Table 2 Clinical and genomic characteristics of patients who achieved either stable disease ≥6 months or partial response (N = 5 patients).
From: Personalized matched targeted therapy in advanced pancreatic cancer: a pilot cohort analysis
Patient ID# Age (in years)/sex | Matched drugs and relevant pathogenic genomic alterations | Matching Score (%) ≥50% versus <50% | PFS (approximate months) | OS (months) | Best response | Comments |
|---|---|---|---|---|---|---|
#20 (69 y/M) | Palbociclib, CDKN2A loss exons 1–2, CDKN2B loss, Trametinib, KRAS G12D, KRAS G12R, Bevacizumab, TP53 R267W | ≥50% | 6.0 | 6.5 | SD ≥ 6 months | |
#12 (74 y/F) | Trametinib, BRAF V600E, SMAD4 loss, Trastuzumab and lapatinib, ERBB2 amplification, Bevacizumab, TP53 V218E | ≥50% | 7.8 | 9.4 | SD ≥ 6 months | |
#24 (63 y/F) | Palbociclib, CDKN2A_p16 R80* Trametinib, KRAS G12D | ≥50% | 9.2 | 19.4 | SD ≥ 6 months | Afatinib also given because KRAS alterations may require EGFR pathway in pancreatic cancer17 |
#22 (82 y/F) | Trametinib, GNAS R201C, KRAS G12D, NF1 D1976fs | ≥50% | 13.6 | 13.9 | SD ≥ 6 months | GNAS, KRAS and NF1 alterations all activate the MEK pathway18,19; trametinib is a MEK inhibitor |
#18 (63 y/F) | Palbociclib, CDKN2A loss exons 1–2, CDKN2B loss Trametinib, KRAS G12D, KRAS G12R, SMAD4 deletion exon 11 Bevacizumab, TP53 R267W. | ≥50% | 17.5+ | 17.5 | PR |
