Vascularization of melanoma by mobilization and remodeling of preexisting latent vessels to patency

Weixin Lu, Alan Jay Schroit

Research output: Contribution to journalArticle

15 Citations (Scopus)

Abstract

Tumors must manipulate the host vasculature to provide a blood supply adequate for their proliferation. Although tumors may arise as avascular masses, there is increasing evidence that some tumors begin to proliferate by first coopting preexisting host blood vessels. By fluorescent vascular imaging, we provide evidence that the vasculature in orthotopically implanted melanoma arises from a preexisting red cell-deficient vascular network that remodels to patency to accommodate the requirements of the expanding tumor mass. Topical application of vascular endothelial growth factor to vascular beds generated immediate and robust vascular transitions that were morphologically similar to tumor-induced transitions. Nφ-nitro-L-arginine, a nitric oxide inhibitor, significantly inhibited the growth of a syngeneic K1735M2 melanoma by reducing blood supply to the tumor by a mechanism independent of endothelial cell proliferation. These findings suggest that tumor-induced remodeling of red cell-deficient vessels to patency contributes to tumor vascularization and growth.

Original languageEnglish (US)
Pages (from-to)913-918
Number of pages6
JournalCancer Research
Volume65
Issue number3
StatePublished - Feb 1 2005

Fingerprint

Melanoma
Blood Vessels
Neoplasms
Growth
Vascular Endothelial Growth Factor A
Arginine
Nitric Oxide
Endothelial Cells
Cell Proliferation

ASJC Scopus subject areas

  • Cancer Research
  • Oncology

Cite this

Vascularization of melanoma by mobilization and remodeling of preexisting latent vessels to patency. / Lu, Weixin; Schroit, Alan Jay.

In: Cancer Research, Vol. 65, No. 3, 01.02.2005, p. 913-918.

Research output: Contribution to journalArticle

Lu, Weixin ; Schroit, Alan Jay. / Vascularization of melanoma by mobilization and remodeling of preexisting latent vessels to patency. In: Cancer Research. 2005 ; Vol. 65, No. 3. pp. 913-918.
@article{49548277e0f94c57afd7ae0e749cae89,
title = "Vascularization of melanoma by mobilization and remodeling of preexisting latent vessels to patency",
abstract = "Tumors must manipulate the host vasculature to provide a blood supply adequate for their proliferation. Although tumors may arise as avascular masses, there is increasing evidence that some tumors begin to proliferate by first coopting preexisting host blood vessels. By fluorescent vascular imaging, we provide evidence that the vasculature in orthotopically implanted melanoma arises from a preexisting red cell-deficient vascular network that remodels to patency to accommodate the requirements of the expanding tumor mass. Topical application of vascular endothelial growth factor to vascular beds generated immediate and robust vascular transitions that were morphologically similar to tumor-induced transitions. Nφ-nitro-L-arginine, a nitric oxide inhibitor, significantly inhibited the growth of a syngeneic K1735M2 melanoma by reducing blood supply to the tumor by a mechanism independent of endothelial cell proliferation. These findings suggest that tumor-induced remodeling of red cell-deficient vessels to patency contributes to tumor vascularization and growth.",
author = "Weixin Lu and Schroit, {Alan Jay}",
year = "2005",
month = "2",
day = "1",
language = "English (US)",
volume = "65",
pages = "913--918",
journal = "Journal of Cancer Research",
issn = "0099-7013",
publisher = "American Association for Cancer Research Inc.",
number = "3",

}

TY - JOUR

T1 - Vascularization of melanoma by mobilization and remodeling of preexisting latent vessels to patency

AU - Lu, Weixin

AU - Schroit, Alan Jay

PY - 2005/2/1

Y1 - 2005/2/1

N2 - Tumors must manipulate the host vasculature to provide a blood supply adequate for their proliferation. Although tumors may arise as avascular masses, there is increasing evidence that some tumors begin to proliferate by first coopting preexisting host blood vessels. By fluorescent vascular imaging, we provide evidence that the vasculature in orthotopically implanted melanoma arises from a preexisting red cell-deficient vascular network that remodels to patency to accommodate the requirements of the expanding tumor mass. Topical application of vascular endothelial growth factor to vascular beds generated immediate and robust vascular transitions that were morphologically similar to tumor-induced transitions. Nφ-nitro-L-arginine, a nitric oxide inhibitor, significantly inhibited the growth of a syngeneic K1735M2 melanoma by reducing blood supply to the tumor by a mechanism independent of endothelial cell proliferation. These findings suggest that tumor-induced remodeling of red cell-deficient vessels to patency contributes to tumor vascularization and growth.

AB - Tumors must manipulate the host vasculature to provide a blood supply adequate for their proliferation. Although tumors may arise as avascular masses, there is increasing evidence that some tumors begin to proliferate by first coopting preexisting host blood vessels. By fluorescent vascular imaging, we provide evidence that the vasculature in orthotopically implanted melanoma arises from a preexisting red cell-deficient vascular network that remodels to patency to accommodate the requirements of the expanding tumor mass. Topical application of vascular endothelial growth factor to vascular beds generated immediate and robust vascular transitions that were morphologically similar to tumor-induced transitions. Nφ-nitro-L-arginine, a nitric oxide inhibitor, significantly inhibited the growth of a syngeneic K1735M2 melanoma by reducing blood supply to the tumor by a mechanism independent of endothelial cell proliferation. These findings suggest that tumor-induced remodeling of red cell-deficient vessels to patency contributes to tumor vascularization and growth.

UR - http://www.scopus.com/inward/record.url?scp=13444252266&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=13444252266&partnerID=8YFLogxK

M3 - Article

C2 - 15705890

AN - SCOPUS:13444252266

VL - 65

SP - 913

EP - 918

JO - Journal of Cancer Research

JF - Journal of Cancer Research

SN - 0099-7013

IS - 3

ER -