Additional file 2: of Dramatic response of BRAF V600E-mutant epithelioid glioblastoma to combination therapy with BRAF and MEK inhibitor: establishment and xenograft of a cell line to predict clinical efficacy

  • Yu Kanemaru (Creator)
  • Manabu Natsumeda (Creator)
  • Masayasu Okada (Creator)
  • Rie Saito (Creator)
  • Daiki Kobayashi (Creator)
  • Takeyoshi Eda (Contributor)
  • Jun Watanabe (Creator)
  • Shoji Saito (Creator)
  • Yoshihiro Tsukamoto (Creator)
  • Makoto Oishi (Creator)
  • Hirotake Saito (Creator)
  • Masayuki Nagahashi (Creator)
  • Takahiro Sasaki (Creator)
  • Rintaro Hashizume (Contributor)
  • Hidefumi Aoyama (Creator)
  • Toshifumi Wakai (Creator)
  • Akiyoshi Kakita (Creator)
  • Yukihiko Fujii (Creator)
  • Manabu Natsumeda (Creator)
  • Daiki Kobayashi (Creator)
  • Makoto Oishi (Creator)
  • Takahiro Sasaki (Creator)
  • Hashizume Rintaro (Contributor)



Figure S1. Genetic profiles of surgical tissue and the NGT41 cell line. BRAF V600E and TERT promotor (C250T) mutation was confirmed by Sanger sequencing (A), and heterozygous loss of CDKN2A/2B was identified by the multiplex ligation-dependent probe amplification method (B). Figure S2. Evaluation of BRAF V600E using ddPCR. Tumor DNA was extracted from the area of vivid tumor cells in the FFPE tissue by laser microdissection (A). Fractional abundance (FA) of mutated BRAF V600E was calculated as copies of mutated DNA/(copies of mutated DNA + wildtype DNA) (B). Scale bar A: 200 μm. Figure S3. Calculation of growth rate value in NGT41 and U87MG after combination treatment. Dose response curves on relative cell count showed marked response to BRAF and/or MEK inhibitor treatment in NGT41 (A), but minimal reduction in U87MG (B). Figure S4. BRAF and MEK inhibitor induced greater apoptosis and G0/G1 arrest in the NGT41 cell line. In BRAF V600E-mutant cell lines, each treatment significantly increased the number of apoptotic cells (n = 3, *p
Date made available2019

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