Array comparative genomic hybridisation analysis of gamma-irradiated human thyrocytes.
The susceptibility of thyroid epithelium to radiation-induced carcinogenesis is well recognised. In this context, thyroid carcinogenesis is associated with specific somatic ret/papillary thyroid carcinoma ( PTC) rearrangements and morphologically with the papillary phenotype. Previous studies have demonstrated the possibility of inducing ret rearrangements in vitro using X-rays. The purpose of our study was to assess whether gamma (gamma) radiation using a Caesium 137 source can induce specific ret rearrangements in a human thyroid epithelial cell culture model. We further hypothesised that if radiation-induced thyroid carcinogenesis is associated with non-random rearrangement events, then DNA copy gain and loss induced by irradiation may also occur in a non-random manner. We irradiated SV40-immortalised human thyroid epithelial cells with incremental doses of gamma-radiation and, using TaqMan reverse-transcription polymerase chain reaction, looked for the presence of the common ret rearrangements. Cohorts showing evidence of ret/ PTC chimeric transcripts were further analysed using microarray comparative genomic hybridisation (CGH) to detect copy gain and loss associated with radiation. Four Grays of gamma-radiation was sufficient to induce ret/PTC-3. In this model, transcripts of ret/PTC-1 were not detected, and we suggest that the type of radiation may influence the resulting rearrangement that occurs. Using array CGH, we have demonstrated a predominant pattern of subtelomeric deletions occurring in association with this radiation cohort and raise the possibility that chromosome 10 may be a hotspot for radiation-induced damage for as yet unknown reasons.[1]References
- Array comparative genomic hybridisation analysis of gamma-irradiated human thyrocytes. Finn, S.P., Smyth, P., O'regan, E., Cahill, S., Flavin, R., O'leary, J., Sheils, O. Virchows Arch. (2004) [Pubmed]
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