Tumor endothelium is characterized by a matrix remodeling signature

Research output: Contribution to journalReview articleAcademicpeer-review

Abstract

Endothelial cells (EC) are attractive targets for therapeutic interference in diseases that are dependent on the formation of novel blood vessels, such as cancer. EC are readily accessible via the blood stream and are considered to be genetically stable, thus enabling efficient and effective drug delivery. However, for targeting of EC in blood vessels of the disease tissue, specific markers are needed. Though various studies have focused on the differences in gene expression in endothelial cells in different in vitro model systems, only few studies have focused on gene expression in EC derived from tumor tissues and corresponding normal tissues. Here, we review the gene expression data sets of EC isolated from tumors of the colon, breast, brain and ovaries. Gene ontology analysis reveals enrichment for genes involved in extracellular matrix turnover and adhesion. Several genes, including collagens 4A1, 4A2 and 1A1, SPARC, THY1 and MMP9 are overexpressed in the endothelium of more than one tumor type, whereas plexin domain containing 1 (PLXDC1), previously known as TEM7, is overexpressed in EC of all four tumor types.

Original languageEnglish
Pages (from-to)216-25
Number of pages10
JournalFrontiers in bioscience (Scholar edition)
Volume1
Publication statusPublished - 1 Jun 2009

Cite this

@article{545954f707ba418598b13f2ab914c090,
title = "Tumor endothelium is characterized by a matrix remodeling signature",
abstract = "Endothelial cells (EC) are attractive targets for therapeutic interference in diseases that are dependent on the formation of novel blood vessels, such as cancer. EC are readily accessible via the blood stream and are considered to be genetically stable, thus enabling efficient and effective drug delivery. However, for targeting of EC in blood vessels of the disease tissue, specific markers are needed. Though various studies have focused on the differences in gene expression in endothelial cells in different in vitro model systems, only few studies have focused on gene expression in EC derived from tumor tissues and corresponding normal tissues. Here, we review the gene expression data sets of EC isolated from tumors of the colon, breast, brain and ovaries. Gene ontology analysis reveals enrichment for genes involved in extracellular matrix turnover and adhesion. Several genes, including collagens 4A1, 4A2 and 1A1, SPARC, THY1 and MMP9 are overexpressed in the endothelium of more than one tumor type, whereas plexin domain containing 1 (PLXDC1), previously known as TEM7, is overexpressed in EC of all four tumor types.",
keywords = "Endothelium, Vascular/pathology, Gene Expression Regulation, Humans, Neoplasms/blood supply, Neovascularization, Pathologic",
author = "{van Beijnum}, {Judy R} and Kjell Petersen and Griffioen, {Arjan W}",
year = "2009",
month = "6",
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language = "English",
volume = "1",
pages = "216--25",
journal = "Frontiers in bioscience (Scholar edition)",
issn = "1945-0516",
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}

Tumor endothelium is characterized by a matrix remodeling signature. / van Beijnum, Judy R; Petersen, Kjell; Griffioen, Arjan W.

In: Frontiers in bioscience (Scholar edition), Vol. 1, 01.06.2009, p. 216-25.

Research output: Contribution to journalReview articleAcademicpeer-review

TY - JOUR

T1 - Tumor endothelium is characterized by a matrix remodeling signature

AU - van Beijnum, Judy R

AU - Petersen, Kjell

AU - Griffioen, Arjan W

PY - 2009/6/1

Y1 - 2009/6/1

N2 - Endothelial cells (EC) are attractive targets for therapeutic interference in diseases that are dependent on the formation of novel blood vessels, such as cancer. EC are readily accessible via the blood stream and are considered to be genetically stable, thus enabling efficient and effective drug delivery. However, for targeting of EC in blood vessels of the disease tissue, specific markers are needed. Though various studies have focused on the differences in gene expression in endothelial cells in different in vitro model systems, only few studies have focused on gene expression in EC derived from tumor tissues and corresponding normal tissues. Here, we review the gene expression data sets of EC isolated from tumors of the colon, breast, brain and ovaries. Gene ontology analysis reveals enrichment for genes involved in extracellular matrix turnover and adhesion. Several genes, including collagens 4A1, 4A2 and 1A1, SPARC, THY1 and MMP9 are overexpressed in the endothelium of more than one tumor type, whereas plexin domain containing 1 (PLXDC1), previously known as TEM7, is overexpressed in EC of all four tumor types.

AB - Endothelial cells (EC) are attractive targets for therapeutic interference in diseases that are dependent on the formation of novel blood vessels, such as cancer. EC are readily accessible via the blood stream and are considered to be genetically stable, thus enabling efficient and effective drug delivery. However, for targeting of EC in blood vessels of the disease tissue, specific markers are needed. Though various studies have focused on the differences in gene expression in endothelial cells in different in vitro model systems, only few studies have focused on gene expression in EC derived from tumor tissues and corresponding normal tissues. Here, we review the gene expression data sets of EC isolated from tumors of the colon, breast, brain and ovaries. Gene ontology analysis reveals enrichment for genes involved in extracellular matrix turnover and adhesion. Several genes, including collagens 4A1, 4A2 and 1A1, SPARC, THY1 and MMP9 are overexpressed in the endothelium of more than one tumor type, whereas plexin domain containing 1 (PLXDC1), previously known as TEM7, is overexpressed in EC of all four tumor types.

KW - Endothelium, Vascular/pathology

KW - Gene Expression Regulation

KW - Humans

KW - Neoplasms/blood supply

KW - Neovascularization, Pathologic

M3 - Review article

VL - 1

SP - 216

EP - 225

JO - Frontiers in bioscience (Scholar edition)

JF - Frontiers in bioscience (Scholar edition)

SN - 1945-0516

ER -