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Updated: Aug 19, 2026

Intravital Microscopy of Tumor-associated Vasculature Using Advanced Dorsal Skinfold Window Chambers on Transgenic Fluorescent Mice
Published on: January 19, 2018
Inadequate vasculature in solid tumours: consequences for cancer research strategies
1CRC Gray Laboratory, Mount Vernon Hospital, Northwood, Middlesex, UK.
Abstract:
In the last decade, since we first postulated that antiproliferating endothelial therapy was a promising new approach to therapy, there have been remarkable developments. Vascular effects have been recognized from completely unrelated and unexpected agents, including hyperthermia, photodynamic therapy, misonidazole, tumour necrosis factor, FAA, interferon and interleukins. These vascular effects may coexist with direct cytotoxicity to the tumour cells or they may explain all of the antitumour activity. In order to benefit from such vascular effects, we need to monitor them, understand their mechanisms of action and ensure that the clinical scheduling is optimized to give the greatest therapeutic advantage. The biologist must re-evaluate the validity of his or her tumour models and the clinician must question whether drugs targeted at tumour cells should be sought or whether it would be more productive to target the nutrient supply through the neovasculature. The molecular biology approaches of oncogene expression in tumour cells and growth factor dependency must be weighed against angiogenesis, the pathophysiology of the tumour mass and its supporting normal stromal elements. Since this is a highly complex field there will be many fascinating years of work elucidating tumour versus normal vascular differences. In the meantime, we need to ensure that we do not reject useful therapeutic agents by inappropriate scheduling based on a misunderstanding of their mode of action, or by the use of inappropriate models for testing potential anticancer agents.
Insights
Antiproliferating endothelial therapy shows promise by targeting tumor vasculature. Optimizing scheduling and understanding mechanisms are key for effective anticancer strategies.
Area of Science:
- Oncology
- Vascular Biology
- Cancer Therapeutics
Background:
- Antiproliferating endothelial therapy has emerged as a significant approach in cancer treatment over the past decade.
- Vascular effects, previously unrecognized, have been observed with various agents, impacting tumor growth.
- These vascular effects can complement or solely account for anticancer activity.
Purpose of the Study:
- To highlight the importance of monitoring and understanding the mechanisms of vascular effects in cancer therapy.
- To emphasize the need for optimized clinical scheduling of therapies targeting tumor vasculature.
- To re-evaluate current tumor models and therapeutic strategies, considering targeting nutrient supply via neovasculature.
Main Methods:
- Review of existing literature on antiproliferating endothelial therapy and its associated vascular effects.
- Analysis of diverse agents exhibiting vascular effects, including hyperthermia, photodynamic therapy, and biological agents.
- Discussion on the interplay between molecular biology approaches and the pathophysiology of tumor vasculature.
Main Results:
- Vascular effects are induced by a wide range of agents, some unrelated to direct tumor cell cytotoxicity.
- The efficacy of antiproliferating endothelial therapy depends on understanding its mechanism and optimizing treatment schedules.
- Current research necessitates a shift in focus from solely targeting tumor cells to targeting the tumor's nutrient supply through neovasculature.
Conclusions:
- Further research is crucial to elucidate the complex differences between tumor and normal vasculature.
- Careful consideration of therapeutic agent scheduling and appropriate model selection is vital to avoid premature rejection of potentially effective treatments.
- Targeting tumor vasculature represents a promising avenue for developing novel and effective anticancer therapies.
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