Sorafenib inhibits vascular endothelial cell proliferation stimulated by anaplastic thyroid cancer cells regardless of BRAF mutation status.

In conclusion, sorafenib more effectively inhibited RAF‑generated growth signals in ATC cells compared with signals generated by its upstream gene, RAS. ATC cells stimulated the growth of HUVECs via humoral factors, including VEGF; this effect was clearly inhibited by sorafenib. The present findings highlighted the potential of sorafenib for the treatment of ATC and provided insight into its mechanism of action.
PMID: 31545405 [PubMed - as supplied by publisher]

Source: International Journal of Oncology - September 18, 2019 Category: Cancer & Oncology Authors: Ishihara S, Onoda N, Noda S, Asano Y, Tauchi Y, Morisaki T, Kashiwagi S, Takashima T, Ohira M Tags: Int J Oncol Source Type: research