Targeted therapy with bevacizumab (Avastin) for metastatic colorectal cancer

Koukourakis, Georgios V.; Sotiropoulou-Lontou, Anastasia

doi:10.1007/s12094-011-0720-z

Cited by 40 publications

(28 citation statements)

References 29 publications

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“…21,22 Therefore, identification of proangiogenic genes and their products that lead to angiogenesis is critical for providing new potential therapeutic targets. In current oncological practice, the VEGF-targeted agent bevacizumab has been established as a first-line treatment for metastatic CRC, [23][24][25] suggesting especially important roles for angiogenic factors in CRC progression. Here, we showed that GPR120 signaling promoted angiogenesis by inducing secretion of proangiogenic factors VEGF, IL-8 and COX-2-derived PGE 2 in vitro and in xenograph mouse model.…”

Section: Gpr120 Is Induced In Human Crc Tissues and Its Expression Ismentioning

confidence: 99%

Identification of G-protein-coupled receptor 120 as a tumor-promoting receptor that induces angiogenesis and migration in human colorectal carcinoma

et al. 2013

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G-protein-coupled receptor 120 (GPR120) functions as a receptor for unsaturated long-chain free fatty acids and has an important role in regulating lipid and glucose metabolism. However, a role for GPR120 in the development of tumors has not yet been clarified. Here, we show that GPR120 signaling promotes angiogenic switching and motility of human colorectal carcinoma (CRC) cells. We show that the expression of GPR120 is significantly induced in CRC tissues and cell lines, which is associated with tumor progression. Activation of GPR120 signaling in human CRC promotes angiogenesis in vitro and in vivo, largely by inducing the expression and secretion of proangiogenic mediators such as vascular endothelial growth factor (VEGF), interleukin-8 and cyclooxygenase-2-derived prostaglandin E 2 . The PI3K/Akt-NF-kB pathway is activated by GPR120 signaling and is required for GPR120 signaling-induced angiogenic switching in CRC cells. And, GPR120 activation enhances the motility of CRC cells and induces epithelial-mesenchymal transition. Furthermore, in vivo study shows that activation of GPR120 promotes angiogenesis and tumor growth. Finally, we find that GPR120 expression is positively correlated with VEGF expression and inversely correlated with the epithelial marker E-cadherin in CRC tissues. Collectively, our results demonstrate that GPR120 functions as a tumor-promoting receptor in CRC and, therefore, shows promise as a new potential target for cancer therapeutics.

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Section: Gpr120 Is Induced In Human Crc Tissues and Its Expression Ismentioning

confidence: 99%

Identification of G-protein-coupled receptor 120 as a tumor-promoting receptor that induces angiogenesis and migration in human colorectal carcinoma

et al. 2013

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“…TSGF, a special substance discovered by Canadian scientists, is produced by malignant tumor cells (Koukourakis et al, 2011;Efferth, 2012;Duffy, 2013). As a new tumor marker, it can promote tumor formation and growth as well as proliferation of a large amount of peripheral capillaries.…”

Section: Discussionmentioning

confidence: 99%

Expression and Significance of TSGF, CEA and AFP in Patients Before and after Radical Surgery for Colon Cancer

Hu¹,

Wang²,

Tao³

et al. 2013

Asian Pacific Journal of Cancer Prevention

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Objective: To explore the expression and significance of tumor specific growth factor (TSGF), carcinoembryonic antigen (CEA) and alpha fetoprotein (AFP) in cancer tissue and serum of patients with colon cancer. Materials and Methods: Radical surgery for colon cancer was performed on 43 patients with laparoscopu under conditions of general anesthesia. The Elisa method was used to detect the levels of serum TSGF, CEA and AFP before and after radical operation, and cancer tissue underwent TSGF, CEA and AFP immunohistochemistry staining after laparoscopic surgery. The decreased conditions of serum TSGF, CEA and AFP in patients with colon cancer at different levels of differentiation and clinical stagings were analyzed, and the relationships of expression rates between histological types, colon cancer morphology, lymph node metastasis and TSGF, CEA as well as AFP in cancer tissue were assessed. Results: Compared with before radical surgery, the levels of serum TSGF, CEA and AFP decreased notably in patients after operations (p<0.01). The decreased degree of TSGF and CEA was the largest in patients with poorly differentiated cancer tissue (p<0.01), while that of AFP was noted in patients with moderately differentiated cancer tissue (p<0.01). The decreased degree of TSGF and AFP was the largest in patients at phase Dukes A (p<0.01), while that of CEA in patients at phase Dukes C (p<0.01). There were no significant differences among the positive expression rates of TSGF, CEA and AFP with different histological types and colon cancer morphologies (p>0.05). The positive expression rates of TSGF and CEA in patients with lymph node metastasis were significantly higher than those without lymph node metastasis (p<0.01). Conclusions: TSGF, CEA and AFP can be used to evaluate the effect of radical operation for colon cancer, and the changed levels of different markers are associated with tumor differentiation, clinical stating and presence or absence of lymph node metastasis.

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“…Bevacizumab (Avastin), a humanized monoclonal antibody against VEGF, the most potent growth factor involved in tumour angiogenesis, was approved in the EU in 2005 for the treatment of carcinoma, non-small-cell lung cancer, colorectal cancer, carcinoma, renal cell cancer, and ovarian cancers [71][72][73][74] . Bevacizumab has been evaluated as first-line treatment in a phase II clinical trial with cisplatin and pemetrexed in patients with advanced mesothelioma.…”

Section: Tyrosine Kinase Inhibitors Against Vegfmentioning

confidence: 99%

Current and prospective pharmacotherapies for the treatment of pleural mesothelioma

Bakker

Guazzelli

Krstic‐Demonacos

et al. 2017

Expert Opinion on Orphan Drugs

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IntroductionMesothelioma is a rare asbestos-linked cancer with an expected incidence peak between 2015-2030. Therapies remain ineffective, thus developing and testing novel treatments is important for both oncologists and researchers. Areas CoveredAfter describing mesothelioma and the shortcomings of current therapies, the article discusses numerous therapies in turn such as immunotherapy (passive and active), gene therapy (such as suicide gene therapy) and targeted therapy such as tyrosine kinase inhibitors. The bases for different therapies and clinical trials at different phases are also described. The article concludes by detailing possible reasons for therapy failure. Expert OpinionDespite the many attempts to uncover new therapeutic options, mesothelioma is still an orphan disease, complicated by factors such as the inflammatory microenvironment and low mutational load. Our opinion is that uncovering the biological mechanisms behind mesothelioma development will assist therapy development. The lack of efficacy of tyrosine kinase inhibitors and modest anti-angiogenic activity indicates a less relevant role for tumour cell proliferation and neoangiogenesis, thus the shortcut of treating mesothelioma with therapies from other cancers may be unsound. Conversely, many lines of evidence indicate that focussing on the survival mechanisms that tumour cells exploit may yield better therapeutics, particularly nutrition and cellular machinery.

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Targeted therapy with bevacizumab (Avastin) for metastatic colorectal cancer

Cited by 40 publications

References 29 publications

Identification of G-protein-coupled receptor 120 as a tumor-promoting receptor that induces angiogenesis and migration in human colorectal carcinoma

Identification of G-protein-coupled receptor 120 as a tumor-promoting receptor that induces angiogenesis and migration in human colorectal carcinoma

Expression and Significance of TSGF, CEA and AFP in Patients Before and after Radical Surgery for Colon Cancer

Current and prospective pharmacotherapies for the treatment of pleural mesothelioma

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