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- Why is the VEGF ligand essential throughout tumor development?
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VEGF and angiogenesis in gastric cancer
— Kösem M, Tuncer I, Kotan Ç, et al. Hepato-Gastroenterology. 20091
...VEGF and the angiogenesis promoted by VEGF play important roles in cancer growth, infiltration and metastasis in gastric carcinoma.
Vascular endothelial growth factor (VEGF) is one of the most potent angiogenic factors discovered to date. It is a signaling molecule secreted by many solid tumors.2,3 High VEGF expression is seen in many human cancer cells, and is also expressed in stromal cells, particularly at sites of relative hypoxia.3-5 VEGF promotes endothelial cell proliferation and migration, and induces angiogenesis.6,7 As its other name—vascular permeability factor (an earlier term for the protein)—suggests, VEGF increases vascular permeability to plasma and its proteins, a characteristic of tumor microvasculature.3
Gastric cancers are overwhelmingly sporadic malignancies, developing in people without a high-risk germ-line mutation.8,9 Adenocarcinomas predominate in the stomach in more than 95% of malignancies. The majority of these express VEGF as an angiogenic factor that results in neovascularization within carcinomas. According to the Lauren classification, these neoplasms are described as intestinal or diffuse types. Intestinal tumors are glandular in nature, while the less common diffuse tumors lack cohesion and functionality.9
Gastric cancer was ranked as the fourth most common global malignancy in 2008, with an estimated 989,600 new cases. About 738,000 people worldwide died from gastric cancer in 2008.10 Gastric carcinoma grows aggressively and, following total gastrectomy, the cancer recurs in nearly 30% of patients.11 Among patients with advanced gastric carcinoma, only 30% are expected to survive 5 or more years after curative resection.12
This section highlights VEGF expression in gastric cancer, as well as the role of VEGF in gastric tumor progression, increased microvessel density (MVD), and malignant metastases.
For more information on a specific topic regarding VEGF and angiogenesis in gastric cancer, click on the links below.
In This Section
References:
- 1.
- Kösem M, Tuncer I, Kotan Ç, et al. Hepatogastroenterology. 2009;56:1236-1240. PMID: 19760978
- 2.
- Suzuki S, Dobashi Y, Hatakeyama Y, et al. BMC Cancer. 2010;10:659. PMID: 21118571
- 3.
- Nagy JA, Feng D, Vasile E, et al. Lab Invest. 2006;86:767-780. PMID: 16732297
- 4.
- Murat A, Migliavacca E, Hussain SF, et al. PLoS One. 2009;4:e5947. PMID: 19536297
- 5.
- Pinto MP, Badtke MM, Dudevoir ML, et al. Cancer Res. 2010;70:2655-2664. PMID: 20332242
- 6.
- Zhao HC, Qin R, Chen XX, et al. World J Gastroenterol. 2006;12:7598-7603. PMID: 17171787
- 7.
- Wang S, Li X, Parra M, et al. Proc Natl Acad Sci U S A. 2008;105:7738-7743. PMID: 18509061
- 8.
- National Cancer Institute dictionary of genetics terms: http://www.cancer.gov/geneticsdictionary?expand=All. Accessed May 16, 2011.
- 9.
- Smith MG, Hold GL, Tahara E, et al. World J Gastroenterol. 2006;12:2979-2990. PMID: 16718776
- 10.
- American Cancer Society. Global cancer facts & figures, 2nd edition, 2011. http://www.cancer.org/acs/groups/content/@epidemiologysurveilance/
documents/document/acspc-027766.pdf. Accessed July 15, 2011. - 11.
- Maeda K, Chung YS, Ogawa Y, et al. Cancer. 1996;77:858-863. PMID: 8608475
- 12.
- Tanigawa N, Amaya H, Matsumura M, et al. Cancer Res. 1996;56:2671-2676. PMID: 8653715