The most common primary mutations are in KIT kinase, representing approximately 75% to 80% of cases, or in PDGFR
kinase, representing approximately 5% to 10% of cases.
Ripretinib is an investigational KIT and PDGFR
? kinase switch control inhibitor in clinical development for the treatment of KIT and/or PDGFR
?-driven cancers, including gastrointestinal stromal tumors, or GIST, systemic mastocytosis, or SM, and other cancers.
Sunitinib malate is a small molecule kinase inhibitor with activity against a number of tyrosine kinase receptors, including VEGFR, PDGFR
, KIT, RET, and FMS-like tyrosine kinase-3 (FLT3) .
Because CM082 plays a role in inhibiting PDGF signaling, we conjecture that CNV regression is a result of PDGFR
inhibition and pericyte dysfunction.
In the dog in this report, the expression of VEGFr, PDGFr
, EGFr, and SCF was demonstrated by immunohistochemistry.
Masson's trichrome; PCNA, proliferating cell nuclear antigen; PDGFR
, platelet-derived growth factor receptor; ROS, reactive oxygen species; SR, sirius red; TGF-15, transforming growth factor-12; TNF-[alpha], tumor necrosis factor-[alpha]; UUO, unilateral ureteral obstruction.
Adult reproductive functions after early postnatal inhibition by imatinib of the two receptor tyrosine kinases, c-kit and PDGFR
, in the rat testis.
In previous studies of glioma , squamous cell carcinoma of the head and neck , colorectal cancer , pancreatic cancer , and T cell lymphoma , PDGFR
activation induced the intracellular signaling pathway and promoted cell migration, invasion, survival, and proliferation .
La senalizacion aberrante de PDGFR
induce la transformacion de pericitos a miofibroblastos, se puede presentar en consecuencia a los efectos del factor de crecimiento de hepatocitos y de TGF-[beta] ya que favorecen la sobreproduccion de PDGF en las celulas del epitelio tubular.
Pleuro-pulmonary solitary fibrous tumors: A clinicopathologic, immunohistochemical, and molecular study of 88 cases confirming the prognostic value of de Perrot staging system and p53 expression, and evaluating the role of c-kit, BRAF, PDGFRs
(alpha/beta), c-met, and EGFR.
To investigate which RTK signaling pathways participate in the proliferation of RO82-W-1 cells, we tested the activity of selective RTK inhibitors [42-46] targeting VEGFR (sorafenib), FGFR (PD166866 and PD173074), KIT (imatinib), and PDGFR
(Ki6783) against 5 DTC cell lines including RO82-W-1 (Table 2), because lenvatinib inhibited these RTKs at [IC.sub.50] values of less than 100 nM (Supplementary Table S1) and RO82-W-1 cells express the mRNA of some of these RTKs (Supplementary Figure S5).
Multikinase inhibitor 20% (1 year survival)  with activity against Raf, VEGF, PDGFR
, Ret, and c-kit Sosa et al.