TABLE 1.
Demographics and clinical characteristics of patients at baseline in total population and by biomarker stratification group (SAF)
| PIK3CA mut (N = 9) | PTEN loss a (N = 3) | Wild‐type (N = 13) | Total population (N = 25) | ||
|---|---|---|---|---|---|
| Median age b , a , years (min‐max) | 63.6 (57.8‐80.7) | 69.0 (62.5‐71.7) | 61.8 (49.0‐80.6) | 62.9 (49.0‐80.7) | |
| BMI [kg/m2], median (min‐max) | 27.9 (17.2‐34.8) | 21.8 (21.2‐27.7) | 24.0 (19.7‐32.8) | 24.2 (17.2‐34.8) | |
| ECOG performance status, n (%) | 0 | 7 (77.8) | 1 (33.3) | 10 (76.9) | 18 (72.0) |
| 1 | 2 (22.2) | 2 (66.7) | 3 (23.1) | 7 (28.0) | |
| 2 | 0 (0.0) | 0 (0.0) | 0 (0.0) | 0 (0.0) | |
| Hormone receptor status, n (%) | ER positive | 9 (100.0) | 3 (100.0) | 13 (100.0) | 25 (100.0) |
| PgR positive | 9 (100.0) | 3 (100.0) | 6 (46.2) | 18 (72.0) | |
| PIK3CA mutation status, by archival tumor tissue, n (%) a | Mutated coding exon 9 | 4 (44.4) | 0 (0) | 0 (0) | 4 (16.0) |
| Mutated coding exon 20 | 5 (55.6) | 0 (0) | 0 (0) | 5 (20.0) | |
| PTEN mutation status, n (%) | PTEN preserved | 9 (100.0) | 0 (0) | 13 (100.0) | 22 (88.0) |
| PTEN loss | 0 (0) | 3 (100.0) | 0 (0) | 3 (12.0) | |
| Tumor status at primary diagnosis—M0/M1 | M0 | 5 (55.6) | 2 (66.7) | 10 (76.9) | 17 (68.0) |
| M1 | 4 (44.4) | 1 (33.3) | 3 (23.1) | 8 (32.0) | |
| DFI, years [median (min‐max)] e | 13.7 (2.4‐15.1) | 14.4 (14.4‐14.4) | 8.2 (2.1‐16.1) | 10.6 (2.1‐16.1) | |
| Median time since primary diagnosis to date of first study treatment, years (min‐max) | 6.1 (1.6‐26.9) | 4.9 (0.9‐17.9) | 8.8 (0.9‐21.4) | 7.8 (0.9‐26.9) | |
| Visceral disease present, n (%) | 8 (88.9) | 3 (100.0) | 10 (76.9) | 21 (84.0) | |
| Metastatic sites c , d | Bone | 9 (100.0) | 2 (66.7) | 8 (61.5) | 19 (76.0) |
| Liver | 5 (55.6) | 1 (33.3) | 8 (61.5) | 14 (56.0) | |
| Lung | 3 (33.3) | 2 (66.7) | 3 (23.1) | 8 (32.0) | |
| Prior (neo‐)adjuvant therapy c , n (%) | ET | 4 (44.4) | 2 (66.7) | 9 (69.2) | 15 (60.0) |
| CHT | 4 (44.4) | 2 (66.7) | 6 (46.2) | 12 (48.0) | |
| Patients with prior palliative treatment, n (%) | Palliative | 9 (100.0) | 2 (66.7) | 11 (84.6) | 22 (88.0) |
| Prior lines of ET in metastatic setting, n (%) | 0 | 0 (0.0) | 1 (33.3) | 4 (30.8) | 5 (20.0) |
| 1 | 7 (77.8) | 2 (66.7) | 5 (38.5) | 14 (56.0) | |
| 2 | 2 (22.2) | 0 (0.0) | 4 (30.8) | 6 (24.0) | |
| Prior ET in metastatic setting c , n (%) | Fulvestrant | 3 (33.3) | 0 (0.0) | 3 (23.1) | 6 (24.0) |
| AI | 8 (88.9) | 1 (33.3) | 9 (69.2) | 18 (72.0) | |
| Prior CHT in metastatic setting, n (%) | 2 (22.2) | 1 (33.3) | 5 (38.5) | 8 (32.0) |
Demographics and clinical characteristics at baseline in the total population and in the prespecified subgroups: PIK3CA mut = “PIK3CA mut/ PTEN preserved”; PTEN loss = “PIK3CA mut or wt/ PTEN loss”; wild‐type = “PIK3CA wt/ PTEN preserved”.
Abbreviations: AI, aromatase inhibitors; BMI, body mass index; CHT, chemotherapy ECOG, Eastern Cooperative Oncology Group; ER, estrogen receptor; ET, endocrine therapy DFI, disease‐free interval; mut, mutant; PI3K, Phosphatidylinositol‐4,5‐bisphosphate 3‐kinase; PgR, Progesterone receptor; PIK3CA, Phosphatidylinositol‐4,5‐bisphosphate 3‐kinase, catalytic subunit alpha; PTEN, Phosphatase and tensin homolog; SAF, safety set; wt, wild‐type.
PIK3CA mutations in coding exons 9 and 20 were mutually exclusive. No patients with mutations in PIK3CA presented additionally PTEN loss, ie, all patients with PIK3CA mutations fell into the ‘PIK3CA mut/ PTEN preserved’ stratification group.
On date of informed consent.
More than one entry per patient possible.
Presented here are metastatic sites at enrolment that showed in ≥30% of total SAF population.
Median disease‐free interval was defined as the time from the last R0 resection of the primary tumor to the date of first local relapse or occurrence of distant metastases. DFI was only calculated for patients with M0 status at primary diagnosis and R0 resection (total population N = 13; PIK3CA mut/ PTEN preserved N = 4; PIK3CA mut or wt/ PTEN loss N = 1; PIK3CA wt/ PTEN preserved N = 8).