Angiogenesis and vascular normalisation models
Models of how tumours recruit blood vessels, and of Rakesh Jain's idea that anti-angiogenic drugs at the right dose normalise rather than destroy those vessels, improving drug and oxygen delivery for a window of days.
Overview
Anderson and Chaplain's 1998 continuum and discrete models simulated capillary sprouting toward a tumour under growth factors, and Jain's group modelled how abnormal vessels raise interstitial pressure and starve tumours of drug. Jain's vascular normalisation hypothesis, that judicious anti-VEGF therapy prunes immature vessels and transiently restores flow, is supported by imaging in glioblastoma and rectal cancer and explains why bevacizumab helps chemotherapy despite cutting blood supply. These models motivate scheduling anti-angiogenic drugs before chemotherapy or radiotherapy and measuring perfusion during treatment.
How it works
Vessel growth follows chemotactic and haptotactic gradients of angiogenic factors; anti-angiogenic therapy at moderate dose reduces vessel density and leakiness, lowering interstitial pressure and improving perfusion transiently.
- Explains combination benefit of anti-VEGF drugs
- Supported by perfusion imaging
- Guides scheduling
- Normalisation window is short and variable
- Hard to measure in routine care
- Models simplify vessel biology
Latest papers
topQuery for this technology: (TITLE:"Angiogenesis and vascular normalisation models" OR ABSTRACT:"Angiogenesis and vascular normalisation models") AND (cancer OR tumor OR tumour OR oncology OR carcinoma OR lymphoma OR leukemia OR leukaemia OR myeloma OR sarcoma OR melanoma OR glioma). Results are unfiltered search hits about Angiogenesis and vascular normalisation models, not a curated reading list.
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