IGF-1R inhibition enhances radiosensitivity and delays double-strand break repair by both non-homologous end-joining and homologous recombination.
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 radiat...
Main Authors: | Chitnis, M, Lodhia, K, Aleksic, T, Gao, S, Protheroe, A, Macaulay, V |
---|---|
Format: | Journal article |
Language: | English |
Published: |
2014
|
Similar Items
-
Depletion of the type 1 IGF receptor delays repair of radiation-induced DNA double strand breaks
by: Turney, B, et al.
Published: (2012) -
Imatinib radiosensitizes bladder cancer by targeting homologous recombination.
by: Qiao, B, et al.
Published: (2013) -
Saccharomyces cerevisiae C1D is implicated in both non-homologous DNA end joining and homologous recombination.
by: Erdemir, T, et al.
Published: (2002) -
Multi-pathway DNA-repair reporters reveal competition between end-joining, single-strand annealing and homologous recombination at Cas9-induced DNA double-strand breaks
by: van de Kooij, Bert, et al.
Published: (2023) -
Inhibition of double-strand break non-homologous end-joining by cisplatin adducts in human cell extracts.
by: Diggle, C, et al.
Published: (2005)