The DOI matches its Crossref record; 18 of the 18 references it cites were found in a registry or an index.
HCC and angiogenesis: possible targets and future directions
Open accessAbstract
Hepatocellular carcinoma (HCC), the most common primary liver tumor, is notoriously resistant to systemic therapies, and often recurs even after aggressive local therapies. HCCs rely on the formation of new blood vessels for growth, and VEGF is critical in this process. A hallmark of new vessel formation in tumors is their structural and functional abnormality. This leads to an abnormal tumor microenvironment characterized by low oxygen tension. The liver is perfused by both arterial and venous blood and the resulting abnormal microenvironment selects for more-aggressive malignancies. Anti-VEGF therapy with sorafenib was the first systemic therapy to demonstrate improved survival in patients with advanced-stage HCC. This important development in the treatment of HCC raises hope as well as critical questions on the future development of targeted agents including other antiangiogenic agents, which hold promise to further increase survival in this aggressive disease.
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“which could potentially enhance the efficacy of radiation and chemotherapy by alleviating hypoxia and tumor invasiveness”
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Cited by
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Self-citationThe Role of Cancer-Associated Fibroblasts and Fibrosis in Liver Cancer
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Metadata
- Authors
- Zhu, A. X., Duda, D. G., Sahani, D. V., & Jain, R. K.
- Venue
- Nature Reviews Clinical Oncology
- Published
- 2011-03-08
- Volume
- 8
- Issue
- 5
- Pages
- 292-301
- ISSN
- 1759-4774 (ISSN-L)
- 1759-4782
- OpenAlex
- W2046623913
- Cited by
- 564
- References
- 18
- FWCI
- 3.53
- Type
- journal article
- Language
- en
- Open access
- green
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- Zhu, A. X., Duda, D. G., Sahani, D. V., & Jain, R. K. (2011). HCC and angiogenesis: possible targets and future directions. Nature Reviews Clinical Oncology. https://doi.org/10.1038/nrclinonc.2011.30
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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