Cell lineStatus FGFR1 DMS-114Gene amplification NCI-H520Gene amplification NCI-H1581Gene amplification FGFR2 NCI-H716Gene amplification KATO-IIIGene amplification.

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Cell lineStatus FGFR1 DMS-114Gene amplification NCI-H520Gene amplification NCI-H1581Gene amplification FGFR2 NCI-H716Gene amplification KATO-IIIGene amplification HSC-39Gene amplification SNU-16Gene amplification SUM-52PEGene amplification MFE-280Gene mutation (S252W) MFE-296Gene mutation (N549K) AN 3CAGene mutation (K310R/N549K) FGFR3 KMS-11 Gene mutation (Y373C), t(4;14) translocation UM-UC-14Gene mutation (S249C) RT-4 Gene rearrangement (FGFR3-TACC3) Others NCI-N87Wild type (ERBB2 amplification) MKN-45Wild type (c-Met amplification) SK-MEL-1Wild type (BRAF V600E) MeWoWild type (NF1 loss) HCT-116Wild type (KRAS G13D) Supplementary Table S1. Supplementary Table S1 Genetic status information of cancer cell lines

Supplementary Table S2. Supplementary Table S2 List of probe that is significantly modulated by CH /Debio 1347 PROBE_IDSYMBOLLog2 ratioLog10 p-value _s_atACOT _atATAD _atCCNG _atCDC25A _s_atCDC _atDKFZp762E _s_atDTL _s_atDUSP _atDUSP _atEIF2B _s_atFEN _s_atFEN _atHSPC _s_atIER _atIFRD _atIPO _atISGF3G _atMAFF _s_atMCM _s_atMCM _atMCM _s_atMCM _s_atMCM _s_atMCM _atNCAPD _atNCAPH _s_atNIP _atNOC3L _s_atNP _x_atORC6L _s_atPAICS _atPBK _atPHLDA _s_atPHLDA _s_atPNO _atPOLE _atPOLR3G _s_atPOLR3K _atRFC _s_atRFC _atRFC _atRRM _atRRP _atSHCBP _atSLC20A _s_atSLC25A _s_atSLCO4A _atTRIB _atTRIP _x_atUCHL5IP _s_atUCK

Supplementary Table S3. Supplementary Table S3 In vivo efficacy data of CH /Debio 1347 Xenograft model FGFR genetic alteration status Tumor growth inhibition (%) CH /Debio 1347 (100 mg/kg) DMS-114 FGFR2 gene amplification 94% SNU-16 FGFR2 gene amplification 147% NCI-N87 Wild type (ERBB2 amplification) -1% MKN-45 Wild type (c-Met amplification) -13%

Supplementary Figure S1. Supplementary Figure S1. MAPK pathway suppression by CH /Debio 1347 in FGFR genetically altered cancer cell lines A MEK-inducible gene signature was obtained from the work from Pratilas et al. From their list for 60 differentially expressed probes upon MEK inhibitor treatment, 56 down-regulated probes were used. Distributions of log-ratio to control were plotted as a histogram. X- axis represents log-ratio. Y-axis represents frequency. Distribution pattern for probes in the MEK-inducible signature were colored in blue, and distribution for other probes were in red. Cells were treated with 1 µM of CH /Debio 1347 or DMSO for 24-h. Total RNA samples from the cells were analyzed with microarray. FGFR2 altered cancers FGFR1 altered cancersFGFR3 altered cancersFGFR wild type NCI-H716 (Amplification) KATO-III (Amplification) HSC-39 (Amplification) DMS-114 (Amplification) NCI-H520 (Amplification) NCI-H1581 (Amplification) KMS-11 (Mutation) UM-UC-14 (Mutation) RT-4 (Fusion) NCI-N87 x Log-ratio Frequency y MFE-280 (Mutation) MFE-296 (Mutation) AN3 CA (Mutation) SNU-16 (Amplification)

Supplementary Figure S2. DUSP6: _at A

Supplementary Figure S2 (Cont.). DUSP6: _s_at B

Supplementary Figure S2 (Cont.) DUSP6: _at Supplementary Figure S2. Modulation of DUSP6 expression in FGFR inhibitor sensitive cancer cell lines Bar graphs shows ratio in signal of probes (a _at, b _s_at, c _at) that recognize DUSP6 compared with the treatment of DMSO in 14 cancer cell lines. Y-axis represents signal intensity. C