Expression of vascular endothelial growth factor (VEGF) and its two receptors (VEGF‐R1‐Flt1 and VEGF‐R2‐Flk1/KDR) in non‐small cell lung carcinomas (NSCLCs): correlation with angiogenesis and survival

Phosphorylated KDR expression in endometrial cancer cells relates to HIF1α/VEGF pathway and unfavourable prognosis

“…16 Cancer cell reactivity was thought to represent VEGF content, as KDR was thought to be confined to endothelial cells, despite reports suggesting the presence of KDR in a variety of human tumours, including breast, lung and endometrial carcinomas. [9][10][11][12][13] Constitutive expression of KDR, however, may not necessarily mean an active KDR pathway.…”

“…7,8 Cancer cells and intratumoral endothelium have also been reported to express VEGF receptors. [9][10][11][12][13] The expression of VEGFRs, however, does not necessarily mean active participation in cancer or endothelial cell biology as this can only be analysed by assessing the activated forms of these receptors. Brekken et al 14 produced monoclonal antibodies that preferentially recognize VEGF bound to its receptor KDR, which presumably reflects the activated KDR receptor.…”

Genetic alterations of multiple tumor suppressors and oncogenes in the carcinogenesis and progression of lung cancer

“…It has been suggested that VEGF expression is induced by HIF-1a responding to hypoxia in lung cancer tissues (Giatromanolaki et al, 2001), while COX-2 and NOS2-mediated stimuli have also been postulated as leading to marked VEGF expression in NSCLC (Marrogi et al, 2000). It remains controversial whether high level of VEGF expression and/or a high microvessel density correlate with a poor prognosis (Fontanini et al, 1999;Yano et al, 2000;Decaussin et al, 1999;Marrogi et al, 2000). VEGF-C promotes lymphangeogenesis through the activation of VEGFR-3-mediated signals, and is expressed in about 40% of NSCLC, raising the possibility of its involvement in lymphatic metastasis (Kajita et al, 2001).…”

Overexpression of vascular endothelial growth factor (VEGF) and its cellular receptor KDR (VEGFR-2) in the bone marrow of patients with acute myeloid leukemia

“…Expression of VEGF, VEGFR-1 and VEGFR-2 protein was semi-quantitatively assessed by scoring the proportion and intensity of stained cells according to published methods, with appropriate modifications. 17,[38][39] At first, the entire bone marrow section was systematically scanned at ϫ100 and ϫ250 magnification and the percentage of positive cells stained with each specific antibody within cellular areas was estimated according to a threegrade scale (1ϵ Ͻ10% positive cells, 2ϵ 10-50% positive cells, 3ϵ Ͼ50% positive cells). Subsequently, the intensity of positive staining was evaluated in three representative ϫ500 fields (0.126 mm 2 field area) selected in each section after the initial screening at ϫ100-ϫ250 magnification.…”

“…A recent study based on the immunohistochemical analyses of lung carcinoma biopsies demonstrated that 75% of the stromal fibroblasts and Ͼ90% of the stromal endothelial cells were positive for VEGFR-2. 38 Bellamy et al 30 investigated the expression of VEGFR-2 by immunohistochemistry of bone marrow clot biopsies of leukemic patients. They were unable to detect VEGFR-2 protein in a group of 17 patients with AML.…”