CDK4/6 inhibitors and endocrine therapies offer a dual benefit: they block estrogen signaling while also reshaping the TIM. CDK4/6 inhibitors, in particular, have shown promise in triggering anti-tumor immunity and reducing recurrence risk. The presentation primarily discusses clinical management strategies for hormone receptor-positive, HER2-negative metastatic breast cancer (HR+/HER2- mBC) after treatment with CDK4/6 inhibitors.
Although CDK4/6 inhibitors show significant progression-free survival (PFS) benefits in initial treatment, resistance eventually emerges. Post-CDK4/6 inhibitor treatment options for HR+/HER2- mBC include continuing CDK4/6 inhibitor-based regimens, switching to other treatments (such as targeted therapy, PARP inhibitors, chemotherapy, antibody-drug conjugates, etc.), and endocrine therapy. The presentation also discusses the optimal treatment choices after CDK4/6 inhibitor treatment and summarizes the results of several studies.
Besides, the importance of the PI3K-AKT-mTOR pathway in HR+ breast cancer, noting that approximately 40% of HR+/HER2- mBC patients harbor PIK3CA mutations in their tumors, which are associated with a poorer prognosis. PIK3CA mutations are considered truncal mutations in HR+HER2- breast cancer, often occurring early in tumor development and being selected for during tumor progression.
The results of several clinical trials, such as the SOLAR-1 trial, which showed that PI3K inhibitors (like alpelisib) have clinical efficacy in HR+HER2- mBC patients with PIK3CA mutations. Additionally, the BYLieve study evaluated the combination of alpelisib and endocrine therapy in HR+HER2- PIK3CA-mutant mBC patients, demonstrating long-term and very-long-term disease control.
In summary, this presentation provides detailed information on treatment options and strategies for HR+/HER2- mBC patients after CDK4/6 inhibitor treatment, highlighting the significance of PIK3CA mutations and their treatment options.
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