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Apoptosis regulator Bcl-2 is an independent prognostic marker for worse overall survival in triple-negative breast cancer patients

Abstract

Background

The objective of this study was to examine the prognostic significance of carbonic anhydrase IX (CAIX), an endogenous marker for tumor hypoxia; the cellular tumor antigen p53; and the apoptosis regulator Bcl-2, in triple-negative breast cancer (TNBC) patients.

Methods

Immunohistochemically determined expression of CAIX, p53, Bcl-2 and proliferation factor Ki-67, analyzed in 64 paraffin-embedded TNBC tissue samples, was used to assess their relation to clinicopathological variables and prognostic implications for overall survival (OS).

Results

Bcl-2 expression was negatively correlated with histological grade of tumor, while expression of p53 was positively correlated with the same clinical variable (p = 0.036 and p = 0.033, respectively). The p53 expression was also positively correlated with tumor size (p = 0.010). Survival analysis showed that patients with high Bcl-2 expression (above cutoff value determined by receiver operator characteristic [ROC] curve analysis) had shorter OS (p = 0.020). The same was observed for patients with tumors larger than 5 cm (p = 0.034) or positive lymph nodes (p = 0.004). Among all 3 examined markers, multivariate analysis showed that only Bcl-2 expression was a strong independent prognostic indicator for decreased OS (hazard ratio [HR] = 15.16, 95% confidence interval [95% CI], 2.881-79.727, p = 0.001).

Conclusions

Elevated expression of Bcl-2 was an independent prognostic factor for poorer OS in TNBC and as such a significant marker for tumor aggressiveness.

Post author correction

Article Type: ORIGINAL RESEARCH ARTICLE

DOI:10.5301/ijbm.5000291

Authors

Petar Ozretic, Ilija Alvir, Bozena Sarcevic, Zeljko Vujaskovic, Zrinka Rendic-Miocevic, Ana Roguljic, Lidija Beketic-Oreskovic

Article History

Disclosures

Financial support: This work was supported by a grant from the Ministry of Science, Education and Sports of the Republic of Croatia (grant no. 074-0982464-1187).
Conflict of interest: The authors declare they have no conflict of interest.
Meeting presentation: The results published in this paper were presented at the 11th Central European Oncology Congress (CEOC) in Opatija, Croatia, June 17-20, 2015, and the 10th European Breast Cancer Conference (EBCC-10) in Amsterdam, Netherlands, March 9-11, 2016.

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Authors

Affiliations

  •  Laboratory for Hereditary Cancer, Division of Molecular Medicine, Rudjer Boskovic Institute, Zagreb - Croatia
  •  Department of Gynecologic Oncology, University Hospital for Tumors, Sestre Milosrdnice Clinical Hospital Center, Zagreb - Croatia
  •  Department of Pathology, University Hospital for Tumors, Sestre Milosrdnice Clinical Hospital Center, Zagreb - Croatia
  •  Division of Translational Radiation Sciences, Department of Radiation Oncology, University of Maryland School of Medicine, Baltimore, Maryland - USA
  •  Department of Radiotherapy and Internal Oncology, University Hospital for Tumors, Sestre Milosrdnice Clinical Hospital Center, Zagreb - Croatia
  • Department of Clinical Oncology, University of Zagreb School of Medicine, Zagreb - Croatia

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