Research Papers:
Prognostic impact of AnxA1 and AnxA2 gene expression in triple-negative breast cancer
Metrics: PDF 1975 views | HTML 2751 views | ?
Abstract
Lee D. Gibbs1 and Jamboor K. Vishwanatha1
1Institute for Molecular Medicine and Texas Center for Health Disparities, University of North Texas Health Science Center, Fort Worth, TX 76017, USA
Correspondence to:
Lee D. Gibbs, email: [email protected]
Keywords: annexin; triple-negative breast cancer; prognosis; survival; relapse
Received: June 12, 2017 Accepted: December 08, 2017 Published: December 23, 2017
ABSTRACT
Objective: Previous studies have shown Annexin A1 (AnxA1) and Annexin A2 (AnxA2) association with the aggressive behavior of Triple Negative Breast Cancer (TNBC). Our aim was to determine the correlation of AnxA1 and AnxA2 with poor prognosis of TNBC patients.
Methods: We analyzed the gene expression of the human annexin family from microarray datasets and correlated with clinical outcomes to determine their ability to predict prognosis.
Results: Within a mean follow-up time of 57.2 months in our TNBC cohort, high AnxA1 expression was an independent indicator of poor overall survival (OS) [hazard ratio (HR), 2.14; 95% confidence interval (CI), 1.22-3.78] and relapse-free survival (RFS) prognosis [HR, 1.66; 95% CI, 1.28-2.17]. Additionally, high AnxA2 expression was an independent indicator of poor OS [HR, 2.66; 95% CI, 1.14-6.25], RFS [HR, 1.45; 95% CI, 1.12-1.89], RFS [HR, 1.45; 95% CI, 1.12-1.89), and distant metastasis free survival (DMFS) prognosis [HR, 1.5; 95% CI, 1.16-1.95]. Analyses of TNBC patients with both high AnxA1 and AnxA2, demonstrates a significant decrease in OS (P=0.0017) and RFS (P=0.0002) when compared to the expression of genes independently. Furthermore, AnxA1 prognostic impact relies on high AnxA2 expression and both are preferential for TNBC when compared to other breast cancer subtypes.
Conclusion: Together these findings indicate that AnxA1 and AnxA2 are preferential dual prognostic predictors among TNBC patients.
All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 4.0 License.
PII: 23627