schliessen

Filtern

 

Bibliotheken

Cover Image

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:
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
Publisher: England: Nature Publishing Group
ID: ISSN: 0028-0836
Link: https://www.ncbi.nlm.nih.gov/pubmed/19759568
Zum Text:
SendSend as email Add to Book BagAdd to Book Bag
Staff View
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


@attributes
NO1
SEARCH_ENGINEprimo_central_multiple_fe
SEARCH_ENGINE_TYPEPrimo Central Search Engine
RANK2.728049
LOCALfalse
PrimoNMBib
record
control
sourceidgale_pubme
recordidTN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_3065241
sourceformatXML
sourcesystemPC
galeidA208694899
sourcerecordidA208694899
originalsourceidFETCH-LOGICAL-1678t-51410db7e759722a43743e4cf3868101c6dcb18b05a1c4cec3fe70ea270449830
addsrcrecordideNp9kl1rFDEUhgdRbF298l6qgigy9WTyOTfCsvQLikKtehkyyZk1MjPZTrLF_ntTd6m7spWEBJLnvOec5C2K5wQOCVD1YTBpOSKoirMHxT5hUpRMKPmw2AeoVAmKir3iSYw_AYATyR4Xe6SWvOZC7Rfw7ejk-IKUxiZ_7dNN6QeHC8zLkA56TCbm6eNBG8beJB-Gp8Wj1nQRn633SfH1-Ohydlqefz45m03PSyKkSiUnjIBrJOZEsqoMo5JRZLalSigCxApnG6Ia4IZYZtHSFiWgqSQwVisKk-LjSnexbHp0Ntczmk4vRt-b8UYH4_X2zeB_6Hm41hQEr3LySXG6Egi5HeNH3Ip1AyYdnK6E1KbiClSTa2ka2krrHNSWE9eCpQ7BZak361rGcLXEmHTvo8WuMwOGZdRCCk6Zggy-_S9IKi4VFwRERl-v0LnpUPuhDbkLe4vraQVK1EzVdaZe7aDswl_pTehwB5SHw97bMGDr8_mW6rutgMwk_JXmZhmjPvtysc2-v5-dXn6ffdpJ2zHEOGJ79-gE9K1b9YZbM_1i84__smt7ZoD8I2d9-mPD3KHv7hF9uYpZHd6JbjK_AVxp_bI
sourcetypeOpen Access Repository
isCDItrue
recordtypearticle
pqid1257856106
display
typearticle
titleVEGFR1-activity-independent metastasis formation
creatorDawson, Michelle R ; Fukumura, Dai ; Jain, Rakesh K ; Duda, Dan G
creatorcontribDawson, Michelle R ; Fukumura, Dai ; Jain, Rakesh K ; Duda, Dan G
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.
identifier
0ISSN: 0028-0836
1EISSN: 1476-4687
2DOI: 10.1038/nature08254
3PMID: 19759568
languageeng
publisherEngland: Nature Publishing Group
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
ispartofNature (London), 2009-09-17, Vol.461 (7262), p.E4-E4
rightsCOPYRIGHT 2009 Nature Publishing Group
lds50peer_reviewed
oafree_for_read
citedbyFETCH-LOGICAL-1678t-51410db7e759722a43743e4cf3868101c6dcb18b05a1c4cec3fe70ea270449830
citesFETCH-LOGICAL-1678t-51410db7e759722a43743e4cf3868101c6dcb18b05a1c4cec3fe70ea270449830
links
openurl$$Topenurl_article
thumbnail$$Usyndetics_thumb_exl
backlink$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19759568$$D View this record in MEDLINE/PubMed
search
creatorcontrib
0Dawson, Michelle R
1Fukumura, Dai
2Jain, Rakesh K
3Duda, Dan G
title
0VEGFR1-activity-independent metastasis formation
1Nature (London)
addtitleNature
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.
subject
0Animals
1Article
2Bone Marrow Cells - cytology
3Cell Movement
4Development and progression
5Lung - pathology
6Lung Neoplasms - secondary
7Metastasis
8Methods
9Mice
10Mice, Inbred C57BL
11Neoplasm Transplantation
12Neoplasms - pathology
13Pharmacogenetics
14Pharmacology, Experimental
15Properties
16Vascular endothelial growth factor
17Vascular Endothelial Growth Factor Receptor-1 - antagonists & inhibitors
18Vascular Endothelial Growth Factor Receptor-1 - deficiency
19Vascular Endothelial Growth Factor Receptor-1 - metabolism
issn
00028-0836
11476-4687
fulltextfalse
rsrctypearticle
creationdate2009
recordtypearticle
recordideNp9kl1rFDEUhgdRbF298l6qgigy9WTyOTfCsvQLikKtehkyyZk1MjPZTrLF_ntTd6m7spWEBJLnvOec5C2K5wQOCVD1YTBpOSKoirMHxT5hUpRMKPmw2AeoVAmKir3iSYw_AYATyR4Xe6SWvOZC7Rfw7ejk-IKUxiZ_7dNN6QeHC8zLkA56TCbm6eNBG8beJB-Gp8Wj1nQRn633SfH1-Ohydlqefz45m03PSyKkSiUnjIBrJOZEsqoMo5JRZLalSigCxApnG6Ia4IZYZtHSFiWgqSQwVisKk-LjSnexbHp0Ntczmk4vRt-b8UYH4_X2zeB_6Hm41hQEr3LySXG6Egi5HeNH3Ip1AyYdnK6E1KbiClSTa2ka2krrHNSWE9eCpQ7BZak361rGcLXEmHTvo8WuMwOGZdRCCk6Zggy-_S9IKi4VFwRERl-v0LnpUPuhDbkLe4vraQVK1EzVdaZe7aDswl_pTehwB5SHw97bMGDr8_mW6rutgMwk_JXmZhmjPvtysc2-v5-dXn6ffdpJ2zHEOGJ79-gE9K1b9YZbM_1i84__smt7ZoD8I2d9-mPD3KHv7hF9uYpZHd6JbjK_AVxp_bI
startdate20090917
enddate20090917
creator
0Dawson, Michelle R
1Fukumura, Dai
2Jain, Rakesh K
3Duda, Dan G
generalNature Publishing Group
scope
0CGR
1CUY
2CVF
3ECM
4EIF
5NPM
6AAYXX
7CITATION
87TO
9H94
107X8
11BOBZL
12CLFQK
135PM
sort
creationdate20090917
titleVEGFR1-activity-independent metastasis formation
authorDawson, Michelle R ; Fukumura, Dai ; Jain, Rakesh K ; Duda, Dan G
facets
frbrtype5
frbrgroupidcdi_FETCH-LOGICAL-1678t-51410db7e759722a43743e4cf3868101c6dcb18b05a1c4cec3fe70ea270449830
rsrctypearticles
prefilterarticles
languageeng
creationdate2009
topic
0Animals
1Article
2Bone Marrow Cells - cytology
3Cell Movement
4Development and progression
5Lung - pathology
6Lung Neoplasms - secondary
7Metastasis
8Methods
9Mice
10Mice, Inbred C57BL
11Neoplasm Transplantation
12Neoplasms - pathology
13Pharmacogenetics
14Pharmacology, Experimental
15Properties
16Vascular endothelial growth factor
17Vascular Endothelial Growth Factor Receptor-1 - antagonists & inhibitors
18Vascular Endothelial Growth Factor Receptor-1 - deficiency
19Vascular Endothelial Growth Factor Receptor-1 - metabolism
toplevelpeer_reviewed
creatorcontrib
0Dawson, Michelle R
1Fukumura, Dai
2Jain, Rakesh K
3Duda, Dan G
collection
0Medline
1MEDLINE
2MEDLINE (Ovid)
3MEDLINE
4MEDLINE
5PubMed
6CrossRef
7Oncogenes and Growth Factors Abstracts
8AIDS and Cancer Research Abstracts
9MEDLINE - Academic
10OpenAIRE (Open Access)
11OpenAIRE
12PubMed Central (Full Participant titles)
jtitleNature (London)
delivery
delcategoryRemote Search Resource
fulltextno_fulltext
addata
au
0Dawson, Michelle R
1Fukumura, Dai
2Jain, Rakesh K
3Duda, Dan G
formatjournal
genrearticle
ristypeJOUR
atitleVEGFR1-activity-independent metastasis formation
jtitleNature (London)
addtitleNature
date2009-09-17
risdate2009
volume461
issue7262
spageE4
epageE4
pagesE4-E4
issn0028-0836
eissn1476-4687
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.
copEngland
pubNature Publishing Group
pmid19759568
doi10.1038/nature08254
tpages3
oafree_for_read