Advertisement

Manipulation of angiogenesis and clinical applications

 "Topic Review"

American Journal of BioMedicine  Volume 3, Issue 3, pages 100-110, March 2015


David B Mulier;Tomoko Zhang; Jill Risau; Petr Folkman;Ling Yao

Abstract

Angiogenesis is the physiological process through which new blood vessels form from pre-existing vessels. However, it is also a fundamental step in the transition of tumors from a benign state to a malignant one, leading to the use of angiogenesis inhibitorsin the treatment of cancer. Mechanical stimulation of angiogenesis is not well characterized. There is a significant amount of controversy with regard to shear stress acting on capillaries to cause angiogenesis. This may be due to an increase in the production of nitric oxide during exercise. Nitric oxide results in vasodilation of blood vessels. While, Chemical stimulation of angiogenesis is performed by various angiogenic proteins, including several growth factors. The purposes of this topic are to review the pathophysiologic angiogenesis process and examine the clinical applications of  antiangiogenic therapy in the prevention and treatment of diseases.

Keywords: Angiogenesis; Blood vessels; Nitric oxide; Chemical stimulation


Limited Access           Full Text-PDF                Feedback


References

1. Shih T, Lindley C. Bevacizumab. an angiogenesis inhibitor for the treatment of solid malignancies.Clinical Therapeutics 2006; 28(11):1779–1802. [PubMed]

2. Siemann DW. The unique characteristics of tumor vasculature and preclinical evidence for its selective disruption by Tumor-Vascular Disrupting Agents. Cancer Treatment Reviews 2011; 37(1):63–74. [PubMed]

3. Draucker JV; Talarico I; Wu L, et al. Notch-3 promote angiogenesis and proliferation of bladder cancer cells through the PI3K/Akt pathway. American Journal of BioMedicine 2014;2(6):724-731. [Abstract/Full-Text]

4. Gotink KJ, Verheul HM. Anti-angiogenic tyrosine kinase inhibitors: what is their mechanism of action? Angiogenesis 2010; 13(1):1–14. [PubMed]

5. Singer BS; Fishbein JA; Blino SK. Critical role of E6 oncoprotein in cervical cancer: involved in cell proliferation, angiogenesis and apoptosis. Pathophysiology of Cell Injury Journal 2014;2(2):31-41. [Abstract/Full-Text]

6.Cook KM, Figg WD. Angiogenesis inhibitors: current strategies and future prospects. CA: A Cancer Journal for Clinicians 2010; 60(4):222–243. [PubMed]

7. Vlaia M; Hoang M; Urzúa V; Scammells H; González-Hernández S. Cardiomyocyte injury: mechanism of doxorubicin toxicity effects. Pathophysiology of Cell Injury Journal  2014; 2(2):68-77. [Abstract/Full-Text]

8. Chen HX, Cleck JN. Adverse effects of anticancer agents that target the VEGF pathway. Nature Reviews Clinical Oncology 2009; 6(8):465–477. [PubMed]

9. Verheul HM, Pinedo HM. Possible molecular mechanisms involved in the toxicity of angiogenesis inhibition. Nature Reviews Cancer 2007; 7(6):475–485. [PubMed]

10. Rispens E; Bron A; Lee J; Fukumoto J. Pathophsiology of Cell Injury Journal 2014;2(1):1-9. [Abstract/Full-Text]

11. Thorpe PE. Vascular targeting agents as cancer therapeutics. Clin Cancer Res 2004;10:415–427. [PubMed]

12. Jin N, Chen W, Blazar BR, et al. Gene therapy of murine solid tumors with T cells transduced with a retroviral vascular endothelial growth factor – immunotoxin target gene. Hum Gene Ther 2002;13:497–508. [PubMed]

13. Siemann DW, Shi W. Efficacy of combined antiangiogenic and vascular disrupting agents in treatment of solid tumors. Int J Radiat Oncol Biol Phys 2004;60:1233–1240. [PubMed]

14. Davis P, Tozer G, Naylor M, et al. Enhancement of vascular targeting by inhibitors of nitric oxide synthase. Int J Radiat Oncol Biol Phys 2002;54:1532–1536. [PubMed]

15. Wankhede M, deDeugd C, Siemann DW, et al. In vivo functional differences in microvascular response of 4T1 and Caki-1 tumors after treatment with OXi4503. Oncol Rep 2010;23:685–692. [PubMed]

16. Zwi L, Baguley B, Gavin J, et al. Correlation between immune and vascular activities of xanthenone acetic acid anti-tumor agents. Oncol Res 1994;6:79–85. [PubMed]

17. Lash CJ, Li AE, Rutland M, et al. Enhancement of the anti-tumour effects of the antivascular agent 5,6-dimethylxanthenone-4-acetic acid (DMXAA) by combination with 5-hydroxytryptamine and bioreductive drugs Br J Cancer. 1998;78:439–445. [PubMed]

18. Siemann D, Horsman M. Vascular targeted therapies in oncology. Cell Tissue Res 2009;335:241–248. [PubMed]

19. Zhao L, Ching LM, Kestell P, et al. Mechanisms of tumor vascular shutdown induced by 5,6-dimethylxanthenone-4-acetic acid (DMXAA): Increased tumor vascular permeability. Int J Cancer 2005;116:322–326. [PubMed]

20. Baguley B. Antivascular therapy of cancer: DMXAA. Lancet Oncol 2003;4:141–148. [PubMed]

21. Parkins C, Holder A, Hill S, et al. Determinants of anti-vascular action by combretastatin A-4 phosphate: role of nitric oxide. Br J Cancer 2000;83:811–816. [PubMed]

22. Slimani H, Zhai Y, Yousif NG, Ao L, Zeng Q, Fullerton DA, Meng X. Enhanced monocyte chemoattractant protein-1 production in aging mice exaggerates cardiac depression during endotoxemia. Crit Care 2014;18(5):527. [PubMed]

 

 

American Journal of Biomedicine © 2017 Frontier Theme
%d bloggers like this: