Vascular endothelium as the vulnerable element in tumours.
The difference between blood vessels in tumours and normal tissues has been recognised for a long time, but little has been done to exploit this in cancer therapy. An overview is presented of the possible contribution of vascular mediated injury with several existing forms of treatment. Interventive radiology and, to some extent, hyperthermia are most obviously mediated through ischaemic cell death. The successful cure of many tumours with radiation, and the complete regressions seen with systemic chemotherapy may also be partially due to a vascular component of damage. The proliferation characteristics of endothelial cells in normal and tumour blood vessels are summarised. These have been derived from single injections or repeated administration of tritiated thymidine. A very large and consistent difference exists between the turnover times. The tumour endothelium is proliferating 20 to 2 000 times faster than any normal tissue endothelium in the adult. The single exception is the placenta which has even more rapid proliferation than the tumour endothelium. The large difference in proliferation rates, coupled with the poor wall structure, lack of innervation and lack of collateral supply, make the blood vessels an attractive target for tumour therapy. Possible means of utilizing this are outlined.
D000818:Animals; D002196:Capillaries; D002455:Cell Division; D002470:Cell Survival; D003250:Constriction; D004727:Endothelium / Q000473:pathology; D006801:Humans; D006979:Hyperthermia, Induced; D007511:Ischemia / Q000378:metabolism / Q000473:pathology; D051379:Mice; D009369:Neoplasms / Q000098:blood supply* / Q000378:metabolism / Q000473:pathology / Q000628:therapy; D009389:Neovascularization, Pathologic; D010100:Oxygen / Q000378:metabolism; D010313:Partial Pressure; D011836:Radiation Tolerance
D010100:Oxygen