2.50
Hdl Handle:
http://hdl.handle.net/10541/96942
Title:
Biological Response Modifiers and Normal Tissue Injury After Irradiation.
Authors:
Hendry, Jolyon H
Abstract:
The reactions of tissues after irradiation can be modified using a variety of biologically based approaches. Cellular radiosensitivity can be changed using growth regulatory molecules (GRM) that have cell-cycle-mediated effects. Radiosensitivity can also be changed using prostaglandins, dose-miodifying factors of up to around 2 can be achieved. Proliferation and differentiation of precursor cells in early-reacting tissues can be promoted by GRM, producing substantial dose-modifying factors in tissues (eg, up to around 2 for marrow failure). Enhanced cell migration probably also plays an important role in the response of epithelial and stromal tissue elements. Antibiotics can prevent or delay the onset of bacterial infection in susceptible tissues (eg, marrow and intestine) to allow time for tissue recovery to occur. Even in situations where injury is already developing, a choice of dietary components in the case of kidney injury or modifiers of the vasculature in general (eg, using essential fatty acids) can delay or reduce the onset of late injury. Biological response modifiers have the potential to attain an increasingly important role in the management of cancer patients receiving radiotherapy as well as in the infrequent cases of high doses received in accidents.
Affiliation:
The Cancer Research Campaign Department of Experimental Radiation Oncology, Paterson Institute for Cancer Research, Manchester, England
Citation:
Biological Response Modifiers and Normal Tissue Injury After Irradiation. 1994, 4 (2):123-132 Semin Radiat Oncol
Journal:
Seminars in Radiation Oncology
Issue Date:
Apr-1994
URI:
http://hdl.handle.net/10541/96942
DOI:
10.1016/S1053-4296(05)80040-2
PubMed ID:
10717099
Type:
Article
ISSN:
1532-9461
Appears in Collections:
All Paterson Institute for Cancer Research

Full metadata record

DC FieldValue Language
dc.contributor.authorHendry, Jolyon Hen
dc.date.accessioned2010-04-20T15:53:25Z-
dc.date.available2010-04-20T15:53:25Z-
dc.date.issued1994-04-
dc.identifier.citationBiological Response Modifiers and Normal Tissue Injury After Irradiation. 1994, 4 (2):123-132 Semin Radiat Oncolen
dc.identifier.issn1532-9461-
dc.identifier.pmid10717099-
dc.identifier.doi10.1016/S1053-4296(05)80040-2-
dc.identifier.urihttp://hdl.handle.net/10541/96942-
dc.description.abstractThe reactions of tissues after irradiation can be modified using a variety of biologically based approaches. Cellular radiosensitivity can be changed using growth regulatory molecules (GRM) that have cell-cycle-mediated effects. Radiosensitivity can also be changed using prostaglandins, dose-miodifying factors of up to around 2 can be achieved. Proliferation and differentiation of precursor cells in early-reacting tissues can be promoted by GRM, producing substantial dose-modifying factors in tissues (eg, up to around 2 for marrow failure). Enhanced cell migration probably also plays an important role in the response of epithelial and stromal tissue elements. Antibiotics can prevent or delay the onset of bacterial infection in susceptible tissues (eg, marrow and intestine) to allow time for tissue recovery to occur. Even in situations where injury is already developing, a choice of dietary components in the case of kidney injury or modifiers of the vasculature in general (eg, using essential fatty acids) can delay or reduce the onset of late injury. Biological response modifiers have the potential to attain an increasingly important role in the management of cancer patients receiving radiotherapy as well as in the infrequent cases of high doses received in accidents.en
dc.languageENG-
dc.subjectIrradiationen
dc.subjectRadiosensitivityen
dc.subjectTissue Injuryen
dc.titleBiological Response Modifiers and Normal Tissue Injury After Irradiation.-
dc.typeArticleen
dc.contributor.departmentThe Cancer Research Campaign Department of Experimental Radiation Oncology, Paterson Institute for Cancer Research, Manchester, Englanden
dc.identifier.journalSeminars in Radiation Oncologyen
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