MINDACT
70-gene signature as an aid to treatment decisions in early-stage breast cancer
Phase 3N = 6,693NCT00433589
- Population
- Women aged 18-70 years with early-stage invasive breast cancer and up to three positive lymph nodes; the results recorded here are for the high clinical risk, low genomic risk group (randomised to chemotherapy or not)
- Design
- Randomised phase 3 study. Genomic risk (70-gene signature) and clinical risk (modified Adjuvant! Online) were both determined; women at low clinical and genomic risk had no chemotherapy, those at high clinical and genomic risk had chemotherapy, and women with discordant results were randomly assigned to chemotherapy or not, using either genomic or clinical risk.
- Primary endpoint
- DMFS
- Arms
- Chemotherapy (control, n = 749): Chemotherapy (high clinical risk, low genomic risk group randomised to receive it)
- No chemotherapy (experimental, n = 748): No chemotherapy (high clinical risk, low genomic risk group randomised to omit it)
- People
- Cardoso F
DMFSHR 0.66 (95% CI 0.48–0.92)Δ 96-month DMFS−2.6 pointsΔ 96-month DMFS−5 pointsΔ 96-month DMFS−0.2 points
Show the numbers
| Endpoint | Analysis | No chemotherapy | Chemotherapy | Effect |
|---|---|---|---|---|
| DMFSHigh clinical risk, low genomic risk, no chemotherapy (primary test population) | primaryCardoso 2016 | 94.7% at 5 y (92.5–96.2%) | — | The 'nochemo' arm here is the primary test population (high clinical risk, low genomic risk, patients not receiving chemotherapy), not the full randomised arm; the 1550 patients (23.2%) in this group are the clinical-high, genomic-low group. The abstract gives an absolute difference of 1.5 percentage points between these patients and those who received chemotherapy, lower without chemotherapy. |
| DMFSHigh clinical risk, low genomic risk, no chemotherapy (primary test population, n=644) | long term-updatemedian follow-up 8.7 yearsPiccart 2021 | 95.1% at 5 y (93.1–96.6%) | — | — |
| DMFSHigh clinical risk, low genomic risk, randomised ITT population | long term-updatemedian follow-up 8.7 yearsPiccart 2021 | 89.4% at 8 y (86.8–91.5%) | 92% at 8 y (89.6–93.8%) | HR 0.66 (95% CI 0.48–0.92)Randomised comparison in this group: chemotherapy n=749, no chemotherapy n=748. The abstract does not state the hazard-ratio direction; HR 0.66 is read as chemotherapy versus no chemotherapy because 8-year DMFS is higher with chemotherapy (92.0% vs 89.4%). The authors describe the benefit as small (2.6 percentage points). |
| DMFSHR-positive, HER2-negative, age 50 years or younger, high clinical risk and low genomic risk (exploratory) | exploratoryPiccart 2021 | 88.6% at 8 y (83.5–92.3%) | 93.6% at 8 y (89.3–96.3%) | Absolute difference 5.0 percentage points (SE 2.8, 95% CI -0.5 to 10.4). Exploratory subgroup analysis, described by the authors as underpowered. |
| DMFSHR-positive, HER2-negative, older than 50 years, high clinical risk and low genomic risk (exploratory) | exploratoryPiccart 2021 | 90% at 8 y (86.6–92.6%) | 90.2% at 8 y (86.8–92.7%) | Absolute difference 0.2 percentage points. Exploratory subgroup analysis. |
| Endpoint | Analysis | No chemotherapy | Chemotherapy | Effect |
|---|---|---|---|---|
| DMFSHigh clinical risk, low genomic risk, no chemotherapy (primary test population) | primaryCardoso 2016 | 94.7% at 5 y (92.5–96.2%) | — | The 'nochemo' arm here is the primary test population (high clinical risk, low genomic risk, patients not receiving chemotherapy), not the full randomised arm; the 1550 patients (23.2%) in this group are the clinical-high, genomic-low group. The abstract gives an absolute difference of 1.5 percentage points between these patients and those who received chemotherapy, lower without chemotherapy. |
| DMFSHigh clinical risk, low genomic risk, no chemotherapy (primary test population, n=644) | long term-updatemedian follow-up 8.7 yearsPiccart 2021 | 95.1% at 5 y (93.1–96.6%) | — | — |
| DMFSHigh clinical risk, low genomic risk, randomised ITT population | long term-updatemedian follow-up 8.7 yearsPiccart 2021 | 89.4% at 8 y (86.8–91.5%) | 92% at 8 y (89.6–93.8%) | HR 0.66 (95% CI 0.48–0.92)Randomised comparison in this group: chemotherapy n=749, no chemotherapy n=748. The abstract does not state the hazard-ratio direction; HR 0.66 is read as chemotherapy versus no chemotherapy because 8-year DMFS is higher with chemotherapy (92.0% vs 89.4%). The authors describe the benefit as small (2.6 percentage points). |
| DMFSHR-positive, HER2-negative, age 50 years or younger, high clinical risk and low genomic risk (exploratory) | exploratoryPiccart 2021 | 88.6% at 8 y (83.5–92.3%) | 93.6% at 8 y (89.3–96.3%) | Absolute difference 5.0 percentage points (SE 2.8, 95% CI -0.5 to 10.4). Exploratory subgroup analysis, described by the authors as underpowered. |
| DMFSHR-positive, HER2-negative, older than 50 years, high clinical risk and low genomic risk (exploratory) | exploratoryPiccart 2021 | 90% at 8 y (86.6–92.6%) | 90.2% at 8 y (86.8–92.7%) | Absolute difference 0.2 percentage points. Exploratory subgroup analysis. |
Data table
| Endpoint | HR | 95% CI |
|---|---|---|
| DMFS | 0.66 | 0.48–0.92 |
Appears in
Sources
Cardoso F, van't Veer LJ, Bogaerts J, Slaets L, Viale G, Delaloge S, et al. 70-Gene Signature as an Aid to Treatment Decisions in Early-Stage Breast Cancer. N Engl J Med. 2016;375(8):717-29.
Piccart M, van 't Veer LJ, Poncet C, Lopes Cardozo JMN, Delaloge S, Pierga JY, et al. 70-gene signature as an aid for treatment decisions in early breast cancer: updated results of the phase 3 randomised MINDACT trial with an exploratory analysis by age. Lancet Oncol. 2021;22(4):476-488.