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. 2021 Jun 28;11(11):2796–2811. doi: 10.1158/2159-8290.CD-20-1647

Table 1.

Actionability of alterations as per ESCAT

Readiness of use in clinical practice ESCAT for alterations in breast cancer Prevalence in the AURORA population Cumulative prevalence in the AURORA population
Tier I Targets ready for implementation in routine clinical decisions ERBB2 amplification (IA), germline BRCA1/2 mutations (IA), PIK3CA mutations (IA), MSI (IC), TRK fusions (IC) 143 (38%) 143 (38%)
Tier II Investigational targets likely to define patients who benefit from a targeted drug, but additional data needed PTEN loss (IIA), ESR1 mutations (IIA), AKT1 mutations (IIB), ERBB2 mutations (IIB) 65 (17%) 193 (51%)
Tier III Clinical benefit previously demonstrated in other tumor type or for similar molecular targets Somatic BRCA1/2 mutations (IIIA), MDM2 amplification (IIIA), ERBB3 mutations (IIIB) 35 (13%) 206 (54%)
Tier IV Preclinical evidence of actionability ARID1A/B, ATM/ATR/PALB2, CDH1, IGF1R, INPP4B loss, MAP2K4/MAP3K1, MT4, MYC, NF1, PIK3R1, RUNX1/CBFB, SF3B1, TP53 (IVA) 233 (61%) 313 (83%)
Tier V Evidence supporting co-targeting approaches
Tier X Lack of evidence of actionability FGFR1 amplification, CCND1 amplification 99 (26%) 328 (86%)

NOTE: We have reproduced the different molecular alterations and their level of evidence as per ESCAT (18). The molecular alterations reported on a sample-per-samples basis in AURORA are in bold.