![]() Curigliano’s talk, he mentioned that TILs are prognostic but not predictive. Tumor infiltrating lymphocytes (TILs) came up as well, where data suggests that having more TILs translates to a better outcome for the patient. Cortes also talked about platinum compounds adding benefit to chemotherapy with paclitaxel. ![]() He suggested similar strategies should be followed for TNBC de-escalation.ĭr. His overview of de-escalation included the APT trial, which evaluated shorter trastuzumab duration, while the ATEMPT trial evaluated TDM1 vs. In the Katherine trial for HER2+ patients, the addition of trastuzumab emtansine (TDM1) increased invasive-DFS rate. More escalation examples included the CREATE-X trial for TNBC, where the addition of capecitabine increased disease-free survival (DFS). ![]() ![]() Keynotte-522 added pembrolizumab to the therapy of TNBC patients while NeoSphere added pertuzumab to the therapy of HER2+ patients, which increased the EFS and the progression free survival (PFS) respectively. First, he talked about escalation of therapy and gave a brief overview of the Keynote-522 and NeoSphere trials as an example of escalation of therapy. Javier Cortes explained escalation strategies in human epidermal growth factor receptor 2-positive (HER2+) and TNBC patients. He posed the questions: Can we de-escalate? Can we give low risk patients chemo free therapy, ADCs alone? Salvage them with chemo when they have residual disease? Finally, he underscored the need to identify optimal responders, not only to IO, but also to chemotherapy.ĭr. He finalized by saying that in TNBC stage it is still unclear how aggressive the treatment should be. For immunotherapy clinical trials he recommended dual endpoints: pCR and EFS. He reasoned that early disease tumors are still plastic and that allows them to change since the beginning of chemotherapy, and with that the PD-L1 status can change. Subgroups with PD-L1+ and PD-L1- have similar EFS and pCR when treated with immune checkpoint inhibitors (ICI). In regards of immunotherapy (IO), nodal status makes no difference for patient response, contrary to what is seen for chemotherapy. Thus, it is possible to generate ADCs for TNBC, characterized by the absence of molecular targets. He talked about antibody drug conjugates (ADCs) and how there is no longer a need to target oncogenic drivers of the disease. TNBC is a very heterogeneous disease, however, he explained that TNBC subtyping provides a better understanding of the disease, but that it has low clinical relevance, at least until now. Peter Schmid talked about the incorporation of novel agents into early TNBC. However, he emphasized the need to generate a framework to understand when to escalate or de-escalate treatment in TNBC patients.ĭr. He talked about tailored chemotherapy escalation in patients with residual disease, and de-escalation in low-risk patients. He reminded the audience that TNBC patients that achieved a pathological complete response (pCR) have better event free survival (EFS), regardless of germline BRCA (gBRCA) status. One option is adding platinum therapy in high risk, node-positive patients and capecitabine in patients with residual disease with wild type BRCA. ![]() He went back to the ABC trials explaining that for early TNBC there is little chance to leave anthracyclines out from the neoadjuvant therapy (NAT) regimens, as they are the basis for systemic therapy along with taxanes. Giuseppe Curigliano focused more on the chemotherapy for TNBC. Giuseppe Curigliano, Peter Schmid and Javier Cortes during a session focused on systemic therapy for early triple negative breast cancer (TNBC).ĭr. Here are our takeaway messages from the conference.Įscalation and de-escalation of care was thoroughly discussed by Drs. Our team was there to present three posters. A well-attended conference covering a broad range of breast cancer topics. The ESMO Breast Cancer 2022 took place in Berlin on May 3 – 5. ![]()
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