VEGF-A is the most potent angiogenic factor in tumour angiogenesis. Its effects are mediated via two receptors VEGFR-1 and VEGFR-2. Primary aim of our study was to examine the expression of VEGFR-1 in breast cancer and its correlation to VEGF expression, lymph node status, tumour size, histological grade, and hormone receptor status. To examine the VEGFR-1 and VEGF expressions in tumour and surrounding tissue of 51 breast cancer patients, and in healthy breast tissue of 30 benign breast diseases patients, we used three-step immunohistochemical staining. VEGFR-1 and VEGF expressions were significantly increased in breast cancer tumour in relation to surrounding tissue ( ), and the VEGF expression was significantly increased in lymph node positive breast cancer patients ( ). VEGFR-1 and VEGF expressions were significantly higher in breast cancer tumour compared with healthy breast tissue ( ). Significant correlation between VEGF and VEGFR-1 expressions was found ( ). No significant correlations between VEGF and VEGFR-1 expressions and tumour size, histological grade, and hormone receptor status were found. Increased expression of VEGFR-1 and VEGF in breast cancer tumour and significant correlation between these proteins suggest the possible role of VEGF/VEGFR-1 signalization in breast cancer development, although VEGFR-1 potential prognostic value was not confirmed. 1. Introduction Breast cancer is the most common cancer and the leading cause of cancer death among women worldwide [1]. Like many other solid cancers, it requires an independent blood supply to enlarge and develop metastases [2, 3]. This process, called tumour angiogenesis, is mediated primarily by vascular endothelial growth factor A (VEGF-A) [4]. A lot of studies have suggested that VEGF expression in tumour tissue is significantly correlated with microvessel density (MVD) and poor prognosis in human cancers including breast cancer [5, 6]. VEGF activates tyrosine kinase receptors, VEGFR-1 (also referred to as FLT1) and VEGFR-2 (or KDR) located in the endothelium, which leads to stimulation of endothelial migration, proliferation, permeability, and survival [7, 8]. Monocyte/macrophages, haematopoietic stem cells, and some tumour cells also express VEGFR-1 [9–11]. Most of the previously mentioned results of VEGF activity are consequences of VEGFR-2 activation [5]. VEGFR-1 has a weak tyrosine kinase activity but higher binding affinity for VEGF than VEGFR-2 [12]. To date, the role of VEGFR-1 in angiogenic signal delivery for VEGF in tumour angiogenesis is poorly examined and still not entirely
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