Week 3: Discussion: Angiogenesis and Metastasis





Week 3: Discussion: Angiogenesis and Metastasis



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Discussion: Angiogenesis and Metastasis

Discussion Topic 1:

  1. In your own words, what is angiogenesis, and what is the importance of this process in cancer progression? 

Angiogenesis is a complex process that results in the formation of new blood vessels. Endogenous systemic or local chemical signals synchronize functions of smooth muscle cells and endothelial cells to repair blood vessels that are damaged. In cancer progression, angiogenesis is crucial as solid tumors require a supply of blood for them to grow in size (Rajabi & Mousa, 2017). The tumor can initiate the blood supply by releasing chemical signals stimulating the process of angiogenesis. Consequently, the tumor cells can also stimulate neighboring normal cells to produce signaling molecules to promote angiogenesis.

  1. In your own words, explain the role of each of these in angiogenesis:
    • VEGF: This is a chemical signal which binds to the receptors on the endothelial cell surface initiating signals within the normal cells, and promoting the survival and growth of new blood vessels (Zuazo-Gaztelu & Casanovas, 2018).
    • MMPs: Specific MMPs have been reported to promote the process of angiogenesis in several ways, including helping in detaching pericytes from blood vessels undergoing the process of angiogenesis, releasing angiogenic growth factors bound to ECM, exposing the binding sites of cryptic proangiogenic integrin in the ECM, generating promigratory components of ECM fragments and cleaving cell-cell adhesion of the endothelial cells (Rajabi & Mousa, 2017).
    • Integrin molecules: In angiogenesis, integrins help in regulating the migration and survival of endothelial cells (Zuazo-Gaztelu & Casanovas, 2018).
    • PDGF: Signals via PDGFRα and PDGFRβ, and stimulates the process of angiogenesis by up-regulating the production of VEGF and modulating the recruitment and proliferation of perivascular cells (Zuazo-Gaztelu & Casanovas, 2018).
  2. List several reasons why angiogenesis is a very active area for cancer therapy research. 

Research on angiogenesis has helped in the development of drugs that prevent cancerous tumors from growing their blood vessels, hence slowing their growth or even shrinking them (Rajabi & Mousa, 2017). Several anti-angiogenesis treatment modalities have been developed through research including drugs that block blood vessels of growth factors, drugs that block cell-to-cell signaling, and those that block signaling within the cell.



Discussion Topic 2:

In your own words, explain metastasis and why this process is important in the prognosis of a patient.   Is this an easy and efficient process for cancer cells, why or why not?

Do you think angiogenesis or metastasis would be the better target for cancer therapy?  Explain.

Metastasis is the spread of cancerous cells to other organs and tissues different from the point of origin. The process of metastasis is important in determining the extent to which cancer has spread in the patient’s body, hence determining how the symptoms can be reduced, cancer growth slowed and the patient’s quality of life improved to promote a better prognosis (Fares et al., 2020). Only a small percentage of the primary cancer cell can successfully metastasize to other areas, despite the process being uncertain. As such, it is quite difficult to target metastasis in cancer therapy. The application of antiandrogens is however simple as specific growth and signaling factors can be developed to slow down the growth of the cancer cells or even shrink them.




Fares, J., Fares, M. Y., Khachfe, H. H., Salhab, H. A., & Fares, Y. (2020). Molecular principles of metastasis: a hallmark of cancer revisited. Signal Transduction and Targeted Therapy5(1).

Rajabi, M., & Mousa, S. (2017). The Role of Angiogenesis in Cancer Treatment. Biomedicines5(4), 34.

Zuazo-Gaztelu, I., & Casanovas, O. (2018). Unraveling the Role of Angiogenesis in Cancer Ecosystems. Frontiers in Oncology8. https://doi.org/10.3389/fonc.2018.00248



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