BACKGROUND: Vascular endothelial growth factor (VEGF) promotes breast cancer progression by inducing angiogenesis via VEGF receptors on endothelial cells but also signals directly through receptors such as VEGFR-1 (Flt-1) expressed on tumour cells. The impact of autocrine signalling loops on treatment with VEGF inhibitors is still unclear. MATERIALS AND METHODS: Six breast cancer cell lines were tested for expression of VEGFR-1 by RT-PCR and Western blot. To assess clinical significance, 93 breast cancer lesions were evaluated for expression of VEGF and VEGFR-1 by immunohistochemistry. RESULTS: VEGFR-1 mRNA was found in all 6 cell lines, while protein expression was found in 5 cell lines. VEGF was expressed in 60% and VEGFR-1 in 39% of breast cancer specimens. VEGFR-1 expression was associated with VEGF expression and with node-negative tumour stage. CONCLUSION: Our data suggest that analysis of VEGF/VEGFR-1 expression might be relevant in identifying patients with different response rates upon treatment with antiangiogenic agents.
BACKGROUND:Vascular endothelial growth factor (VEGF) promotes breast cancer progression by inducing angiogenesis via VEGF receptors on endothelial cells but also signals directly through receptors such as VEGFR-1 (Flt-1) expressed on tumour cells. The impact of autocrine signalling loops on treatment with VEGF inhibitors is still unclear. MATERIALS AND METHODS: Six breast cancer cell lines were tested for expression of VEGFR-1 by RT-PCR and Western blot. To assess clinical significance, 93 breast cancer lesions were evaluated for expression of VEGF and VEGFR-1 by immunohistochemistry. RESULTS:VEGFR-1 mRNA was found in all 6 cell lines, while protein expression was found in 5 cell lines. VEGF was expressed in 60% and VEGFR-1 in 39% of breast cancer specimens. VEGFR-1 expression was associated with VEGF expression and with node-negative tumour stage. CONCLUSION: Our data suggest that analysis of VEGF/VEGFR-1 expression might be relevant in identifying patients with different response rates upon treatment with antiangiogenic agents.
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