RAD51 as a potential surrogate marker for DNA repair capacity in solid malignancies
Mariam Gachechiladze, Josef Škarda, Alex Soltermann & Markus Joerger
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abstract
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Targeting deficient mechanisms of cellular DNA repair still
represents the basis for the treatment of the majority of solid
tumors, and increased DNA repair capacity is a hallmark mechanism of
resistance not only to DNA-damaging treatments such as cytotoxic
drugs and radiotherapy, but also to small molecule targeted drugs
such as inhibitors of poly-ADP ribose polymerase (PARP). Hence,
there is substantial medical need for potent and convenient
biomarkers of individual response to DNA-targeted treatment in
personalized cancer care. RAD51 is a highly conserved protein that
catalyzes DNA repair via homologous recombination, a major DNA
repair pathway which directly modulates cellular sensitivity to
DNA-damaging treatments. The clinical and biological significance of
RAD51 protein expression is still under investigation. Pre-clinical
studies consistently show the important role of nuclear RAD51
immunoreactivity in chemo- and radioresistance. Validating data from
clinical trials however is limited at present, and some clinical
studies show controversial results. This review gives a
comprehensive overview on the current knowledge about the prognostic
and predictive value of RAD51 protein expression and genetic
variability in patients with solid malignancies.
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citation
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Gachechiladze M, Škarda J, Soltermann A, Joerger M. RAD51 as a
potential surrogate marker for DNA repair capacity in solid
malignancies. Int J Cancer 2017; 141:1286-1294.
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type
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journal paper/review (English)
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date of publishing
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19-05-2017
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journal title
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Int J Cancer (141/7)
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ISSN electronic
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1097-0215
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pages
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1286-1294
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PubMed
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28477336
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DOI
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10.1002/ijc.30764
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