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Expression of topoisomerase II-α in triple negative breast cancer

Ivana Mrklić1, Zenon Pogorelić, Vesna Ćapkun

  • 1Departments of *Pathology, Forensic Medicine and Cytology †Pediatric Surgery ‡Nuclear Medicine, Split University Hospital Centre, School of Medicine, University of Split, Split, Croatia.

Applied Immunohistochemistry & Molecular Morphology : AIMM
|May 25, 2013
PubMed

Insights

Triple negative breast cancer (TNBC) lacks targeted therapies. High topoisomerase II-alpha (topoIIα) expression in TNBC suggests anthracycline chemotherapy may be effective for this aggressive cancer.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Triple-negative breast cancer (TNBC) presents a poor prognosis due to aggressive tumor biology and limited targeted therapy options.
  • Estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER2) negativity defines TNBC.
  • Topoisomerase II-alpha (topoIIα) is an intracellular target for anthracycline chemotherapy, with elevated expression noted in TNBC.

Purpose of the Study:

  • To investigate the prevalence of basal-like (BL) immunophenotype in TNBC.
  • To assess the correlation between BL immunophenotype, proliferation markers, and tumor characteristics.
  • To evaluate the expression of topoIIα in TNBC and its potential therapeutic implications.

Main Methods:

  • Immunohistochemical staining was performed on 83 TNBC patient samples (surgery dates: Jan 2003 - Dec 2009).
  • Markers analyzed included CK5/6, CK14, EGFR, Ki-67, and topoIIα.
  • Basal-like (BL) immunophenotype was defined by positivity for CK5/6, CK14, or EGFR.

Main Results:

  • 66.26% of TNBC cases exhibited the BL immunophenotype, significantly associated with higher mitotic count, BL morphology, histologic grade, and Ki-67 proliferation rate.
  • TopoIIα expression showed significant correlation with invasive ductal carcinoma NOS, higher mitotic count, histologic grade, and Ki-67.
  • A strong association was found between topoIIα expression and high proliferation rates (Ki-67).

Conclusions:

  • TNBC's lack of ER, PR, and HER2 expression limits targeted therapies, making chemotherapy the primary systemic treatment.
  • The observed topoIIα expression in TNBC suggests potential efficacy of anthracycline-based chemotherapy.
  • Targeting topoIIα could represent a viable therapeutic strategy for TNBC patients.

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