ESMO E-Learning: The Value and Role of Anti-Angiogenesis in Solid Tumours and the Mechanism to Inhibit Angiogenesis
- To provide an update on neoangiogenesis in solid tumours and the value of its inhibition
- To provide an update on anti-angiogenic agents, their mechanism of action, and the role they have in the management of various solid tumours
- To summarise results from the clinical studies with anti-angiogenic agents in various solid tumours
|Title||Duration||Content||CME Points||CME Test|
|The value and role of anti-angiogenesis in solid tumours and the mechanism to inhibit angiogenesis||33 min.||75 slides||1||Take Test|
Angiogenesis is a crucial mechanism required for many physiological events. Neoangiogenesis is a multistep process and in recent years the use of anti-angiogenic drugs has become wider practice in cancer therapy. Anti-angiogenic drugs demonstrated activity in different types of solid tumours, including colorectal, lung, breast, ovarian, gastric, hepatocellular, renal cell cancers, neuroendocrine gastro-entero-pancreatic tumours, and sarcomas.
This E-learning module provides an essential update on angiogenesis and mechanisms of neoangiogenesis, as well as describing the role that both processes have in the organism. Furthermore, it provides a list of principal pro- and anti-angiogenesis factors and describes VEGFR pathway.
The authors further segment the module according to agents targeting the VEGF pathway: anti-VEGF antibodies ( bevacizumab), anti–VEGFR-2 antibodies (ramucirumab), soluble VEGF receptors (aflibercept), and principal small molecule inhibitors ( sunitinib, sorafenib, pazopanib, and regorafenib).
For each of the above mentioned agents, the authors provide a comprehensive overview of relevant clinical studies in a range of solid tumours, in particular those in which the concept of anti-angiogenesis has shown clinically meaningful activity. Among the described different angiogenesis inhibitors, the authors underline that they share similar “class specific” adverse events such as hypertension, bleeding, thrombosis, fatigue, and hand and foot syndrome.
Finally, by providing key efficacy results, the authors touch the issue of a more personalised management and cover the current research results in term of biomarkers, concluding that better markers of efficacy are needed for anti-VEGF agents.
F. Ciardiello has participated in advisory board with Roche, Merck Serono, Astellas and Bayer. E. Martinelli, V. Gambardella, T. Troiani have reported no conflict of interest.