What "helps" tumors evade vascular targeting treatment?
OBJECTIVE
To throw a light on the possible factors which might induce resistance of vascular targeting treatment in tumors by reviewing the recent publications in the field of tumor angiogenesis and vascular targeting treatment. Data sources The data used in this review were mainly from Medline and PubMed for relevant English language articles published from 1971 to January 2008. The search terms were "angiogenesis", "vascular targeting treatment" and "endothelial progenitor cells". Study selection Articles involved in the possible influence factors during angiogenesis and vascular targeting treatment were selected, including angiogenic or anti-angiogenic mechanism, tumor vasculature, tumor cells, cancer stem cells and endothelial progenitor cells.


RESULTS
As a promising strategy vascular targeting treatment still has experimental and clinical setbacks which may term tumor vasculature's resistance to anti-angiogenesis agents. There are several possible explanations for such a resistance that might account for clinical and preclinical failures of anti-angiogenic treatment against tumor. Proangiogenic effect of hypoxia, normal tumor vasculature, escape of tumor cells and tumor vasculogenesis are included. This review reveals some clues which might be helpful to direct future research in order to remove obstacles to vascular targeting treatment.


CONCLUSIONS
Generally and undoubtedly vascular targeting treatment remains a promising strategy. But we still have to realize the existence of a challenging future. Further research is required to enhance our knowledge of vascular targeting treatment strategy before it could make a more substantial success.
Si
Zhi-chao
ZC
Clinical Medical Institute, Aarhus University Hospital-Skejby, Arhus 8210, Denmark.
Liu
Jie
J
D000970:Antineoplastic Agents / Q000494:pharmacology*; D001808:Blood Vessels / Q000187:drug effects*; D015687:Cell Hypoxia; D042783:Endothelial Cells / Q000166:cytology; D006801:Humans; D009369:Neoplasms / Q000098:blood supply* / Q000188:drug therapy*; D014411:Neoplastic Stem Cells / Q000187:drug effects; D018919:Neovascularization, Physiologic / Q000187:drug effects; D010641:Phenotype; D013234:Stem Cells / Q000166:cytology
D000970:Antineoplastic Agents