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.
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.
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.
Bevacizumab is a humanised antibody that soaks up VEGF-A, the signal tumours use to grow new blood vessels. Approved in 2004, it partners chemotherapy in colorectal, ovarian, cervical, lung, kidney and liver cancer and glioblastoma, and adds to trifluridine/tipiracil in late-line bowel cancer; hypertension, protein in the urine and bleeding are its characteristic side effects.
Query 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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