Table 5.
Correlations of CINSARC classes with therapeutic response/vulnerability in Luminal B breast cancers.
| Therapies | Characteristics | N | CINSARC classes | p-value | ||
|---|---|---|---|---|---|---|
| Low-risk | High-risk | |||||
| Chemotherapy | 107-gene signature | No pCR-like | 1587 | 663 (83%) | 924 (75%) | 1.43E−04 |
| pCR-like | 441 | 140 (17%) | 301 (25%) | |||
| pCR | No pCR | 124 | 49 (88%) | 75 (80%) | 0.270 | |
| pCR | 26 | 7 (12%) | 19 (20%) | |||
| Hormone therapy | E2F4-activation signature | Low | 496 | 348 (43%) | 148 (12%) | 3.73E−57 |
| High | 1532 | 455 (57%) | 1077 (88%) | |||
| CDK4/6 inhibitors | RBsig signature | Score | 2028 | 0.01 (−0.9–1.6) | 0.44 (−0.6–2.6) | 1.57E−100 |
| E2F regulon signature | Score | 2028 | 0.11 (−0.6–0.6) | 0.3 (−0.5–0.73) | 5.36E−56 | |
| PARP inhibitors | HRD signature | Low | 248 | 94 (94%) | 154 (81%) | 2.59E−03 |
| High | 42 | 6 (6%) | 36 (19%) | |||
| Immune checkpoint inhibitorss | ICR signature | Score | 2028 | −0.33 (−2.31–2.6) | −0.21 (−1.8–3.1) | 8.07E−04 |
| TIS signature | Score | 2028 | −0.35 (−2.3–2.2) | −0.24 (−2.1–2.8) | 2.68E−03 | |
| TLS signature | Score | 2028 | −0.32 (−2.2–1.8) | −0.17 (−3.2–2.3) | 1.69E−05 | |
| IA ESCAT alterations | ERBB2 amplification1 | No | 764 | 305 (100%) | 459 (98%) | 0.156 |
| Yes | 8 | 1 (0%) | 7 (2%) | |||
| PIK3CA mutation | No | 575 | 219 (72%) | 356 (76%) | 0.151 | |
| (E542K, E545K/A, H1047R/L) | Yes | 197 | 87 (28%) | 110 (24%) | ||
| IIA ESCAT alterations | ESR1 mutation | No | 772 | 306 (100%) | 466 (100%) | — |
| (E380Q, Y537S/C/N, D538G) | Yes | 0 | 0 (0%) | 0 (0%) | ||
| PTEN loss2 | No | 766 | 305 (100%) | 461 (99%) | 0.411 | |
| Yes | 6 | 1 (0%) | 5 (1%) | |||
| IIB ESCAT alterations | AKT1 mutation | No | 752 | 296 (97%) | 456 (98%) | 0.361 |
| (E17K) | Yes | 20 | 10 (3%) | 10 (2%) | ||
| ERBB2 mutation3 | No | 761 | 302 (99%) | 459 (98%) | 1 | |
| Yes | 11 | 4 (1%) | 7 (2%) | |||
pCR: pathological complete response; 1: >= 6 copies; 2homozigous deletion, truncated mutations and kown inactivating missense mutations (e.g., R130Q/G); 3hotspot activating missense mutations (e.g., S310F/Y, L755S, V777L), inframe insertion exon 2 O (e.g., Y772_A775dup).