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Molecular mechanisms and clinical applications of angiogenesis
Open accessAbstract
Blood vessels deliver oxygen and nutrients to every part of the body, but also nourish diseases such as cancer. Over the past decade, our understanding of the molecular mechanisms of angiogenesis (blood vessel growth) has increased at an explosive rate and has led to the approval of anti-angiogenic drugs for cancer and eye diseases. So far, hundreds of thousands of patients have benefited from blockers of the angiogenic protein vascular endothelial growth factor, but limited efficacy and resistance remain outstanding problems. Recent preclinical and clinical studies have shown new molecular targets and principles, which may provide avenues for improving the therapeutic benefit from anti-angiogenic strategies.
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“In clinical settings, this approach has been proven to be ineffective when used alone [23].”
From Approaches to Improve EPR-Based Drug Delivery for Cancer Therapy and Diagnosis (2023) · cites this paper as [23]
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“In addition to increasing drug resistance, a high SS could influence tumor cells' gene expression, comprise immune cells ability to kill cancerous cells or even turn macrophages to tumorfriendly cells, thereby enhancing the metastatic potential of cancer cells [180-184].”
From Microfluidic modelling of the tumor microenvironment for anti-cancer drug development (2019) · cites this paper as [184]
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“This disparity is, in part, attributed to VEGF-independent nonangiogenic mechanisms of vascularization (such as vessel co-option) that are exploited by cancer cells at the early stages of metastasis formation6,9,55,56”
From Enhancing cancer immunotherapy using antiangiogenics: opportunities and challenges (2018) · cites this paper as [9]
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“Several cellular and molecular mechanisms of escape from antiangiogenic therapies have been postulated and investigated, including activation of alternative angiogenic pathways, recruitment of proangiogenic myeloid cells, increased pericyte cell coverage of tumour blood vessels, increased tumour cell invasion, and alternative modes of vessel recruitment7,9,80”
From Enhancing cancer immunotherapy using antiangiogenics: opportunities and challenges (2018) · cites this paper as [9]
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Metadata
- Authors
- Carmeliet, P., & Jain, R. K.
- Affiliations
- Harvard University (US)
- Corresponding author
- Carmeliet, Peter
- Jain, Rakesh K.
- ORCID
- Carmeliet, Peter
- Venue
- Nature
- Published
- 2011-05
- Volume
- 473
- Issue
- 7347
- Pages
- 298-307
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- PMC
- PMC4049445
- OpenAlex
- W1992112921
- Semantic Scholar
- cc1723f25e863386b91340ea03cd76a22de359ae
- Cited by
- 5,467
- References
- 100
- Citations by year
- 2026: 238 · 2025: 316 · 2024: 308 · 2023: 364 · 2022: 393 · 2021: 442 · 2020: 399 · 2019: 399 · 2018: 384 · 2017: 454 · 2016: 369 · 2015: 375 · 2014: 326 · 2013: 342 · 2012: 284
- FWCI
- 29.09
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- Funders
- National Cancer Institute (R01CA115767, R01CA085140, P01CA080124, R01CA126642, R01CA163815)
- 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, angiogenesis inhibitors, vascular endothelial growth factor, VEGF inhibitors, drug resistance, molecular targets, cancer, eye diseases, blood vessel development
- MeSH terms
- Animals, Blood Vessels, Fibroblast Growth Factors, Humans, Platelet-Derived Growth Factor, Transforming Growth Factor beta, Neovascularization, Physiologic, Angiogenesis Inhibitors, Vesicular Transport Proteins, Vascular Endothelial Growth Factor A
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