title: First-line endocrine therapy alone could be a reasonable treatment option for hormone-positive, HER2-positive metastatic breast cancer.
abstract: OBJECTIVE
  The treatment strategy for hormone receptor-positive (ER+) HER2-positive (HER2+) metastatic breast cancer has been modified since several randomized trials have proven the effectiveness of anti-HER2 targeted therapy. Previously validated clinical practice guidelines recommending the use of endocrine therapy alone in first line might be changed.
  
  
  METHODS
  This study focused on the outcomes of women with ER+ HER2+ metastatic breast cancer receiving first-line endocrine therapy alone at the Léon-Bérard Centre, Lyon, France.
  
  
  RESULTS
  Of 290 patients with ER+ HER2+ tumors, 32 (11%) met the criteria for inclusion. The median age was 54 years (29-79 years). Eighteen patients (56%) had only bone and/or soft tissue metastases. Most patients (n = 21; 65%) had only one metastatic site. Fifteen (47%) had histological grade III disease. The median progression free survival (PFS) was 8.2 months (95% CI: 0.1-16.3) and the median overall survival (OS) was 48 months (95% CI: 22.9-72.9). The overall response rate was 25% (95% CI: 11-49%), including one patient with complete response and seven with partial responses. Ten patients (31%) had stable disease. After failure of endocrine therapy, all patients received trastuzumab. The median PFS after first-line chemotherapy was 8.4 months (95% CI: 5.1-11.8). We identified a group of 10 patients with good prognostic factor (tumor grade < 3 tumors and no visceral metastases), for whom median PFS was 15.5 months (95% CI: 7-23).
  
  
  CONCLUSIONS
  Our result suggests that first-line endocrine therapy is a viable therapeutic option for a selected population of metastatic breast cancer patients with HER2-positive tumors. Genomic and transcriptomic signature could help to identify tumors that remain dependant of estrogen-signaling pathway.
authors.affiliation: Centre Léon-Bérard, Department of Medical Oncology, 28, rue Laennec, 69008 Lyon, France. julien.peron@ymail.com
authors.forename: Julien
authors.initials: J
authors.lastname: Peron
authors.forename: Olivier
authors.initials: O
authors.lastname: Tredan
authors.forename: Isabelle
authors.initials: I
authors.lastname: Ray-Coquard
authors.forename: Thomas
authors.initials: T
authors.lastname: Bachelot
authors.forename: Sana Intidhar
authors.initials: SI
authors.lastname: Labidi Galy
authors.forename: Bertrand
authors.initials: B
authors.lastname: Favier
authors.forename: Isabelle
authors.initials: I
authors.lastname: Treilleux
authors.forename: Jean-Paul
authors.initials: JP
authors.lastname: Guastalla
mesh_terms: D000328:Adult; D000368:Aged; D061067:Antibodies, Monoclonal, Humanized / Q000627:therapeutic use; D018931:Antineoplastic Agents, Hormonal / Q000627:therapeutic use*; D047072:Aromatase Inhibitors / Q000627:therapeutic use; D001943:Breast Neoplasms / Q000188:drug therapy* / Q000378:metabolism / Q000401:mortality / Q000473:pathology; D018450:Disease Progression; D018572:Disease-Free Survival; D004965:Estrogen Antagonists / Q000627:therapeutic use*; D005260:Female; D006801:Humans; D008875:Middle Aged; D009363:Neoplasm Proteins / Q000037:antagonists & inhibitors / Q000378:metabolism; D018719:Erb-b2 Receptor Tyrosine Kinases / Q000037:antagonists & inhibitors / Q000378:metabolism; D011960:Receptors, Estrogen / Q000037:antagonists & inhibitors / Q000378:metabolism; D011980:Receptors, Progesterone / Q000037:antagonists & inhibitors / Q000378:metabolism; D012189:Retrospective Studies; D013629:Tamoxifen / Q000627:therapeutic use; D000068878:Trastuzumab
chemical_list: D061067:Antibodies, Monoclonal, Humanized; D018931:Antineoplastic Agents, Hormonal; D047072:Aromatase Inhibitors; D004965:Estrogen Antagonists; D009363:Neoplasm Proteins; D018719:Erb-b2 Receptor Tyrosine Kinases; D011960:Receptors, Estrogen; D011980:Receptors, Progesterone; D013629:Tamoxifen; D000068878:Trastuzumab