Volume 13 Supplement 2

IX Madrid Breast Cancer Conference

Open Access

BCL2 is a predictive marker of adjuvant CMF regimen in triple-negative breast cancer patients

  • K Bouchalova1,
  • M Cizkova1, 2,
  • R Trojanec1,
  • V Koudelakova1,
  • L Radova1,
  • J Furstova1,
  • B Melichar2,
  • K Cwiertka2,
  • G Kharaishvili3,
  • Z Kolar3 and
  • M Hajduch1
Breast Cancer Research201113(Suppl 2):P8

https://doi.org/10.1186/bcr3029

Published: 16 November 2011

Introduction

Triple-negative breast cancers (TNBCS) are aggressive with poor prognosis. Patients cannot benefit from targeted treatment. Moreover, little is known of which TNBC patients will benefit from nontargeted adjuvant treatment. The objective was to search for predictors of adjuvant chemotherapy in TNBC.

Methods

The study included 67 TNBC patients in clinical stages I to III, all but 22 had undergone adjuvant chemotherapy (CMF - 27 patients). FISH using p53, HER1, centromere 7 and 17 probes was performed on tumor tissue. Bcl2 was detected by immunohistochemistry.

Results

HER1 amplification was found in 23.9%, p53 deletion was detected in 29.7% and bcl2 positivity was present in 32.8% tumors. A lower p53/chromosome 17 ratio correlated with higher grading (P = 0.003) and showed a strong trend toward HER1/chromosome 7 ratio (P = 0.053). Patients with a chromosome 17 copy number ≥1.9 had better overall survival than patients with a copy number <1.9 (Kaplan-Meier, P = 0.014). Bcl2-positive patients treated with adjuvant CMF had significantly better disease-free survival than bcl2-negative patients treated with adjuvant CMF (Kaplan-Meier, P < 0.035).

Conclusion

Initial data support the use of a classical CMF regimen in TNBC patients. However, the biomarker of CMF responsiveness is needed for clinical practice. We confirmed the bcl2 positivity as a predictor of CMF sensitivity in TNBC. Thus, validation of this marker in a larger study is needed. Higher chromosome 17 copy number was associated with better outcome, suggesting the importance of its assessment.

Declarations

Acknowledgements

Supported by grants IGA NS10286-3, NS9956, MSM6198959216 and Biomedreg CZ.1.05/2.1.00/01.0030.

Authors’ Affiliations

(1)
Laboratory of Experimental Medicine, Institute of Molecular and Translational Medicine, Faculty of Medicine and Dentistry, Palacky University and Faculty Hospital
(2)
Oncology Clinic, Faculty of Medicine and Dentistry, Palacky University and Faculty Hospital
(3)
Laboratory of Molecular Pathology, Faculty of Medicine and Dentistry, Palacky University and Faculty Hospital

Copyright

© Bouchalova et al. 2011

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