title: Celecoxib decreases prostaglandin E2 concentrations in nipple aspirate fluid from high risk postmenopausal women and women with breast cancer.
abstract: BACKGROUND
  Celecoxib inhibits PGE2 production in cancerous tissue. We previously reported that PGE2 levels in nipple aspirate fluid (NAF) and plasma were not decreased in women at increased breast cancer risk who received celecoxib 200 mg twice daily (bid). The endpoints of the current study were to determine if a short course of celecoxib 400 mg bid would decrease PGE2 levels in women 1) at increased breast cancer risk, and 2) with established breast cancer.
  
  
  METHODS
  NAF and plasma samples were collected before, 2 weeks after taking celecoxib 400 mg bid, and two weeks after washout from 26 women who were at increased breast cancer risk. From 13 women with newly diagnosed breast cancer, NAF from the incident breast and plasma were collected before and on average 2 weeks after taking celecoxib. Additionally, in nine of the 13 women with breast cancer, NAF was collected from the contralateral breast.
  
  
  RESULTS
  No consistent change in NAF or plasma PGE2 levels was noted in high risk premenopausal women. NAF PGE2 levels decreased after celecoxib administration in postmenopausal high risk women (p = 0.02), and in both the NAF (p = 0.02) and plasma (p = 0.03) of women with breast cancer.
  
  
  CONCLUSIONS
  Celecoxib 400 mg bid taken on average for 2 weeks significantly decreased NAF, but not plasma, PGE2 levels in postmenopausal high risk women, and decreased both NAF and plasma PGE2 levels in women with newly diagnosed breast cancer. PGE2 levels may predict celecoxib breast cancer prevention and treatment efficacy. Our observations are preliminary, and larger studies to confirm and extend these findings are warranted.
authors.affiliation: Surgery, University of Missouri, Columbia, MO 65212, USA. sautere@health.missouri.edu
authors.forename: Edward R
authors.initials: ER
authors.lastname: Sauter
authors.forename: Wenyi
authors.initials: W
authors.lastname: Qin
authors.forename: Lisa
authors.initials: L
authors.lastname: Schlatter
authors.forename: John E
authors.initials: JE
authors.lastname: Hewett
authors.forename: John T
authors.initials: JT
authors.lastname: Flynn
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001145:Arrhythmias, Cardiac / Q000139:chemically induced; D001826:Body Fluids / Q000737:chemistry / Q000187:drug effects*; D001943:Breast Neoplasms / Q000378:metabolism* / Q000517:prevention & control; D018270:Carcinoma, Ductal, Breast / Q000378:metabolism* / Q000517:prevention & control; D002285:Carcinoma, Intraductal, Noninfiltrating / Q000378:metabolism* / Q000517:prevention & control; D000068579:Celecoxib; D052246:Cyclooxygenase 2 Inhibitors / Q000008:administration & dosage / Q000009:adverse effects / Q000494:pharmacology* / Q000627:therapeutic use; D003967:Diarrhea / Q000139:chemically induced; D015232:Dinoprostone / Q000032:analysis* / Q000097:blood; D004305:Dose-Response Relationship, Drug; D004487:Edema / Q000139:chemically induced; D005260:Female; D006801:Humans; D008875:Middle Aged; D009558:Nipples; D010352:Patient Dropouts; D017698:Postmenopause / Q000097:blood; D017697:Premenopause / Q000097:blood; D011720:Pyrazoles / Q000008:administration & dosage / Q000009:adverse effects / Q000494:pharmacology* / Q000627:therapeutic use; D012307:Risk Factors; D013449:Sulfonamides / Q000008:administration & dosage / Q000009:adverse effects / Q000494:pharmacology* / Q000627:therapeutic use
chemical_list: D052246:Cyclooxygenase 2 Inhibitors; D011720:Pyrazoles; D013449:Sulfonamides; D000068579:Celecoxib; D015232:Dinoprostone