title: Tumor response and estrogen suppression in breast cancer patients treated with aromatase inhibitors.
abstract: BACKGROUND
  The rationale for the hormonal treatment of breast cancer (BC) is based on depriving tumor cells of estrogenic stimulation. Aromatase inhibitors (Als) block the conversion of peripheral tissue androgens to estrogens with different levels of potency. In an attempt to investigate the relationship between tumor response and estrogen suppression, we reviewed the hormonal and clinical data of two previous studies with formestane (250 and 500 mg i.m. fortnightly) in advanced BC patients.
  
  
  METHODS
  Two hundred four BC patients were selected on the basis of the availability of records concerning their plasma estrone (El) and estradiol (E2) levels assessed at scheduled times. The degree of estrogen suppression and the best clinical response of each patient during the trials were considered.
  
  
  RESULTS
  There was a positive and significant (P < 0.05) correlation between baseline and post-formestane E1 and E2 levels, with a decrease in the levels of both hormones irrespective of any antitumor response. In particular, the degree of plasma estrogen suppression was similar in the patients who experienced a complete remission and those with progressive disease (PD).
  
  
  CONCLUSIONS
  The plasma estrogen suppression induced by aromatase inhibition is not the only mechanism accounting for its clinical activity. Many clinical trials have demonstrated that all AIs induce a similar antitumor response regardless of their potency, and further investigations are warranted in order to improve our understanding as to why the patients with PD also show a significant plasma estrogen suppression. It is possible that intratumoral aromatase activity may be a marker for selecting the BC patients most likely to respond to AI treatment.
authors.affiliation: Division of Medical Oncology Unit B, Istituto Nazionale per lo Studio e la Cura dei Tumori, Milan, Italy. bajetta@istitutotumori.mi.it
authors.forename: E
authors.initials: E
authors.lastname: Bajetta
authors.forename: N
authors.initials: N
authors.lastname: Zilembo
authors.forename: E
authors.initials: E
authors.lastname: Bichisao
authors.forename: A
authors.initials: A
authors.lastname: Martinetti
authors.forename: R
authors.initials: R
authors.lastname: Buzzoni
authors.forename: P
authors.initials: P
authors.lastname: Pozzi
authors.forename: P
authors.initials: P
authors.lastname: Bidoli
authors.forename: L
authors.initials: L
authors.lastname: Ferrari
authors.forename: L
authors.initials: L
authors.lastname: Celio
mesh_terms: D000368:Aged; D018931:Antineoplastic Agents, Hormonal / Q000627:therapeutic use*; D047072:Aromatase Inhibitors; D001943:Breast Neoplasms / Q000188:drug therapy* / Q000473:pathology; D018450:Disease Progression; D004791:Enzyme Inhibitors / Q000627:therapeutic use*; D004958:Estradiol / Q000097:blood; D004970:Estrone / Q000097:blood; D005260:Female; D006801:Humans; D008875:Middle Aged; D012189:Retrospective Studies; D016896:Treatment Outcome
chemical_list: D018931:Antineoplastic Agents, Hormonal; D047072:Aromatase Inhibitors; D004791:Enzyme Inhibitors; D004970:Estrone; D004958:Estradiol