The DOI matches its Crossref record; 101 of the 101 references it cites were found in a registry or an index.
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]
In the citing paper
“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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Citations
Cites
Normalization of Tumor Vasculature: An Emerging Concept in Antiangiogenic Therapy
Jain, R. K. (2005) · Science · doi:10.1126/science.1104819 · Cited by 5,527 · cited 1×
“Tumour vessels become abnormal in almost all aspects of their structure and functio”
BackgroundSelf-citationAngiogenesis in health and disease
Carmeliet, P. (2003) · Nature Medicine · doi:10.1038/nm0603-653 · Cited by 4,379
Self-citationIntegrins in cancer: biological implications and therapeutic opportunities
Desgrosellier, J. S., & Cheresh, D. A. (2009) · Nature reviews. Cancer · doi:10.1038/nrc2748 · Cited by 3,815
Microenvironmental regulation of metastasis
Joyce, J. A., & Pollard, J. W. (2009) · Nature Reviews Cancer · doi:10.1038/nrc2618 · Cited by 3,684
Angiogenesis in life, disease and medicine
Carmeliet, P. (2005) · Nature · doi:10.1038/nature04478 · Cited by 3,551
Self-citationVEGFR1-positive haematopoietic bone marrow progenitors initiate the pre-metastatic niche
Kaplan, R. N., Riba, R. D., Zacharoulis, S., Bramley, A. H., Vincent, L., Costa, C., MacDonald, D. D., Jin, D. K., Shido, K., Kerns, S. A., et al. (2005) · Nature · doi:10.1038/nature04186 · Cited by 3,288
Modes of resistance to anti-angiogenic therapy
Bergers, G., & Hanahan, D. (2008) · Nature Reviews Cancer · doi:10.1038/nrc2442 · Cited by 2,953 · cited 1×
“Aberrant FGF signalling promotes tumour angiogenesis and mediates the escape of tumour vascularization from VEGF- or epidermal growth factor receptor (EGFR)-inhibitor treatmen”
BackgroundMatrix metalloproteinase-9 triggers the angiogenic switch during carcinogenesis
Bergers, G., Brekken, R., McMahon, G., Vu, T. H., Itoh, T., Tamaki, K., Tanzawa, K., Thorpe, P., Itohara, S., Werb, Z., et al. (2000) · Nature Cell Biology · doi:10.1038/35036374 · Cited by 2,797
Molecular regulation of vessel maturation
Jain, R. K. (2003) · Nature Medicine · doi:10.1038/nm0603-685 · Cited by 2,594
Self-citationHypoxia-inducible factors and the response to hypoxic stress
Majmundar, A. J., Wong, W. J., & Simon, M. C. (2010) · Molecular Cell · doi:10.1016/j.molcel.2010.09.022 · Cited by 2,380
Cited by
Sorted by citations
Microenvironmental regulation of tumor progression and metastasis
Quail, D. F., & Joyce, J. A. (2013) · Nature Medicine · doi:10.1038/nm.3394 · Cited by 7,994
Accessories to the Crime: Functions of Cells Recruited to the Tumor Microenvironment
Hanahan, D., & Coussens, L. M. (2012) · Cancer Cell · doi:10.1016/j.ccr.2012.02.022 · Cited by 4,632
PLGA-based nanoparticles: An overview of biomedical applications
Danhier, F., Ansorena, E., Silva, J. M., Coco, R., Breton, A. L., & Véronique Préat, A. (2012) · Journal of Controlled Release · doi:10.1016/j.jconrel.2012.01.043 · Cited by 4,006
Basic and Therapeutic Aspects of Angiogenesis
Potente, M., Gerhardt, H., & Carmeliet, P. (2011) · Cell · doi:10.1016/j.cell.2011.08.039 · Cited by 2,771
Self-citationMao, X., Xu, J., Wang, W., Liang, C., Hua, J., Liu, J., Zhang, B., Meng, Q., Yu, X., & Shi, S. (2021) · Molecular Cancer · doi:10.1186/s12943-021-01428-1 · Cited by 2,290
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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