FMS-like tyrosine kinase 3 (FLT3) amplification in patients with metastatic colorectal cancer

Hiroko Hasegawa, Hiroya Taniguchi, Yoshiaki Nakamura, Takeshi Kato, Satoshi Fujii, Hiromichi Ebi, Manabu Shiozawa, Satoshi Yuki, Toshiki Masuishi, Ken Kato, Naoki Izawa, Toshikazu Moriwaki, Eiji Oki, Yoshinori Kagawa, Tadamichi Denda, Tomohiro Nishina, Akihito Tsuji, Hiroki Hara, Taito Esaki, Tomohiro NishidaHisato Kawakami, Yasutoshi Sakamoto, Izumi Miki, Wataru Okamoto, Kentaro Yamazaki, Takayuki Yoshino

Research output: Contribution to journalArticlepeer-review

5 Citations (Scopus)


FMS-like tyrosine kinase 3 (FLT3) plays a key role in hematopoiesis. However, the oncogenic role of FLT3 amplification in patients with metastatic colorectal cancer (mCRC) remains unclear. Here, we aimed to evaluate the characteristics, prognosis, and treatment efficacy of an FLT3 inhibitor (regorafenib) in patients with mCRC with FLT3 amplifications. Tumor tissue samples from 2329 patients were sequenced using NGS in the Nationwide Cancer Genome Screening Project in Japan. The effects of clinicopathological features, co-altered genes, prognosis, and efficacy of regorafenib were investigated. Between April 2015 and June 2018, 85 patients with mCRC with FLT3 amplification were observed. There were no differences in baseline characteristics between patients with or without FLT3 amplification. The frequency of RAS or other gene co-alterations was inversely correlated with the copy number status. Median survival time in patients with FLT3 amplification was significantly shorter compared with those with non-FLT3 amplification. Further investigations of FLT3 amplification as a potential treatment target in mCRC are warranted.

Original languageEnglish
Pages (from-to)314-322
Number of pages9
JournalCancer Science
Issue number1
Publication statusPublished - Jan 2021

All Science Journal Classification (ASJC) codes

  • Oncology
  • Cancer Research


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