CoChat
Sign Up
Cited by 748Angiogenesis and VEGF in CancerLymphatic System and DiseasesVascular Tumors and Angiosarcomas

The DOI matches its Crossref record; 231 of the 231 references it cites were found in a registry or an index.

Angiogenesis: regulators and clinical applications

Liekens, Sandra, De Clercq, Erik, Neyts, Johan·2001·Biochemical Pharmacology
DOI 10.1016/s0006-2952(00)00529-3
Open this paper in CoChat — free account

Abstract

Angiogenesis is a fundamental process in reproduction and wound healing. Under these conditions, neovascularization is tightly regulated. Unregulated angiogenesis may lead to several angiogenic diseases and is thought to be indispensable for solid tumor growth and metastasis. The construction of a vascular network requires different sequential steps including the release of proteases from "activated" endothelial cells with subsequent degradation of the basement membrane surrounding the existing vessel, migration of endothelial cells into the interstitial space, endothelial cell proliferation, and differentiation into mature blood vessels. These processes are mediated by a wide range of angiogenic inducers, including growth factors, chemokines, angiogenic enzymes, endothelial specific receptors, and adhesion molecules. Finally, when sufficient neovascularization has occurred, angiogenic factors are down-regulated or the local concentration of inhibitors increases. As a result, the endothelial cells become quiescent, and the vessels remain or regress if no longer needed. Thus, angiogenesis requires many interactions that must be tightly regulated in a spatial and temporal manner. Each of these processes presents possible targets for therapeutic intervention. Synthetic inhibitors of cell invasion (marimastat, Neovastat, AG-3340), adhesion (Vitaxin), or proliferation (TNP-470, thalidomide, Combretastatin A-4), or compounds that interfere with angiogenic growth factors (interferon-alpha, suramin, and analogues) or their receptors (SU6668, SU5416), as well as endogenous inhibitors of angiogenesis (endostatin, interleukin-12) are being evaluated in clinical trials against a variety of solid tumors. As basic knowledge about the control of angiogenesis and its role in tumor growth and metastasis increases, it may be possible in the future to develop specific anti-angiogenic agents that offer a potential therapy for cancer and angiogenic diseases.

Overview

Integrity signals

Registry

Crossref · 10.1016/s0006-2952(00)00529-3

Cites

231 of 231 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Verification

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Citations

Cites

Items 201–231 of 231

Research works printed but not linked: 6

  1. Moore, 1998, CXC chemokine modulation of angiogenesis, J Investig Med, 46, 113
  2. Montesano, 1992, Modulation of angiogenesisin vitro, EXS, 61, 129
  3. Liekens, 1999, A novel animal model for hemangiomas, Cancer Res, 59, 2376
  4. Tozer, 1999, Combretastatin A-4 phosphate as a tumor vascular-targeting agent, Cancer Res, 59, 1626
  5. Im, 1999, Antiangiogenesis treatment for gliomas, Cancer Res, 59, 895
  6. Kumar, 1999, Breast carcinoma, Cancer Res, 59, 856

Cited by

Sorted by citations

See all 748

Related

See all

Metadata

Authors
Liekens, S., De Clercq, E., & Neyts, J.
Affiliations
Rega Institute for Medical Research (BE)
Corresponding author
Liekens, Sandra
ORCID
Venue
Biochemical Pharmacology
Publisher
Elsevier BV
Published
2001-02
Volume
61
Issue
3
Pages
253-270
ISSN
0006-2952 (ISSN-L)
DOI
10.1016/s0006-2952(00)00529-3
OpenAlex
W2109197670
Cited by
748
References
231
Citations by year
2026: 5 · 2025: 10 · 2024: 11 · 2023: 14 · 2022: 16 · 2021: 22 · 2020: 20 · 2019: 16 · 2018: 17 · 2017: 25 · 2016: 33 · 2015: 39 · 2014: 44 · 2013: 30 · 2012: 28
FWCI
16.00
Type
journal article
Language
en
Open access
closed
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Biochemical Pharmacology (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Angiogenesis and VEGF in Cancer
  • Health Sciences › Medicine › Oncology › Lymphatic System and Diseases
  • Health Sciences › Medicine › Oncology › Vascular Tumors and Angiosarcomas
Keywords
angiogenesis, neovascularization, angiogenesis inhibitors, anti-angiogenic therapy, tumor growth, metastasis, angiogenic factors, endothelial cell migration, basement membrane degradation, endostatin, marimastat, combretastatin A-4, thalidomide, wound healing, reproduction
MeSH terms
Humans, Neoplasms, Neovascularization, Pathologic, Neovascularization, Physiologic, Angiogenesis Inhibitors, Angiogenesis Inducing Agents

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review