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      Role of VEGFA gene polymorphisms in colorectal cancer patients who treated with bevacizumab

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          Abstract

          Objectives

          This study aimed to explore the effects of vascular endothelial growth factor A ( VEGFA) gene polymorphisms (rs699947 and rs833061) on Bevacizumab (BEV) treatment in colorectal cancer (CRC) patients.

          Methods

          125 CRC cases receiving BEV plus FOLFIRI treatment were recruited in this study. VEGFA polymorphisms were genotyped using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method. Correlation of VEGFA gene polymorphisms with the response rate and progression free survival (PFS) was evaluated. Multivariate analyses were performed to estimate the effects of VEGFA polymorphisms on the therapeutic effects of BEV treatment in CRC patients.

          Results

          Rs699947 variants did not show significant association with BEV treatment. For rs833061 analysis, TT and TC genotype carriers had significantly higher ORR (objective response rate) than CC carriers ( P=0.048 and P=0.021, respectively). Moreover, TT carriers underwent a well DCR (disease control rate) compared to CC carriers ( P=0.002). PFS time also showed obvious correlation with rs833061 polymorphism (log rank test, P=0.002). Multivariate analyses demonstrated that TT and TC genotypes of rs833061 polymorphism were significantly correlated with enhanced therapeutic effects and prolonged PFS in CRC patients.

          Conclusion

          VEGFA rs833061 polymorphism is significantly associated with the therapeutic efficiency of bevacizumab in CRC patients.

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          Cellular abnormalities of blood vessels as targets in cancer.

          Hiroya Hashizume, Peter Baluk, Sarah McDonald (2005)
          Tumor blood vessels have multiple structural and functional abnormalities. They are unusually dynamic, and naturally undergo sprouting, proliferation, remodeling or regression. The vessels are irregularly shaped, tortuous, and lack the normal hierarchical arrangement of arterioles, capillaries and venules. Endothelial cells in tumors have abnormalities in gene expression, require growth factors for survival and have defective barrier function to plasma proteins. Pericytes on tumor vessels are also abnormal. Aberrant endothelial cells and pericytes generate defective basement membrane. Angiogenesis inhibitors can stop the growth of tumor vessels, prune existing vessels and normalize surviving vessels. Loss of endothelial cells is not necessarily accompanied by simultaneous loss of pericytes and surrounding basement membrane, which together can then provide a scaffold for regrowth of tumor vessels. Rapid vascular regrowth reflects the ongoing drive for angiogenesis and bizarre microenvironment in tumors that promote vascular abnormalities and thereby create therapeutic targets.
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            Anticancer strategies involving the vasculature.

            Roy Bicknell, Victoria Heath (2009)
            The growth and metastasis of solid tumors critically depends on their ability to develop their own blood supply, a process known as tumor angiogenesis. Over the past decade much work has been performed to understand this process, and modifying this process provides a key point of therapeutic intervention in the fight against cancer. This Review explores the development of anti-VEGF-based antiangiogenic therapies, of which there are currently three licensed for clinical use worldwide. Although originally anticipated to inhibit the growth of tumor vessels, the induction of vascular normalization caused by these approved agents has provided a novel means of effective delivery of known chemotherapeutic agents. The development of small molecules that target VEGF receptors has resulted in the generation of inhibitors with not only vascular activity but antitumor activity in certain cancers. This Review will address the current status of vascular-disrupting strategies, such as therapies designed to induce tumor collapse by selectively destroying existing tumor vessels. These therapies can be broadly divided into small-molecular-weight vascular-disrupting agents and ligand-directed approaches. We discuss the current status of development, drug mechanisms of actions, combination with conventional chemotherapy and radiotherapy, and potential future targets for therapeutic intervention.
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              Molecular controls of arterial morphogenesis.

              Michael Simons, Anne Eichmann (2015)
              Formation of arterial vasculature, here termed arteriogenesis, is a central process in embryonic vascular development as well as in adult tissues. Although the process of capillary formation, angiogenesis, is relatively well understood, much remains to be learned about arteriogenesis. Recent discoveries point to the key role played by vascular endothelial growth factor receptor 2 in control of this process and to newly identified control circuits that dramatically influence its activity. The latter can present particularly attractive targets for a new class of therapeutic agents capable of activation of this signaling cascade in a ligand-independent manner, thereby promoting arteriogenesis in diseased tissues.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Oncotarget
                Journal ID (iso-abbrev): Oncotarget
                Journal ID (publisher-id): Oncotarget
                Journal ID (publisher-id): ImpactJ
                Title: Oncotarget
                Publisher: Impact Journals LLC
                ISSN (Electronic): 1949-2553
                Publication date Collection: 1 December 2017
                Publication date (Electronic): 6 November 2017
                Volume: 8
                Issue: 62
                Pages: 105472-105478
                Affiliations
                1 Department of General Surgery, The Military General Hospital of Beijing PLA, Beijing 100700, China
                2 Department of Health, The Military General Hospital of Beijing PLA, Beijing 100700, China
                Author notes
                Correspondence to: Bo Yu, sdklfod@ 123456yeah.net
                Article
                Publisher ID: 22295
                DOI: 10.18632/oncotarget.22295
                PMC ID: 5739652
                PubMed ID: 29285265
                SO-VID: dd781580-d360-40fe-a6b9-5d37904c1339
                Copyright © Copyright: © 2017 Cui et al.
                License:

                This article is distributed under the terms of the Creative Commons Attribution License (CC-BY), which permits unrestricted use and redistribution provided that the original author and source are credited.

                History
                Date received : 21 March 2017
                Date accepted : 26 August 2017
                Categories
                Subject: Research Paper

                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: vegfa,polymorphisms,bevacizumab,colorectal cancer
                Data availability:
                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: vegfa, polymorphisms, bevacizumab, colorectal cancer

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