iodine-131).
Overview of fundamental study of pazopanib in cancer.
Tianjin, China. In Thorac Cancer, 2014
Through the exploration of inhibitors of vascular endothelial growth factor receptor (VEGFR)-2, deemed as the major angiogenesis pathway, pazopanib was found as a small molecular pan-VEGFR and pan-platelet-derived growth factor receptor (PDGFR) inhibitor, with suitable pharmacodynamic and pharmacokinetic parameters to be an oral drug.
State of the Art in the Treatment of Gastrointestinal Stromal Tumors.
Magdeburg, Germany. In Gastrointest Tumors, 2014
Despite their biological and clinical heterogeneity, the majority of these tumors are positive for the receptor tyrosine kinase KIT and are driven by KIT- or platelet-derived growth factor receptor alpha (PDGFRA)-activating mutations.