FMS-like tyrosine kinase 3 (FLT3) amplification in patients with metastatic colorectal cancer.
Hiroko HasegawaHiroya TaniguchiYoshiaki NakamuraTakeshi KatoSatoshi FujiiHiromichi EbiManabu ShiozawaSatoshi YukiToshiki MasuishiKen KatoNaoki IzawaToshikazu MoriwakiEiji OkiYoshinori KagawaTadamichi DendaTomohiro NishinaAkihito TsujiHiroki HaraTaito EsakiTomohiro NishidaHiasto KawakamiYasutoshi SakamotoIzumi MikiWataru OkamotoKentaro YamazakiTakayuki YoshinoPublished in: Cancer science (2020)
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.
Keyphrases
- tyrosine kinase
- epidermal growth factor receptor
- metastatic colorectal cancer
- nucleic acid
- acute myeloid leukemia
- copy number
- genome wide
- end stage renal disease
- label free
- chronic kidney disease
- dna methylation
- prognostic factors
- risk assessment
- peritoneal dialysis
- newly diagnosed
- young adults
- cross sectional
- high resolution
- patient reported