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dc.contributor.authorQuarmby, Steven L
dc.contributor.authorKumar, Patricia
dc.contributor.authorKumar, Shant
dc.date.accessioned2009-12-15T16:05:30Z
dc.date.available2009-12-15T16:05:30Z
dc.date.issued1999-07-30
dc.identifier.citationRadiation-induced normal tissue injury: role of adhesion molecules in leukocyte-endothelial cell interactions. 1999, 82 (3):385-95 Int. J. Canceren
dc.identifier.issn0020-7136
dc.identifier.pmid10399956
dc.identifier.doi10.1002/(SICI)1097-0215(19990730)82:3<385::AID-IJC12>3.0.CO;2-5
dc.identifier.urihttp://hdl.handle.net/10541/88028
dc.description.abstractThe late onset of necrosis and fibrosis in normal tissues can be a serious consequence of radiotherapy in cancer patients. Because radiation-induced vascular injury precedes the tissue damage, vascular injury is regarded as crucial in the pathogenesis of tissue damage. An understanding of the processes responsible is essential to develop strategies for the amelioration of radiation-induced normal tissue damage. Leukocyte infiltration is commonly observed at sites of irradiation and is likely to lead to the acceleration and/or induction of parenchymal atrophy, fibrosis and necrosis in normal tissues following radiotherapy. The molecular mechanisms mediating leukocyte infiltration of tissues during inflammation have been studied extensively. It is now well established that cell adhesion molecules (CAMs) expressed on leukocytes and endothelial cells control the trafficking of leukocytes from the blood vessel lumen in these conditions. CAMs including E (endothelial), P (platelet) and L (leukocyte)-selectins, intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1), beta1 and beta2 integrins and CD31 are involved in the cascade of events resulting in rolling, arrest and transmigration of leukocytes through the inflamed endothelium. Whether a similar sequence of molecular events induces leukocyte sequestration in irradiated normal tissues is not known. This review is focussed on the role of CAMs in radiation-induced leukocyte infiltration of normal tissues and the therapeutic implications of these findings.
dc.language.isoenen
dc.subject.meshAnimals
dc.subject.meshCell Adhesion Molecules
dc.subject.meshCell Communication
dc.subject.meshCell Cycle
dc.subject.meshCell Movement
dc.subject.meshEndothelium, Vascular
dc.subject.meshHumans
dc.subject.meshLeukocytes
dc.subject.meshRadiation Injuries, Experimental
dc.titleRadiation-induced normal tissue injury: role of adhesion molecules in leukocyte-endothelial cell interactions.en
dc.typeArticleen
dc.contributor.departmentDepartment of Pathological Sciences, Manchester University and Christie Hospital, UK.en
dc.identifier.journalInternational Journal of Canceren
html.description.abstractThe late onset of necrosis and fibrosis in normal tissues can be a serious consequence of radiotherapy in cancer patients. Because radiation-induced vascular injury precedes the tissue damage, vascular injury is regarded as crucial in the pathogenesis of tissue damage. An understanding of the processes responsible is essential to develop strategies for the amelioration of radiation-induced normal tissue damage. Leukocyte infiltration is commonly observed at sites of irradiation and is likely to lead to the acceleration and/or induction of parenchymal atrophy, fibrosis and necrosis in normal tissues following radiotherapy. The molecular mechanisms mediating leukocyte infiltration of tissues during inflammation have been studied extensively. It is now well established that cell adhesion molecules (CAMs) expressed on leukocytes and endothelial cells control the trafficking of leukocytes from the blood vessel lumen in these conditions. CAMs including E (endothelial), P (platelet) and L (leukocyte)-selectins, intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1), beta1 and beta2 integrins and CD31 are involved in the cascade of events resulting in rolling, arrest and transmigration of leukocytes through the inflamed endothelium. Whether a similar sequence of molecular events induces leukocyte sequestration in irradiated normal tissues is not known. This review is focussed on the role of CAMs in radiation-induced leukocyte infiltration of normal tissues and the therapeutic implications of these findings.


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