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Cited by 1,434

The DOI matches its Crossref record; 88 of the 88 references it cites were found in a registry or an index.

Angiogenesis in cancer

Open access
Nishida, Naoyo, Yano, Hirohisa, Nishida, Takashi, Kamura, Toshiharu, Kojiro, Masamichi·2006·Vascular Health and Risk Management
DOI 10.2147/vhrm.2006.2.3.213
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Abstract

New growth in the vascular network is important since the proliferation, as well as metastatic spread, of cancer cells depends on an adequate supply of oxygen and nutrients and the removal of waste products. New blood and lymphatic vessels form through processes called angiogenesis and lymphangiogenesis, respectively. Angiogenesis is regulated by both activator and inhibitor molecules. More than a dozen different proteins have been identified as angiogenic activators and inhibitors. Levels of expression of angiogenic factors reflect the aggressiveness of tumor cells. The discovery of angiogenic inhibitors should help to reduce both morbidity and mortality from carcinomas. Thousands of patients have received antiangiogenic therapy to date. Despite their theoretical efficacy, antiangiogeic treatments have not proved beneficial in terms of long-term survival. There is an urgent need for a new comprehensive treatment strategy combining antiangiogenic agents with conventional cytoreductive treatments in the control of cancer.

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Metadata

Authors
Nishida, N., Yano, H., Nishida, T., Kamura, T., & Kojiro, M.
Venue
Vascular Health and Risk Management
Publisher
Informa UK Limited
Published
2006-08
Volume
2
Issue
3
Pages
213-219
ISSN
1176-6344 (ISSN-L)
DOI
10.2147/vhrm.2006.2.3.213
OpenAlex
W2032347891
Cited by
1,434
References
88
FWCI
4.17
Type
journal article
Language
en
Open access
green

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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.

Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.