VEGFR1-activity-independent metastasis formation

Michelle R. Dawson (), Dan G. Duda (), Dai Fukumura () and Rakesh K. Jain ()
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Michelle R. Dawson: Steele Laboratory, Massachusetts General Hospital, Harvard Medical School
Dan G. Duda: Steele Laboratory, Massachusetts General Hospital, Harvard Medical School
Dai Fukumura: Steele Laboratory, Massachusetts General Hospital, Harvard Medical School
Rakesh K. Jain: Steele Laboratory, Massachusetts General Hospital, Harvard Medical School

Nature, 2009, vol. 461, issue 7262, E4-E4

Abstract: Abstract Arising from: R. N. Kaplan et al. Nature 438, 820–827 (2005)10.1038/nature04186 ; Kaplan et al. reply Molecules 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)1, which may subsequently be recruited to tumours and facilitate tumour growth and metastasis2,3. A study4 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 model5,6,7,8. Therefore, alternative pathways probably mediate the priming of tissues for metastasis.

Date: 2009
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DOI: 10.1038/nature08254

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