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<p>Pathological complete response (pCR) after neoadjuvant chemoimmunotherapy (NACi) is associated with improved patient outcomes in early triple-negative breast cancer (TNBC). This study aimed to identify factors associated with pCR after NACi. This cohort included all patients with stage II-III TNBC treated with NACi who underwent surgery at Institut Curie hospitals between 08/2021-06/2023. Among 208 patients, the overall pCR rate was 70% and was similar in ER &lt; 1% (69%) and ER-low TNBC (73%, <i>p</i> = 0.6). In a multivariate model, Ki-67 ≥ 30% (OR 5.19 [1.73–17.3]), centralized TILs ≥ 30% (OR = 3.08 [1.42–7.04]), absence of DCIS at initial biopsy (OR = 2.56 [1.08–6.25]) and germline mutations in homologous recombination genes (OR = 9.50 [2.37–67.7]) remained strong independent predictors of pCR. These findings may guide treatment decisions in patients with TNBC undergoing NACi. Almost all patients with germline mutations in HR genes achieved pCR, supporting de-escalation trials. We suggest that ER-low tumors should be managed as TNBC tumors.</p>

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Clinico-pathological factors predicting pathological response in early triple-negative breast cancer

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年2月13日

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  • Clara Helal,
  • Lounes Djerroudi,
  • Toulsie Ramtohul,
  • Enora Laas,
  • Anne Vincent-Salomon,
  • Maxime Jin,
  • Romain-David Seban,
  • Ivan Bieche,
  • Diana Bello-Roufai,
  • Francois-Clement Bidard,
  • Paul Cottu,
  • Delphine Loirat,
  • Matthieu Carton,
  • Florence Lerebours,
  • Nicolas Kiavue,
  • Emanuela Romano,
  • Claire Bonneau,
  • Luc Cabel

摘要

Pathological complete response (pCR) after neoadjuvant chemoimmunotherapy (NACi) is associated with improved patient outcomes in early triple-negative breast cancer (TNBC). This study aimed to identify factors associated with pCR after NACi. This cohort included all patients with stage II-III TNBC treated with NACi who underwent surgery at Institut Curie hospitals between 08/2021-06/2023. Among 208 patients, the overall pCR rate was 70% and was similar in ER < 1% (69%) and ER-low TNBC (73%, p = 0.6). In a multivariate model, Ki-67 ≥ 30% (OR 5.19 [1.73–17.3]), centralized TILs ≥ 30% (OR = 3.08 [1.42–7.04]), absence of DCIS at initial biopsy (OR = 2.56 [1.08–6.25]) and germline mutations in homologous recombination genes (OR = 9.50 [2.37–67.7]) remained strong independent predictors of pCR. These findings may guide treatment decisions in patients with TNBC undergoing NACi. Almost all patients with germline mutations in HR genes achieved pCR, supporting de-escalation trials. We suggest that ER-low tumors should be managed as TNBC tumors.