PubMed · 2774009
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M R Creasy. 1989. Complex chromosomal rearrangements.. https://doi.org/10.1002/ajmg.1320320434
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The induction of collateral radioresistance after the development of cisplatin resistance is a well-documented phenomenon; however, the exact processes that are responsible for the cisplatin-induced radioresistance remain to be elucidated. There was no obvious difference in the level of radiation-induced DNA double strand breaks (DSBs), in DSB rejoining rates, or the level of the catalytic subunit of the DNA-dependent protein kinase (DNA-PKcs) in the cisplatin- and radiation-sensitive 2780/WT and cisplatin-resistant 2780/CP cell lines. However, there was a significantly (P < 0.01) lower level of DSB misrejoining activity within nuclear protein extracts derived from the cisplatin- and radiation-sensitive 2780/WT and OAW42/WT tumour cell lines than in similar extracts from their cisplatin- (and radiation-) resistant 2780/CP and OAW42/CP counterparts. All of the DSB misrejoining events involved deletions of between 134 and 444 bp that arose through illegitimate recombination at short repetitive sequences, such as those that arise through non-homologous repair (NHR). These data further support the notion that the radiosensitivity of DSB repair proficient human tumour cell lines may be partly determined by the predisposition of these cell lines to activate non-conservative DSB rejoining pathways. Furthermore, our data suggest that the induction of acquired cisplatin resistance is associated with a two- to threefold decrease in the activity of a non-conservative DSB rejoining mechanism that appears to be a manifestation of NHR.
The inverted chromosome 16 is commonly associated with acute myelomonocytic leukaemia (AML) M4 with bone marrow eosinophilia. Cytogenetic identification of the inverted chromosome 16 can be difficult. To help identify the inversion in bone marrow samples from patients referred for the diagnosis of AML-M4, we applied the molecular cytogenetic technique of chromosome painting using chromosome 16 p-arm paint. The results were concordant with standard chromosome analyses and clearly allowed for the identification of a pericentric inversion within chromosome 16 even in poor-quality metaphase spreads.