2025乳房醫學線上研討會，今年度共3場會議，將於6/27, 7/25, 08/29，在乳e學院線上進行，歡迎有意報考乳房專科醫師的學員及各位會員踴躍上網觀看影片!

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.

CDK4/6 inhibitors have emerged as an important treatment option for advanced hormone receptor-positive breast cancer. They work by blocking the activity of proteins called CDK4 and CDK6, which are involved in cell division. By doing this, these inhibitors can prevent cancer cells from growing and dividing.

Several CDK4/6 inhibitors are currently approved for use, including Ribociclib , Palbociclib and Abemaciclib. They are commonly used in combination with hormone therapy as first-line treatment for advanced hormone receptor-positive breast cancer, and have been shown to significantly prolong progression-free survival in this patient population.

It has been observed that certain markers may predict response to treatment, although further research is needed in this area. For example, patients with hormone receptor-positive breast cancer seem to respond better to CDK4/6 inhibitors compared to those with hormone receptor-negative cancer. There is also some evidence to suggest that alterations in certain genes such as PIK3CA could predict resistance to CDK4/6 inhibitors.

Overall, CDK4/6 inhibitors have brought a significant improvement in the management of advanced hormone receptor-positive breast cancer, offering a balance of efficacy and tolerability that can help to optimise patient outcomes.

This course provides an overview of T-DXd reimbursement updates in Taiwan, specifically for HER2+ 2L metastatic breast cancer (mBC) patients and HER2-low, HR- mBC patients under NHIA coverage. It covers policy changes, clinical implications, and eligibility criteria. Additionally, the course highlights T-DXd’s strong efficacy while maintaining a manageable safety profile as an ADC therapy. The session will also explore key adverse event (AE) management strategies, including the prevention and management of nausea and vomiting using three types of antiemetics for high-emetic-risk drugs, and the prevention and management of interstitial lung disease (ILD). The focus will be on proactive monitoring, early intervention, and best practices to optimize patient outcomes.

In hormone receptor-positive (HR+) breast cancer, the tumor immune microenvironment (TIM) is uniquely shaped by estrogen signaling, which not only suppresses immune activity but also fosters a microenvironment conducive to late recurrence. This makes late recurrence a critical issue that must not be underestimated in these patients. 

Estrogen promotes immunosuppressive mechanisms, such as polarizing macrophages toward the M2 subtype and enhancing Tregs and myeloid-derived suppressor cells (MDSCs). Conversely, 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. Excitingly, ongoing research is exploring how different CDK4/6 inhibitors uniquely modulate the TIM, potentially paving the way for more precise and effective treatment strategies in HR+ breast cancer.

Sacituzumab Govitecan (SG; Trodelvy) is a targeted therapy designed for adults with hormone receptor (HR)-positive and human epidermal growth factor receptor 2 (HER2)-negative metastatic breast cancer (MBC) who have received hormone therapy and at least two additional treatments for metastatic disease. It is an antibody-drug conjugate that binds to the Trop-2 antigen, delivering a potent chemotherapy directly to cancer cells6. Clinical trials have demonstrated that SG significantly improves progression-free survival and overall survival compared to traditional chemotherapy in this patient population. This therapy offers a new treatment option for patients with HR+/HER2- MBC, who historically have had limited treatment choices and poor survival outcomes. SG's mechanism of action and clinical efficacy make it a valuable addition to the treatment landscape for this challenging form of breast cancer.