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Published on: November 23, 2014
Escaping Antiangiogenic Therapy: Strategies Employed by Cancer Cells
Mauricio P Pinto1, Paula Sotomayor2, Gonzalo Carrasco-Avino3
1Department of Physiology, Faculty of Biological Sciences, Pontificia Universidad Católica de Chile, Santiago 8331150, Chile. mauricio_pinto@outlook.com.
Abstract:
Tumor angiogenesis is widely recognized as one of the "hallmarks of cancer". Consequently, during the last decades the development and testing of commercial angiogenic inhibitors has been a central focus for both basic and clinical cancer research. While antiangiogenic drugs are now incorporated into standard clinical practice, as with all cancer therapies, tumors can eventually become resistant by employing a variety of strategies to receive nutrients and oxygen in the event of therapeutic assault. Herein, we concentrate and review in detail three of the principal mechanisms of antiangiogenic therapy escape: (1) upregulation of compensatory/alternative pathways for angiogenesis; (2) vasculogenic mimicry; and (3) vessel co-option. We suggest that an understanding of how a cancer cell adapts to antiangiogenic therapy may also parallel the mechanisms employed in the bourgeoning tumor and isolated metastatic cells delivering responsible for residual disease. Finally, we speculate on strategies to adapt antiangiogenic therapy for future clinical uses.
Insights
Tumor cells can resist anti-angiogenic therapy by developing new blood vessels or hijacking existing ones. Understanding these escape routes is key to improving cancer treatment strategies.
Area of Science:
- Oncology
- Cancer Biology
- Molecular Medicine
Background:
- Tumor angiogenesis, the formation of new blood vessels, is a critical hallmark of cancer.
- Anti-angiogenic therapies are established cancer treatments, but tumor resistance remains a significant challenge.
- Understanding resistance mechanisms is crucial for advancing cancer therapy.
Purpose of the Study:
- To review the primary mechanisms by which tumors escape anti-angiogenic therapy.
- To explore the parallels between therapy escape and intrinsic tumor growth strategies.
- To propose future directions for adapting anti-angiogenic therapies.
Main Methods:
- Literature review and synthesis of existing research on tumor angiogenesis and therapy resistance.
- Detailed analysis of three key escape mechanisms: compensatory angiogenesis, vasculogenic mimicry, and vessel co-option.
- Exploration of the link between therapy escape and residual disease development.
Main Results:
- Identified and detailed three principal mechanisms of anti-angiogenic therapy escape.
- Highlighted the role of compensatory angiogenesis, vasculogenic mimicry, and vessel co-option in treatment failure.
- Suggested that tumor adaptation to therapy mirrors mechanisms in primary tumor growth and metastasis.
Conclusions:
- Tumor resistance to anti-angiogenic therapy is multifaceted, involving adaptive strategies.
- Understanding these escape mechanisms can inform the development of more effective, combination therapies.
- Future strategies should aim to overcome or circumvent these resistance pathways for improved clinical outcomes.
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