• Dépistage, diagnostic, pronostic

  • Évaluation des technologies et des biomarqueurs

  • Sein

Circulating Tumor DNA Guides Prognosis in Metastatic Triple-Negative Breast Cancer

Menée à partir de l'analyse de 506 échantillons plasmatiques prélevés sur 164 patientes atteintes d'un cancer du sein triplement négatif, cette étude évalue l'association entre la proportion de l'ADN circulant d'origine tumorale ou le niveau d'altération du nombre de copies somatiques et la survie des patientes

Triple-negative breast cancer (TNBC) constitutes up to 15% of all breast cancers but accounts for > 25% of breast cancer–related deaths, with limited improvements in overall survival over the past 20 years.1-3 It is a diagnosis of exclusion, defined by the lack of expression of estrogen receptor (ER), progesterone receptor (PR) and human epidermal growth factor receptor 2 (HER2), and is consequently accompanied by a lack of targeted therapeutic options. TNBC tumors frequently have inferior clinical outcomes and are biologically more aggressive than other breast cancer subtypes, with chemotherapy remaining the therapy of choice.1-3 Although diagnosed as a single tumor entity, there is a high degree of molecular heterogeneity within TNBC. Several attempts have been made to subdivide TNBC into clinically relevant subgroups, and there is early clinical evidence of a differential response to therapy depending on the underlying molecular features.4-9 Emerging clinical trials of targeted agents offer glimpses of hope, including the use of poly ADP ribose polymerase inhibitors in TNBCs with DNA repair defects,10,11 antiandrogen therapy in patients who are androgen receptor positive,12 and phosphatidylinositol 3-kinase inhibitors, which may sensitize BRCA-proficient TNBCs to poly ADP ribose polymerase inhibition.13 Moreover, a subset of TNBCs seems to be immunogenic, with high levels of tumor-infiltrating lymphocytes, providing a strong rationale for ongoing efforts to explore the role of immunotherapies.14,15 Improved understanding of the molecular heterogeneity of TNBC and the relevant pathways involved will undoubtedly hold the key to better outcomes for patients with this disease.

Journal of Clinical Oncology , éditorial en libre accès, 2017

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