Show simple item record

dc.contributor.authorZienolddiny, S
dc.contributor.authorRyberg, D
dc.contributor.authorSvendsrud, DH
dc.contributor.authorEilertsen, E
dc.contributor.authorSkaug, V
dc.contributor.authorHewer, A
dc.contributor.authorPhillips, DH
dc.contributor.authorRiele, HT
dc.contributor.authorHaugen, A
dc.date.accessioned2018-09-04T11:47:46Z
dc.date.issued2006-06-01
dc.identifier11
dc.identifier.citationINTERNATIONAL JOURNAL OF CANCER, 2006, 118 pp. 2899 - 2902
dc.identifier.issn0020-7136
dc.identifier.urihttps://repository.icr.ac.uk/handle/internal/2534
dc.identifier.doi10.1002/ijc.21686
dc.description.abstractDNA mismatch repair (MMR) is essential for repair of single-base mismatches and insertion/deletion loops. MMR proteins also participate in cellular response to DNA damaging agents such as various alkylating agents. Mice deficient in the MMR gene Msh2 develop tumors earlier after exposure to alkylating agents when compared to unexposed mice. The interaction between the MMR system and polycyclic aromatic hydrocarbons such as benzo[a]pyrene (B[a]P) has not been investigated in vivo. Here, we show that treatment of Msh2-deficient mice with B[a]P enhances susceptibility to lymphomagenesis. Carrying at least one intact copy of the Msh2 gene had a protective effect. B[a]P treatment only induced lymphomas in 3 of the 40 (7.5%) mice with at least one intact copy of the Msh2 gene as compared to 13 of the 17 (76.5%) Msh2-deficient mice and occurs only after a much longer time period. The B[a]P-DNA adduct levels measured in lung, liver, spleen and forestomach of B[a]P-treated Msh2(-/-) mice were not significantly different from B[a]P-treated Msh2(+/+) mice. In summary, the results suggest that B[a]P accelerates lymphomagenesis in Msh2-deficient mice. Furthermore, Msh2 deficiency does not have any significant effect on B[a]P-DNA adduct levels. (c) 2005 Wiley-Liss, Inc.
dc.format.extent2899 - 2902
dc.languageeng
dc.language.isoeng
dc.titleMsh2 deficiency increases susceptibility to benzo[a]pyrene-induced lymphomagenesis
dc.typeJournal Article
rioxxterms.versionofrecord10.1002/ijc.21686
rioxxterms.licenseref.startdate2006-06-01
rioxxterms.typeJournal Article/Review
dc.relation.isPartOfINTERNATIONAL JOURNAL OF CANCER
pubs.notesresearcherid-numbers: Zienolddiny, Shanbeh/O-7392-2015 orcid-numbers: Zienolddiny, Shan/0000-0001-9747-9625 Phillips, David/0000-0001-8509-3485 unique-id: ISI:000237029300036
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/Closed research teams
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Closed research teams/Human Biomonitoring & Carcinogen Activation
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/Closed research teams
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Closed research teams/Human Biomonitoring & Carcinogen Activation
pubs.volume118
pubs.embargo.termsNot known
icr.researchteamHuman Biomonitoring & Carcinogen Activationen_US
dc.contributor.icrauthorPhillips, David Hunteren


Files in this item

FilesSizeFormatView

There are no files associated with this item.

This item appears in the following collection(s)

Show simple item record