The high expression of Ki67 and Bcl-2 in combination with the non-functional p53 could have contributed to cell tumourigenicity, regrowth of tumour cells, and the formation of radiation-damaged multinucleated giant cells with improper chromosome segregation and cell division behaviours [41, 45, 46].
These structures may potentially be the source for the formation of radiation-induced chromosomal aberrations.
These data elucidate the mechanisms involved in the formation of radiation-induced chromatid aberrations and propose that these mechanisms contribute to chromosome instability in pluripotent cells in vivo.
Downregulation of Rad51 or Brca2 by siRNA led to significant reduction in the spontaneous SCE level and completely abolished the formation of radiation-induced SCEs.
However, evidence that mammospheres, such as the monolayer cells, employ both NHEJ and HR was indicated by the formation of radiation-induced 53BP1 and Rad51 foci [see Additional file 3].
The results indicate that WR-1065 is an effective protector against the formation of radiation-induced double-strand breaks in DNA as measured using a neutral elution technique at either pH.
Our results indicate the indirect involvement of topoisomerase II α in the formation of radiation-induced chromatid breaks from DSB, and suggest topoisomerase II α as a possible factor in the inter-individual variation in chromatid radiosensitivity.
KPNA2 also controls both the nuclear localisation of the MRN complexes with the formation of radiation-induced focus (Tseng et al, 2005); therefore, the suppression of KPNA2 prevents the double-stranded breaks (induced by ionising radiation), which will lead to suppression of NSB-mediated DNA repair pathway.
We used As-oligodeoxynucleotide (ODN) specific for Rad51 mRNA in order to analyse its effect on Rad51-foci formation, rejoining of radiation induced DNA-Dsb and apoptosis in NSCLC cell lines.
