Serial topoisomerase II expression in primary breast cancer and response to neoadjuvant anthracycline-based chemotherapy

M Martin-Richard*, M Munoz, J Albanell, L Colomo, M Bellet, MJ Rey, J Tabernero, C Alonso, A Cardesa, P Gascon, PL Fernandez

*Corresponding author for this work

Research output: Contribution to journalArticleResearchpeer-review

44 Citations (Scopus)

Abstract

Objective: We analyzed the value of topoisomerase IIalpha ( Topo II) in predicting the clinical response to anthracycline-based neoadjuvant chemotherapy in breast cancers and the potential changes in Topo II after chemotherapy. In parallel, HER2, which is commonly coexpressed with Topo II, and p53, a modulator of chemotherapy activity, were also analyzed. Methods: Forty-one patients with primary breast cancer and treated with neoadjuvant anthracycline-based chemotherapy (FAC or FEC) were included for the present study. Topo II, HER2 and p53 expression were measured by immunohistochemistry in pre and post chemotherapy ( at the time of surgery), tumor specimens and the results were correlated with the clinical response. Results: Topo II was overexpressed in 16 of 41 (31%) tumors before treatment, and this overexpression was significantly associated with clinical response ( p = 0.03). HER2 and p53 were unrelated to response. Notably, Topo II overexpression, but not HER2 or p53, was lost in specimens after chemotherapy ( p = 0.01). Conclusion: The observed link between Topo II and the clinical response to neoadjuvant anthracycline-based chemotherapy, together with its after chemotherapy, implies that Topo II deserves further testing in a prospective setting as a predictive marker. Copyright (C) 2004 S. Karger AG, Basel.

Original languageEnglish
Pages (from-to)388-394
Number of pages7
JournalOncology (Basel)
Volume66
Issue number5
DOIs
Publication statusPublished - 2004

Keywords

  • predictive factor
  • topoisomerase II alpha
  • doxorubicin
  • HER2
  • p53
  • breast cancer
  • INDUCTION CHEMOTHERAPY
  • ADJUVANT THERAPY
  • ALPHA
  • P53
  • AMPLIFICATION
  • DOXORUBICIN
  • RESISTANCE
  • ERBB-2
  • HER-2
  • MODULATION

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