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VEGFR1-activity-independent metastasis formation

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), wh... Full description

Journal Title: Nature (London) 2009-09-17, Vol.461 (7262), p.E4-E4
Main Author: Dawson, Michelle R
Other Authors: Fukumura, Dai , Jain, Rakesh K , Duda, Dan G
Format: Electronic Article Electronic Article
Language: English
Subjects:
Publisher: England: Nature Publishing Group
ID: ISSN: 0028-0836
Link: https://www.ncbi.nlm.nih.gov/pubmed/19759568
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recordid: cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_3065241
title: VEGFR1-activity-independent metastasis formation
format: Article
creator:
  • Dawson, Michelle R
  • Fukumura, Dai
  • Jain, Rakesh K
  • Duda, Dan G
subjects:
  • Animals
  • Article
  • Bone Marrow Cells - cytology
  • Cell Movement
  • Development and progression
  • Lung - pathology
  • Lung Neoplasms - secondary
  • Metastasis
  • Methods
  • Mice
  • Mice, Inbred C57BL
  • Neoplasm Transplantation
  • Neoplasms - pathology
  • Pharmacogenetics
  • Pharmacology, Experimental
  • Properties
  • 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
ispartof: Nature (London), 2009-09-17, Vol.461 (7262), p.E4-E4
description: 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.
language: eng
source:
identifier: ISSN: 0028-0836
fulltext: no_fulltext
issn:
  • 0028-0836
  • 1476-4687
url: Link


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descriptionArising 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.
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subjectAnimals ; Article ; Bone Marrow Cells - cytology ; Cell Movement ; Development and progression ; Lung - pathology ; Lung Neoplasms - secondary ; Metastasis ; Methods ; Mice ; Mice, Inbred C57BL ; Neoplasm Transplantation ; Neoplasms - pathology ; Pharmacogenetics ; Pharmacology, Experimental ; Properties ; 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
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descriptionArising 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.
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abstractArising 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.
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