title: Receptor status change from primary to residual breast cancer after neoadjuvant chemotherapy and analysis of survival outcomes.
abstract: BACKGROUND
  To evaluate the frequency of receptor change from pretreatment to residual breast cancer after NCT and their correlation with outcomes.
  
  
  METHODS
  Three hundred ninety-eight women were identified retrospectively. Estrogen receptor, progesterone receptor, and HER2 were reviewed. Patients were classified as not having receptor change versus any receptor change. Kaplan-Meier was used to estimate survival outcomes according to changes. Cox proportional hazards models were used to determine the association of receptor status changes with outcomes after adjustment for patient and tumor characteristics.
  
  
  RESULTS
  One hundred sixty-two (40.7%) patients had a change in at least 1 of the receptors from pretreatment to residual disease. Patients who had no change in receptor status had a significantly greater triple-negative breast cancer (TNBC) rate at baseline (P = .0001). Of the 193 hormone receptor (HR)-positive tumors, 9 (4.7%) and 29 (15.1%) became HER2-positive and TNBC, respectively. Of the 72 HER2-positive tumors, 20 (27.8%) and 9 (12.5%) became HR-positive and TNBC, respectively. Of the 128 TNBC tumors, only 2 (1.6%) and 33 (25.8%) became HER2-positive and HR-positive, respectively. At a median follow up of 40 months, 5-year overall survival (OS) was 73% and 63%; and 5-year relapse-free survival (RFS) was 63% and 48% for patients with or without any receptor change (P = .07 and P = .003), respectively. Any receptor change was associated with better RFS (hazard ratio, 0.63; 95% confidence interval [CI], 0.44-0.9) but not OS. (hazard ratio, 0.79; 95% CI, 0.53-1.18).
  
  
  CONCLUSIONS
  Changes in receptor status between the pretreatment and residual disease after NCT are frequent and appear to be associated with improved RFS because of the receptor stability of TNBC.
authors.affiliation: Department of Breast Medical Oncology, The University of Texas M.D. Anderson Cancer Center, Houston, TX.
authors.forename: Napa
authors.initials: N
authors.lastname: Parinyanitikul
authors.affiliation: Department of Biostatistics, The University of Texas M.D. Anderson Cancer Center, Houston, TX.
authors.forename: Xiudong
authors.initials: X
authors.lastname: Lei
authors.affiliation: Department of Breast Medical Oncology, The University of Texas M.D. Anderson Cancer Center, Houston, TX.
authors.forename: Mariana
authors.initials: M
authors.lastname: Chavez-MacGregor
authors.affiliation: Department of Breast Medical Oncology, The University of Texas M.D. Anderson Cancer Center, Houston, TX.
authors.forename: Shuying
authors.initials: S
authors.lastname: Liu
authors.affiliation: Department of Surgical Oncology, The University of Texas M.D. Anderson Cancer Center, Houston, TX.
authors.forename: Elizabeth A
authors.initials: EA
authors.lastname: Mittendorf
authors.affiliation: Department of Breast Medical Oncology, The University of Texas M.D. Anderson Cancer Center, Houston, TX.
authors.forename: Jennifer K
authors.initials: JK
authors.lastname: Litton
authors.affiliation: Department of Radiation Oncology, The University of Texas M.D. Anderson Cancer Center, Houston, TX.
authors.forename: Wendy
authors.initials: W
authors.lastname: Woodward
authors.affiliation: Department of Pathology, The University of Texas M.D. Anderson Cancer Center, Houston, TX.
authors.forename: Amy Hong
authors.initials: AH
authors.lastname: Zhang
authors.affiliation: Department of Breast Medical Oncology, The University of Texas M.D. Anderson Cancer Center, Houston, TX.
authors.forename: Gabriel N
authors.initials: GN
authors.lastname: Hortobagyi
authors.affiliation: Department of Breast Medical Oncology, The University of Texas M.D. Anderson Cancer Center, Houston, TX.
authors.forename: Vicente
authors.initials: V
authors.lastname: Valero
authors.affiliation: Department of Surgical Oncology, The University of Texas M.D. Anderson Cancer Center, Houston, TX; Department of Investigational Cancer Therapeutics, The University of Texas M.D. Anderson Cancer Center, Houston, TX. Electronic address: fmeric@mdanderson.org.
authors.forename: Funda
authors.initials: F
authors.lastname: Meric-Bernstam
authors.affiliation: Department of Breast Medical Oncology, The University of Texas M.D. Anderson Cancer Center, Houston, TX; Department of Systems Biology, The University of Texas M.D. Anderson Cancer Center, Houston, TX.
authors.forename: Ana M
authors.initials: AM
authors.lastname: Gonzalez-Angulo
mesh_terms: D000328:Adult; D000368:Aged; D000970:Antineoplastic Agents / Q000627:therapeutic use*; D014408:Biomarkers, Tumor / Q000032:analysis*; D001943:Breast Neoplasms / Q000188:drug therapy* / Q000401:mortality*; D017024:Chemotherapy, Adjuvant; D018572:Disease-Free Survival; D005260:Female; D006801:Humans; D053208:Kaplan-Meier Estimate; D008875:Middle Aged; D020360:Neoadjuvant Therapy; D018365:Neoplasm, Residual / Q000378:metabolism*; D016016:Proportional Hazards Models; D018719:Erb-b2 Receptor Tyrosine Kinases / Q000096:biosynthesis; D011960:Receptors, Estrogen / Q000096:biosynthesis; D011980:Receptors, Progesterone / Q000096:biosynthesis
chemical_list: D000970:Antineoplastic Agents; D014408:Biomarkers, Tumor; D018719:Erb-b2 Receptor Tyrosine Kinases; D011960:Receptors, Estrogen; D011980:Receptors, Progesterone; C508053:ERBB2 protein, human
keywords: Estrogen receptor; Her2; Molecular evolution; Receptor changes; Triple negative breast cancer