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dc.contributor.authorMorgan, G
dc.date.accessioned2018-07-11T10:53:07Z
dc.date.issued2004
dc.identifierhttp://publications.icr.ac.uk/6746/
dc.identifier.citationIARC SCIENTIFIC PUBLICATIONS, 2004, (157), pp. 373 - 392
dc.identifier.issn0300-5038
dc.identifier.urihttps://repository.icr.ac.uk/handle/internal/2030
dc.description.abstractIn this chapter, we apply the molecular epidemiological paradigm of biomarkers of exposure, early effect and susceptibility to causal models of leukaemia and lymphoma. The aim is to enhance the development of biomarkers for use in studying the causes of these haematopoeitic cancers in the general population. Two causal models of acute myeloid leukaemia are discussed in detail: chemotherapy-induced and benzene-induced acute myeloid leukaemia. Specific chromosomal changes found in acute myeloid leukaemia may serve as useful biomarkers of early effect in these models, and genetic variants in glutathione S-transferases, NQO1 and DNA-repair enzymes may serve as useful biomarkers of susceptibility. Several causal models of lymphoma exist in which biomarkers could be developed and validated. These include human immunodeficiency virus (HIV) immunosuppression, families with inherited disorders and workers exposed to petroleum products, pesticides or organochlorines. Biomarkers of early effect could include markers of DNA double-strand breaks and aberrant V(D)J recombination, and susceptibility may be related to polymorphisms in genes controlling DNA repair and immunological status. We predict that biomarkers of susceptibility will continue to be studied in the case-control format, perhaps in large pooled studies, but that for biomarkers of early effect, there will be a move away from the study of diseased populations to the study of individuals 'at risk' in the causal models described above.
dc.format.extent373 - 392
dc.languageeng
dc.language.isoeng
dc.titleCausal models of leukaemia and lymphoma
dc.typeJournal Article
rioxxterms.licenseref.startdate2004
rioxxterms.typeJournal Article/Review
dc.relation.isPartOfIARC SCIENTIFIC PUBLICATIONS
pubs.issue157
pubs.notesNot known
pubs.organisational-group/ICR
pubs.organisational-group/ICR/Primary Group
pubs.organisational-group/ICR/Primary Group/ICR Divisions
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Clinical Studies
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Clinical Studies/Molecular Haematology (including Cytogenetics Group and Cell Markers)
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Molecular Pathology
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Molecular Pathology/Molecular Haematology (including Cytogenetics Group and Cell Markers)
pubs.organisational-group/ICR
pubs.organisational-group/ICR/Primary Group
pubs.organisational-group/ICR/Primary Group/ICR Divisions
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Clinical Studies
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Clinical Studies/Molecular Haematology (including Cytogenetics Group and Cell Markers)
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Molecular Pathology
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Molecular Pathology/Molecular Haematology (including Cytogenetics Group and Cell Markers)
pubs.embargo.termsNot known
icr.researchteamMolecular Haematology (including Cytogenetics Group and Cell Markers)en_US
dc.contributor.icrauthorMorgan, Gareth Johnen


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