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Cells deficient in base-excision repair reveal cancer hallmarks originating from adjustments to genetic instability

Abstract:

Genetic instability, provoked by exogenous mutagens, is well linked to initiation of cancer. However, even in unstressed cells, DNA undergoes a plethora of spontaneous alterations provoked by its inherent chemical instability and the intracellular milieu. Base excision repair (BER) is the major cellular pathway responsible for repair of these lesions, and as deficiency in BER activity results in DNA damage it has been proposed that it may trigger the development of sporadic cancers. Neverthel...

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Publication status:
Published
Peer review status:
Peer reviewed

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Publisher copy:
10.1093/nar/gkv222

Authors


More by this author
Institution:
University of Oxford
Division:
MSD
Department:
NDM
Sub department:
Target Discovery Institute
Role:
Author
More by this author
Institution:
University of Oxford
Division:
MSD
Department:
NDM
Sub department:
Target Discovery Institute
Role:
Author
More by this author
Institution:
University of Oxford
Division:
MSD
Department:
Oncology
Sub department:
CRUK/MRC Ox Inst for Radiation Oncology
Role:
Author
Publisher:
Oxford University Press Publisher's website
Journal:
Nucleic Acids Research Journal website
Volume:
43
Issue:
7
Pages:
3667-3679
Publication date:
2015-03-23
Acceptance date:
2015-03-04
DOI:
EISSN:
1362-4962
ISSN:
0305-1048
Source identifiers:
516651
Language:
English
Keywords:
Pubs id:
pubs:516651
UUID:
uuid:547a714f-d5da-461c-aecd-a443edfd52e3
Local pid:
pubs:516651
Deposit date:
2016-06-17

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