Mechanisms of normal and tumor-derived angiogenesis

Papetti, Michael; Herman, Ira M.

doi:10.1152/ajpcell.00389.2001

Cited by 809Angiogenesis and VEGF in CancerLymphatic System and DiseasesMathematical Biology Tumor Growth

Mechanisms of normal and tumor-derived angiogenesis

Papetti, Michael, Herman, Ira M.·2002·American Journal of Physiology-Cell Physiology

DOI 10.1152/ajpcell.00389.2001

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Abstract

Often those diseases most evasive to therapeutic intervention usurp the human body's own cellular machinery or deregulate normal physiological processes for propagation. Tumor-induced angiogenesis is a pathological condition that results from aberrant deployment of normal angiogenesis, an essential process in which the vascular tree is remodeled by the growth of new capillaries from preexisting vessels. Normal angiogenesis ensures that developing or healing tissues receive an adequate supply of nutrients. Within the confines of a tumor, the availability of nutrients is limited by competition among actively proliferating cells, and diffusion of metabolites is impeded by high interstitial pressure (Jain RK. Cancer Res 47: 3039–3051, 1987). As a result, tumor cells induce the formation of a new blood supply from the preexisting vasculature, and this affords tumor cells the ability to survive and propagate in a hostile environment. Because both normal and tumor-induced neovascularization fulfill the essential role of satisfying the metabolic demands of a tissue, the mechanisms by which cancer cells stimulate pathological neovascularization mimic those utilized by normal cells to foster physiological angiogenesis. This review investigates mechanisms of tumor-induced angiogenesis. The strategies used by cancer cells to develop their own blood supply are discussed in relation to those employed by normal cells during physiological angiogenesis. With an understanding of blood vessel growth in both normal and abnormal settings, we are better suited to design effective therapeutics for cancer.

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Hypoxic stress induces angiogenic signaling by upregulating vascular endothelial growth factor (VEGF).
“This hypoxic stress acts as a potent inducer of angiogenic signaling, upregulating key factors such as vascular endothelial growth factor (VEGF) [51].”
From Modeling Tumor Microenvironment Complexity In Vitro: Spheroids as Physiologically Relevant Tumor Models and Strategies for Their Analysis (2025) · cites this paper as [51]
As a tumor expands beyond ~1-2 mm3, limited diffusion results in hypoxic regions that drive tumor dormancy.
“As the tumor expands beyond this size, the limited diffusion capacity results in the formation of hypoxic regions, which drive tumor dormancy [50,51].”
From Modeling Tumor Microenvironment Complexity In Vitro: Spheroids as Physiologically Relevant Tumor Models and Strategies for Their Analysis (2025) · cites this paper as [51]
Some tumors co-opt existing vasculature and grow along the vessels until demand for nutrients and oxygen becomes too large and angiogenesis starts again.
“Instead of triggering angiogenesis, some tumors co-opt existing vasculature and grow along the vessels [53][54][55][56], until the demand for nutrients and oxygen becomes too large and angiogenesis starts again [53,55].”
From Cancer-on-chip models for metastasis: importance of the tumor microenvironment (2024) · cites this paper as [53]
VEGF-A presence is essential for initiation of the angiogenic program.
“its presence is essential for initiation of the angiogenic program (76,77)”
From Adipose tissue remodeling and obesity (2011) · cites this paper as [76]
VEGF-A is the only bona fide endothelial cell growth factor.
“VEGF-A is the only bona fide endothelial cell growth factor”
From Adipose tissue remodeling and obesity (2011) · cites this paper as [76]

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Authors: Papetti, M., & Herman, I. M.
Affiliations: Tufts University (US)
ORCID: Herman, Ira M.
Venue: American Journal of Physiology-Cell Physiology
Publisher: American Physiological Society
Published: 2002-05-01
Volume: 282
Issue: 5
Pages: C947-C970
ISSN: 0363-6143 (ISSN-L)
1522-1563
DOI: 10.1152/ajpcell.00389.2001
OpenAlex: W2050499474
Cited by: 809
References: 271
Citations by year: 2026: 11 · 2025: 15 · 2024: 19 · 2023: 33 · 2022: 38 · 2021: 32 · 2020: 36 · 2019: 28 · 2018: 20 · 2017: 41 · 2016: 36 · 2015: 45 · 2014: 42 · 2013: 46 · 2012: 41
FWCI: 2.10
Type: journal article
Language: en
Open access: closed
Locations: American Journal of Physiology-Cell Physiology (publishedVersion)
PubMed (publishedVersion)
Funders: National Institutes of Health (5r01gm055110-04)
National Eye Institute (R01EY009033, EY09033)
National Institute of General Medical Sciences (GM55110)
National Institute of Diabetes and Digestive and Kidney Diseases (P30DK034928)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Angiogenesis and VEGF in Cancer
Health Sciences › Medicine › Oncology › Lymphatic System and Diseases
Physical Sciences › Mathematics › Modeling and Simulation › Mathematical Biology Tumor Growth
Keywords: tumor angiogenesis, physiological angiogenesis, tumor blood supply, vascular remodeling, capillary proliferation, interstitial fluid pressure, tumor microenvironment, cancer metabolism
MeSH terms: Blood Vessels, Growth Substances, Humans, Models, Cardiovascular, Neoplasms, Neovascularization, Pathologic, Proteins, Receptors, Cell Surface, Neovascularization, Physiologic, Receptor Protein-Tyrosine Kinases, Angiopoietin-2, Receptors, TIE

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Mechanisms of normal and tumor-derived angiogenesis

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