title: Increasing Use of Neoadjuvant Treatment for T1 and T2 HER2-Positive Tumors.
abstract: BACKGROUND
  Use of targeted therapy for human epidermal growth factor receptor-2 (HER2)-positive breast cancer has led to improvements in survival. Furthermore, neoadjuvant chemotherapy (NAC) with dual HER2 agents demonstrated improved pathological complete response (pCR) rates. With these data, and with US FDA approval in September 2013 of pertuzumab in the neoadjuvant setting, we hypothesized that the use of NAC for early-stage HER2-positive patients is increasing.
  
  
  METHODS
  With Institutional Review Board approval, we reviewed 267 patients with 268 clinical T1 and T2 HER2-positive tumors treated from October 2008 to September 2014. We compared treatment in the early (October 2008-September 2013) to recent (October 2013-September 2014) periods. Statistical analysis was performed using Chi square tests.
  
  
  RESULTS
  Mean patient age was 59 years. Clinical T stage included 6 (2%) T1mic, 11 (4%) T1a, 41 (15%) T1b, 95 (35%) T1c, and 115 (43%) T2. Targeted therapy included combinations of trastuzumab, lapatinib, pertuzumab, and neratinib. NAC use increased from 53/219 (24.2%) in the early group to 19/49 (38.8%) in the recent group (p = 0.04). Forty-two percent (8/19) of patients in the recent group received neoadjuvant pertuzumab versus 0/53 in the early group (p < 0.0001). More clinically node-negative (cN0) patients received NAC in the recent (12/41, 29.3%) versus early (20/167, 12.0%) period (p = 0.01). For T1 tumors, the use of NAC more than doubled between the two time periods (5.6-17.2%; p = 0.06), while NAC use increased from 48 to 70% for T2 tumors (p = 0.08). The overall pCR rate after NAC was 48.6% (35/72).
  
  
  CONCLUSIONS
  NAC for HER2-positive breast cancer patients is increasing. Most striking was a substantial increase in NAC for patients with T1 tumors and cN0 disease.
authors.affiliation: Department of Surgery, Mayo Clinic, Rochester, MN, 55905, USA.
authors.forename: Zahraa
authors.initials: Z
authors.lastname: Al-Hilli
authors.forename: Judy C
authors.initials: JC
authors.lastname: Boughey
authors.forename: Tanya L
authors.initials: TL
authors.lastname: Hoskin
authors.forename: Courtney N
authors.initials: CN
authors.lastname: Heins
authors.forename: Tina J
authors.initials: TJ
authors.lastname: Hieken
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000970:Antineoplastic Agents / Q000627:therapeutic use*; D001943:Breast Neoplasms / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D018270:Carcinoma, Ductal, Breast / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D018275:Carcinoma, Lobular / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D005260:Female; D005500:Follow-Up Studies; D015972:Gene Expression Regulation, Neoplastic / Q000187:drug effects*; D006801:Humans; D007124:Immunoenzyme Techniques; D008875:Middle Aged; D058990:Molecular Targeted Therapy; D020360:Neoadjuvant Therapy / Q000706:statistics & numerical data*; D009361:Neoplasm Invasiveness; D009364:Neoplasm Recurrence, Local / Q000188:drug therapy / Q000473:pathology; D009367:Neoplasm Staging; D011379:Prognosis; D018719:Erb-b2 Receptor Tyrosine Kinases / Q000037:antagonists & inhibitors* / Q000378:metabolism
chemical_list: D000970:Antineoplastic Agents; D018719:Erb-b2 Receptor Tyrosine Kinases; C508053:ERBB2 protein, human