ESMO 2025 Breaking New Ground in Breast Cancer: Five Trials to Know

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This year’s wave of data in early breast cancer continues to reshape how we think about curative-intent therapy. Below are five pivotal trials with clear clinical relevance—from adjuvant cyclin-dependent kinase 4/6 (CDK4/6) inhibition, through next-generation antibody-drug conjugates (ADCs), and beyond into novel endocrine-resistance combinations.

1. monarchE (Adjuvant CDK4/6 in HR+, HER2–): Why OS matters

The primary overall survival (OS) analysis of the phase 3 monarchE trial confirms that abemaciclib plus endocrine therapy provides a statistically significant survival benefit in high-risk HR-positive/HER2-negative (HR+/HER2–) node-positive early breast cancer. At 76 months of follow-up, abemaciclib reduced the risk of death by 15.8% versus endocrine therapy alone (HR, 0.842; P = .0273), with 7-year OS rates of 86.8% versus 85.0%. 

Long-term invasive disease-free survival (HR, 0.734) and distant relapse-free survival (HR, 0.746) benefits were sustained, reflecting a 6%–7% absolute improvement and durable prevention of metastatic recurrence long after treatment ends. Abemaciclib is now the first CDK4/6 inhibitor to demonstrate a significant OS benefit in the adjuvant setting, firmly establishing CDK4/6 inhibition as a curative-intent option for this highest-risk, node-positive population.

2. ASCENT-03 & TROPION-Breast02 (ADC in 1st-line mTNBC)

These trials highlight the increasing ADC momentum now shaping earlier-stage therapeutic strategy. In ASCENT-03, first-line sacituzumab govitecan improved progression-free survival (PFS) to 9.7 versus 6.9 months (HR, 0.62) in programmed cell death ligand 1 (PD-L1)-ineligible metastatic triple-negative breast cancer (mTNBC). Crossover to SG after progression was allowed, which may blunt OS separation, but mirrors real-world access. Toxicity was manageable without mandated granulocyte colony-stimulating factor. 

Meanwhile, TROPION-Breast02 enrolled a poorer-prognosis population (15% of patients relapsed within 6 months), yet demonstrated stronger separation for datopotamab deruxtecan (Dato-DXd), with a PFS of 10.8 versus 5.6 months (HR, 0.57; P < .001) and statistically significant OS improvement (23.7 vs 18.7 months; HR, 0.79). The absence of doublet chemotherapy and no ADC crossover limit interpretability, though Dato-DxD-associated mucositis and ocular toxicity require proactive management. Together, these trials reaffirm that ADCs outperform chemotherapy in frontline mTNBC and support a shift toward deploying ADCs earlier in the disease course.

3. DESTINY-Breast05 (Adjuvant ADC in HER2+ residual disease): A Practice-Changer

In HER2+ early breast cancer with residual invasive disease after neoadjuvant therapy, adjuvant trastuzumab deruxtecan (T-DXd) reduced the risk of invasive disease recurrence or death by 53% compared with trastuzumab emtansine (T-DM1, HR, 0.47; P < .0001), with 3-year invasive disease-free survival (IDFS) of 92.4% versus 83.7%. OS data remain immature, but trend strongly in favor of T-DXd (HR, 0.61). This very high-risk group (inoperable or node-positive residual disease with heavy pre-treatment) clearly benefits from escalation with ADC therapy. DESTINY-Breast05 is poised to redefine adjuvant HER2+ management, while questions remain about whether T-DM1 retains a role for lower-risk residual disease.

4. DESTINY-Breast11 (Neoadjuvant ADC in HER2+ early disease): The Future Frontier

In a high-risk neoadjuvant HER2+ cohort, T-DXd followed by THP (trastuzumab, pertuzumab, taxane) achieved a higher pathogenic complete response rate than standard THP (ddAC→THP, 67.3% vs 56.3%; P = .003). Event-free survival and OS data remain immature. The T-DXd monotherapy induction arm was closed early due to higher-than-expected adjudicated interstitial lung disease/pneumonitis, highlighting that safety margins narrow when de-escalating chemotherapy in curative settings. DESTINY-Breast11 signals a potentially chemotherapy-reducing future for HER2+ disease, but more maturity and refined selection are required before practice changes.

5. evERA (Oral endocrine / ESR1-resistance combo): Tackling Post-CDK4/6 Escape

With adjuvant CDK4/6 inhibition expanding, strategies to address endocrine-resistant relapse must evolve. evERA evaluated giredestrant (oral selective estrogen receptor degrader [SERD]) plus everolimus versus endocrine therapy plus everolimus in ER-positive, /HER2– advanced breast cancer after CDK4/6 inhibition. 

The trial met both co-primary PFS endpoints—a 44% risk reduction overall and 62% reduction in the ESR1-mutated subgroup, with a positive OS trend. While currently metastatic, this lays groundwork for moving modern endocrine-resistance strategies earlier, particularly for ESR1-driven recurrence. This strategy is distinct from other ongoing trials recycling CDK4/6 inhibitors combined with oral SERD.

Where This Leaves Us

With these five studies, early breast cancer is entering an era of precision escalation—curative-intent ADCs and CDK4/6 inhibitors applied earlier and smarter, while oral SERDs and biology-driven combinations aim to prevent or delay resistance. The challenge ahead is not just adopting new breakthroughs, but in sequencing them intelligently—maximizing cure potential while minimizing toxicity and overtreatment.