VEGFR1-activity-independent metastasis formation

• Published in: Nature (London) Vol. 461; no. 7262; p. E4
• Main Authors: Dawson, Michelle R, Fukumura, Dai, Jain, Rakesh K, Duda, Dan G
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 17-09-2009; Nature Publishing Group
• Subjects: Animals; Bone Marrow Cells - cytology; brief-communications-arising; Cell Movement; Development and progression; Humanities and Social Sciences; Lung - pathology; Lung Neoplasms - secondary; Metastasis; Methods; Mice; Mice, Inbred C57BL; multidisciplinary; Neoplasm Transplantation; Neoplasms - pathology; Pharmacogenetics; Pharmacology, Experimental; Properties; Science; Science (multidisciplinary); Vascular endothelial growth factor; Vascular Endothelial Growth Factor Receptor-1 - antagonists & inhibitors; Vascular Endothelial Growth Factor Receptor-1 - deficiency; Vascular Endothelial Growth Factor Receptor-1 - metabolism
• ISSN: 0028-0836; 1476-4687
• DOI: 10.1038/nature08254

Arising from: R. N. Kaplan et al. Nature 438, 820-827 (2005); Kaplan et al. replyMolecules such as vascular endothelial growth factor (VEGF) or placental growth factor-critical regulators of tumour angiogenesis-are also thought to mobilize into blood circulation bone marrow-derived cells (BMDCs), which may subsequently be recruited to tumours and facilitate tumour growth and metastasis. A study has suggested that BMDCs form 'metastatic niches' in lungs before arrival of cancer cells, and showed that pharmacological inhibition of VEGF receptor 1 (VEGFR1, also known as Flt1)-cognate receptor for VEGF and placental growth factor-prevented BMDC infiltration in lungs and 'metastatic niche' formation. Here we report that blockade of VEGFR1 activity does not affect the rate of spontaneous metastasis formation in a clinically relevant and widely used preclinical model. Therefore, alternative pathways probably mediate the priming of tissues for metastasis.