Τίτλος:
EPHA2, EPHA4, and EPHA7 Expression in Triple-Negative Breast Cancer
Γλώσσες Τεκμηρίου:
Αγγλικά
Περίληψη:
Ongoing research continues to elucidate the complex role of ephrin
receptors (EPHs) and their ligands (ephrins) in breast cancer
pathogenesis, with their varying expression patterns implied to have an
important impact on patients’ outcome. The current study aims to
investigate the clinical significance of EPHA2, EPHA4, and EPHA7
expression in triple-negative breast cancer (TNBC) cases. EPHA2, EPHA4,
and EPHA7 protein expression was assessed immunohistochemically on
formalin-fixed and paraffin-embedded (FFPE) TNBC tissue sections from 52
TNBC patients and correlated with key clinicopathologic parameters and
patients’ survival data (overall survival (OS); disease-free survival
(DFS)). EPHA2, EPHA4, and EPHA7 expression was further examined in TNBC
cell lines. EPHA2 overexpression was observed in 26 (50%) of the TNBC
cases, who exhibited a shorter OS and DFS than their low-expression
counterparts, with EPHA2 representing an independent prognostic factor
for OS and DFS (p = 0.0041 and p = 0.0232, respectively). EPHA4
overexpression was associated with lymph node metastasis in TNBC
patients (p = 0.0546). Alterations in EPHA2, EPHA4, and EPHA7 expression
levels were also noted in the examined TNBC cell lines. Our study
stresses that EPHA2 expression constitutes a potential prognostic factor
for TNBC patients. Given the limited treatment options and poorer
outcome that accompany the TNBC subtype, EPHA2 could also pose as a
target for novel, more personalized, and effective therapeutic
approaches for those patients.
Συγγραφείς:
Nikas, Ilias
Giaginis, Constantinos
Petrouska, Kalliopi and
Alexandrou, Paraskevi
Michail, Artemis
Sarantis, Panagiotis and
Tsourouflis, Gerasimos
Danas, Eugene
Pergaris, Alexandros and
Politis, Panagiotis K.
Nakopoulou, Lydia
Theocharis, Stamatios
Περιοδικό:
DIAGNOSTIC ONCOLOGY
Λέξεις-κλειδιά:
biomarker; basal-like breast cancer; EPH; ephrin; targeted therapy
DOI:
10.3390/diagnostics12020366
