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IGF-1R inhibition enhances radiosensitivity and delays double-strand break repair by both non-homologous end-joining and homologous recombination.

Abstract:

Inhibition of type 1 insulin-like growth factor receptor (IGF-1R) enhances tumor cell sensitivity to ionizing radiation. It is not clear how this effect is mediated, nor whether this approach can be applied effectively in the clinic. We previously showed that IGF-1R depletion delays repair of radiation-induced DNA double-strand breaks (DSBs), unlikely to be explained entirely by reduction in homologous recombination (HR) repair. The current study tested the hypothesis that IGF-1R inhibition i...

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Publication status:
Published

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Publisher copy:
10.1038/onc.2013.460

Authors


Chitnis, MM More by this author
Lodhia, KA More by this author
Aleksic, T More by this author
Protheroe, AS More by this author
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Journal:
Oncogene
Volume:
33
Issue:
45
Pages:
5262-5273
Publication date:
2014-11-05
DOI:
EISSN:
1476-5594
ISSN:
0950-9232
URN:
uuid:f22b4dd6-a235-4b7b-a342-aad03d15f995
Source identifiers:
434126
Local pid:
pubs:434126

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