Literature DB >> 21729671

Phase II trial of neoadjuvant exemestane in combination with celecoxib in postmenopausal women who have breast cancer.

Maryam B Lustberg1, Stephen P Povoski, Weiqiang Zhao, Rebecca M Ziegler, Yasuro Sugimoto, Amy S Ruppert, Amy M Lehman, Donna R Shiels, Ewa Mrozek, Bhuvaneswari Ramaswamy, Rachel M Layman, Robert W Brueggemeier, Charles L Shapiro.   

Abstract

PURPOSE: Within breast tissue, aromatase expression and activity is increased by prostaglandin E2, providing a rationale for combining the COX-2 inhibitor celecoxib with an aromatase inhibitor. To evaluate the effect of these drugs on aromatase and other biomarkers, a phase II trial of neoadjuvant exemestane followed sequentially by celecoxib plus exemestane was performed.
METHODS: Postmenopausal women with estrogen receptor (ER) and/or progesterone (PR) positive stages II-III breast cancers received 8 weeks of exemestane 25 mg daily, followed by 8 weeks of exemestane 25 mg daily and celecoxib 400 mg twice daily. Core biopsies were collected pretreatment, after 8 weeks of exemestane, and at definitive breast cancer surgery. A tissue microarray was constructed and immunohistochemistry (IHC) for aromatase, ER, PR, HER-2, Ki-67, and COX-2 was performed.
RESULTS: Twenty-two women were enrolled. Celecoxib was discontinued in 4 (18%) women for toxicity (all grade 1 and 2) and 2 (9%) developed serious cardiac events occurring at 1 and 4 months after completing treatment. By US, there were 8 (36%)-partial responses and 12 (55%)-stable disease. There were no pathological complete responses (pCR). There were statistically significant decreases in ER (P = .003), PR (P = .002), Ki-67 (P < .001), and COX-2 (P = .004) expression. No significant differences in aromatase or HER-2 expression were observed (P = .13 and P = .39, respectively).
CONCLUSION: The addition of celecoxib to exemestane was tolerated by the majority of women and anti-tumor response was observed. Additional studies, including gene expression, are required to more fully understand the basis for the decreased expression of ER, PR, Ki-67, and COX-2.
Copyright © 2011. Published by Elsevier Inc.

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Year:  2011        PMID: 21729671      PMCID: PMC3440773          DOI: 10.1016/j.clbc.2011.03.022

Source DB:  PubMed          Journal:  Clin Breast Cancer        ISSN: 1526-8209            Impact factor:   3.225


  21 in total

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