BCL2 is an independent predictor of outcome in basal-like triple-negative breast cancers treated with adjuvant anthracycline-based chemotherapy
Jazyk angličtina Země Spojené státy americké Médium print-electronic
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
25616695
DOI
10.1007/s13277-015-3061-7
PII: 10.1007/s13277-015-3061-7
Knihovny.cz E-zdroje
- MeSH
- adjuvantní chemoterapie MeSH
- antracykliny aplikace a dávkování MeSH
- dospělí MeSH
- erbB receptory biosyntéza genetika MeSH
- Kaplanův-Meierův odhad MeSH
- lidé středního věku MeSH
- lidé MeSH
- lokální recidiva nádoru farmakoterapie genetika patologie MeSH
- přežití po terapii bez příznaků nemoci MeSH
- protoonkogenní proteiny c-bcl-2 biosyntéza genetika MeSH
- senioři MeSH
- triple-negativní karcinom prsu farmakoterapie genetika patologie MeSH
- Check Tag
- dospělí MeSH
- lidé středního věku MeSH
- lidé MeSH
- senioři MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- antracykliny MeSH
- EGFR protein, human MeSH Prohlížeč
- erbB receptory MeSH
- protoonkogenní proteiny c-bcl-2 MeSH
Neither targeted therapies nor predictors for chemotherapy sensitivity are available for triple-negative breast cancer (TNBC). Our study included 187 patients with TNBC, 164 of whom were treated with anthracycline-based adjuvant chemotherapy. Eleven molecular biomarkers were analyzed. BCL2, epidermal growth factor receptor (EGFR), MYC, TOP2A, and Ki-67 protein expression was evaluated by immunohistochemistry. The status of the EGFR, MYC, and TOP2A genes and chromosomes 7, 8, and 17 was assessed using fluorescence in situ hybridization. High BCL2 expression predicted poor relapse-free survival (RFS) in patients treated with anthracycline-based adjuvant chemotherapy (p = 0.035), poor breast cancer-specific survival (BCSS) (p = 0.048), and a trend to poor overall survival (OS) (p = 0.085). High levels of BCL2 expression predicted poor OS in basal-like (BL) TNBC patients treated with adjuvant anthracycline-based regimens (log-rank p = 0.033, hazard ratio (HR) 3.04, 95 % confidence interval (CI) 1.04-8.91) and a trend to poor RFS (log-rank p = 0.079) and poor BCSS (log-rank p = 0.056). Multivariate analysis showed that BCL2 status, tumor size, and nodal status all had independent predictive significance for RFS (p = 0.005, p = 0.091, p = 0.003, respectively; likelihood ratio test for the whole model, p = 0.003), BCSS (p = 0.012, p = 0.077, p = 0.01, respectively; likelihood ratio test for the whole model, p = 0.016), and OS (p = 0.008, p = 0.004, p = 0.004, respectively; likelihood ratio test for the whole model, p = 0.0006). Similarly, multivariate analysis for BL TNBC showed BCL2, tumor size, and nodal status all had independent predictive significance for RFS (likelihood ratio test for the whole model, p = 0.00125), BCSS (p = 0.00035), and OS (p = 0.00063). High EGFR expression was associated with poor BCSS (p = 0.039) in patients treated with anthracycline-based adjuvant chemotherapy. Patients who underwent anthracycline-based adjuvant chemotherapy and exhibited CMYC amplification had a trend to worse BCSS (p = 0.066). In conclusion, high BCL2 expression is a significant independent predictor of poor outcome in TNBC patients treated with anthracycline-based adjuvant chemotherapy, and this is the first study showing the BCL2 prediction in BL TNBC. BCL2 expression analysis could facilitate decision making on adjuvant treatment in TNBC patients.
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J Pathol. 2012 Jan;226(1):97-107 PubMed
J Clin Oncol. 2005 Oct 20;23(30):7483-90 PubMed
J Clin Invest. 2011 Jul;121(7):2750-67 PubMed
Nat Clin Pract Oncol. 2005 Aug;2(8):416-22 PubMed
Breast Cancer Res Treat. 2009 Jul;116(2):317-28 PubMed
Clin Cancer Res. 2008 Dec 1;14(23):7909-16 PubMed
Clin Cancer Res. 2004 Aug 15;10(16):5367-74 PubMed
Cancer Invest. 2004;22(2):248-56 PubMed
Neoplasma. 2006;53(5):393-401 PubMed
Tumour Biol. 2014 Dec;35(12):12255-63 PubMed
J Clin Oncol. 2011 Apr 20;29(12):1578-86 PubMed
J Pathol. 2014 Jan;232(2):142-50 PubMed
Cancer Res. 2012 Aug 15;72 (16):4193-203 PubMed
Eur J Cancer. 2004 Jan;40(2):205-11 PubMed
Br J Cancer. 2010 Aug 24;103(5):668-75 PubMed
Clin Cancer Res. 2013 Oct 1;19(19):5533-40 PubMed
Breast. 2012 Feb;21(1):20-6 PubMed
Ann Oncol. 2013 Nov;24(11):2801-7 PubMed
Breast Cancer Res Treat. 2010 Aug;123(1):171-5 PubMed
Mol Hum Reprod. 1998 Dec;4(12):1099-109 PubMed
Mol Pathol. 2000 Feb;53(1):15-8 PubMed
Breast Cancer Res Treat. 2012 Jul;134(1):277-82 PubMed
Med Oncol. 2012 Jun;29(2):401-5 PubMed
Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub. 2009 Mar;153(1):13-7 PubMed
J Clin Oncol. 2010 Mar 1;28(7):1145-53 PubMed
Nat Rev Cancer. 2005 May;5(5):341-54 PubMed
Nature. 2012 Apr 04;486(7403):395-9 PubMed
Histopathology. 2008 Jan;52(1):108-18 PubMed
Curr Drug Targets. 2014;15(12):1166-75 PubMed
Cancer Control. 2005 Apr;12(2):73-81 PubMed
Nature. 2009 Dec 24;462(7276):1005-10 PubMed
Am J Pathol. 2000 Mar;156(3):839-47 PubMed
Breast Cancer Res Treat. 2010 Aug;123(1):163-9 PubMed
Oncologist. 2012;17(10):1246-55 PubMed
Breast. 2014 Aug;23(4):473-81 PubMed
Breast Cancer Res Treat. 2003 Mar;78(1):97-103 PubMed
Cancer. 2000 Dec 1;89(11):2145-52 PubMed
J Clin Oncol. 2011 Mar 1;29(7):859-67 PubMed
J Exp Med. 2012 Apr 9;209(4):679-96 PubMed
Clin Cancer Res. 2007 Aug 1;13(15 Pt 1):4429-34 PubMed
Breast Cancer Res. 2011 Oct 06;13(5):R97 PubMed
Breast Cancer Res. 2005;7(6):R940-52 PubMed
Mol Oncol. 2010 Apr;4(2):161-8 PubMed
