Breast Cancer Res Treat (2017) 165:383–389 DOI 10.1007/s10549-017-4284-7 CLINICAL TRIAL COX2 induction: a mechanism of endocrine breast cancer resistance? 1 2 1,3 • • Brandi L. Clark Michael A. Murphy Landry K. Kamdem Received: 1 April 2017 / Accepted: 4 May 2017 / Published online: 21 June 2017 Springer Science+Business Media New York 2017 Abstract administration. We found no statistically signiﬁcant cor- Purpose Urine prostaglandin E2 (PGE2) levels have relations between fold increase in urine PGE2 levels and shown to be a risk factor of breast cancer, and the use of the pharmacokinetics of either exemestane or 17-hy- nonsteroidal anti-inﬂammatory drugs (NSAIDs) is known droexemestane (major in vivo metabolite of exemestane). to be beneﬁcial in preventing breast cancer risk and/or Conclusion Our results indicate that one of the pharma- recurrence with or without aromatase inhibitors. We cological effects to aromatase inhibitors (e.g., exemestane) hypothesized that the use of an aromatase inhibitor triggers involves the activation of the inﬂammatory pathway via the activation of the inﬂammatory pathway via release of release of PGE2. Further in vitro mechanistic and in vivo PGE2. translational studies designed to elucidate the role of this Methods A single oral 25 mg dose of an aromatase
Breast Cancer Research and Treatment – Springer Journals
Published: Jun 21, 2017
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