Table 1 Characteristics of the patients treated in WINTHER trial investigated with DDPP.

From: Digital Display Precision Predictor: the prototype of a global biomarker model to guide treatments with targeted therapy and predict progression-free survival

Study ID Age Sex Cancer site Prior lines PFS months DNA—list of molecular alterations (Foundation Medicine report)a Drug_given
203 67 F GI/NE 1 60.0+ No mutation Everolimus
148 82 M GI/NE 2 11.6 BCOR N1652fs*34; CDKN1B E126fs*1 Everolimus
6 64 F UP 1 8.1 TSC1 splice site 913 + 1G > T; BRCA1 truncation, intron 11; CDKN2A/B loss; DNMT3A R882H; LRP1B loss Everolimus
117 34 M HN 2 1.9 TSC2 S1431L; TP53 G245S; BCOR K374fs*19; SMARCA4 R1135W Everolimus
227 56 M LS 4 1.7 STK11 F354L; STK11 F354L; TERT promoter —124C > T Everolimus
90 74 M HN 2 1.3 PIK3CA Q546R; EP300 D1154fs*30; NOTCH1 L1746fs*40 Everolimus
83 59 M HN 4 8.8 MTOR L2209V; ETV6 trunc intron 5; CIC S333fs*36; MLL2 G3698 fs*51 Axitinib
223 65 F HN 3 7.1 CCND1 T2861 Axitinib
259 53 F HN 4 6.2 PDGFRA amp Axitinib
25 65 M HN 2 5.3 TP53 I195F; KDM6A L725fs*4; MSH6 K1358fs*2; NFE2L2 R18Q Axitinib
88 56 M Lung 1 2.9 DNMT3A R635P; KRAS G12C; TP53 Y220C; MLL2 T1246M Axitinib
149 54 F CRC 5 7.4 KRAS G12V; ARID1A SPLICE SITE 2733-1G > A Trametinib
100 43 M Lung 2 6.6 BRAF A598_T599insT; IDH1 R132C Trametinib
118 78 F Lung 3 3.1 KRAS G12C; CDKN2A/B loss; TP53 V157F, Y220 fs*27; MUTYH G382D Trametinib
156 71 F Lung 2 14.3 EGFR E746_A750del, T790M; CDKN2A/B loss; CTNNB1 S33F; MYC amplification; SMAD4 P186fs*6; STAG2 splice site 1535-12_1630del108 Afatinib + cetuximab
235 60 F Lung 1 11.3 ERBB2 A775_G776insYVMA Afatinib
136 79 M Lung 3 0.4 ERBB3 amp; MET splice site 3028 + 1G > A; STK11 Q100* ATM L2450fs*11; BRCA1 E23fs*17; CDK4 amp; CDKN2A/B loss; MDM2 amp; APC I1307K; KDM5C truncation; MAP3K1 S1475* Afatinib
237 47 M HN 6 19.3 CCND1 amp; FGFR2 amp; CDKN2A/B loss; FGF19 amp; FGF4 amp; BAP1 trunc exon 3; FGF3 amp; MAGI2 Q1077*; PBRM1 E1155fs*17 NCT01004224 BGJ398
247 67 M Esophagus 2 1.6 FGFR2 amp; CDKN2A/B loss; TP53 W91*; ASXL1 splice site 472-2A > G NCT02052778 TAS-120
228 38 M CRC 5 0.7 FGFR1 amp; TP53 C176F; APC E1322*, R213*; SMAD4 loss; SOX9 V163fs*21 NCT02052778 TAS-120
183 66 M CRC 2 61.0+ RBB3; V104M; MAP2K1; E203K; CDKN2A/B loss; FBXW7 R465C; PIK3CA E39K; PIK3R1 R348*, R639*; PTEN R233*, splice site 801 + 2T > G; TP53 R158H, R273H; APC R1450*, R499*; ARID1A P1115fs*46, Q1306fs*17; ATRX Q2422*; CDH1 D433N; EP300 R2263*; FAM123B R631*; FAT1 A4305V; FLCN H429fs*39; MSH6 L1330fs*12, S279fs*12 Pembrolizumab
(TMB: 74.8)
(MSI: +)
294 57 M HN 1 1.7 BRCA2 K3408* Nivolumab
(TMB: 0)
(MSI: −)
270 76 F CRC 3 0.9 FLT4 amp; FLT3 amp equivocal; BARD1 C53fs*5; MYC amp; PARK2 loss exons 3–5; TP53 R175H; APC T1556fs*3; BCL2L1 amp; CDK8 amp; ETV6 rearrangement intron 5; FAM123B R497*; GATA6 amp equivocal; KDM6A-Y215*; MUTYH-Y165C; NOTCH1 Q2123* Atezolizumab
(TMB: 10.4)
(MSI: −)
  1. Foundation Medicinea10; ID 203, PFS 60+ and OS60+ are censored values, updated from the WINTHER trial Supplemental Table 3, Abbreviations: GI gastrointestinal, NE neuroendocrine, HN head and neck, UP unknown primary, LS liposarcoma, TMB tumor mutation burden, MSI microsatellite instability, amp amplification, del deletion, trunc truncation.