title: Immunohistochemical evaluation of hormone receptor status for predicting response to endocrine therapy in metastatic breast cancer.
abstract: BACKGROUND
  The importance of establishing hormone receptor status of tumors for the treatment of women with hormone receptor-positive breast cancer has been emphasized, however, there is no general agreement as to how immunohistochemical assays should be evaluated. It is critical to evaluate hormone receptor status when considering response to endocrine therapy.
  
  
  METHODS
  Estrogen receptor (ER) and progesterone receptor (PgR) expression was examined by immunohistochemistry using Allred's score for primary breast tumors from 75 metastatic breast cancer patients who received first-line treatment with endocrine therapy (56 patients received tamoxifen, 11 patients received aromatase inhibitors, and 8 patients received LH-RH agonist or other endocrine reagents) on relapse. Correlation between hormone receptor status and response to endocrine therapy as well as post-relapse survival was analyzed.
  
  
  RESULTS
  The most significant correlation between positive ER expression and response to any endocrine therapy (p = 0.011) or tamoxifen only (p = 0.030) occurred when the cutoff score was set at 10%. When the evaluation was based on Allred's score (TS), a cutoff point of TS>or=4 showed a more significant association between positive ER expression and response to all kinds of endocrine therapy (p = 0.020) or tamoxifen only (p = 0.047). When evaluated at a cutoff point of 1% positive cells, there were fifteen patients with both ER- and PgR-negative tumors, and three patients (20.0%) responded to the therapy. Patients with 1% or more ER or PgR positive cells had better survival after relapse (p = 0.0005 and p = 0.0008, respectively).
  
  
  CONCLUSIONS
  The proportion score alone might be enough to predict hormone responsiveness and post-relapse survival in metastatic breast cancer. The cutoff might be set low, for example 1%, especially for metastatic disease.
authors.affiliation: Oncology and Immunology, Nagoya City University Graduate School of Medical Sciences, 1, Kawasumi, Nagoya 467-8601, Japan. hirokoy@med.nagoya-cu.ac.jp
authors.forename: Hiroko
authors.initials: H
authors.lastname: Yamashita
authors.forename: Yoshiaki
authors.initials: Y
authors.lastname: Yando
authors.forename: Mariko
authors.initials: M
authors.lastname: Nishio
authors.forename: Zhenhuan
authors.initials: Z
authors.lastname: Zhang
authors.forename: Maho
authors.initials: M
authors.lastname: Hamaguchi
authors.forename: Keiko
authors.initials: K
authors.lastname: Mita
authors.forename: Shunzo
authors.initials: S
authors.lastname: Kobayashi
authors.forename: Yoshitaka
authors.initials: Y
authors.lastname: Fujii
authors.forename: Hirotaka
authors.initials: H
authors.lastname: Iwase
mesh_terms: D018931:Antineoplastic Agents, Hormonal / Q000627:therapeutic use*; D001943:Breast Neoplasms / Q000188:drug therapy* / Q000378:metabolism* / Q000556:secondary; D017024:Chemotherapy, Adjuvant; D005260:Female; D020249:Hormone Replacement Therapy; D006801:Humans; D007124:Immunoenzyme Techniques; D008875:Middle Aged; D009364:Neoplasm Recurrence, Local / Q000188:drug therapy / Q000378:metabolism / Q000473:pathology; D011379:Prognosis; D011960:Receptors, Estrogen / Q000378:metabolism*; D011980:Receptors, Progesterone / Q000378:metabolism*; D015996:Survival Rate; D013629:Tamoxifen / Q000627:therapeutic use*
chemical_list: D018931:Antineoplastic Agents, Hormonal; D011960:Receptors, Estrogen; D011980:Receptors, Progesterone; D013629:Tamoxifen