We have analyzed the distribution of bleomycin-induced breaks in a subline of the ATL9 lymphoblastoid line, derived from peripheral lymphocytes of an ataxia telangiectasia patient, transformed in vitro by Epstein-Barr virus (EBV). As reported elsewhere (Caporossi et al., 1988), the major feature of this subline, ATL9/g, is a stable achromatic gap at 1p32 in one of the chromosomes 1, overlapping a preferential site of EBV localization. The results of this paper show that this gap is highly sensitive to bleomycin-induced damage. In addition, the breaks induced by bleomycin in ATL9 cells are distributed nonrandomly and are preferentially localized in bands where fragile sites have been mapped.
Caporossi, D., Tedeschi, B., Vernole, P., Porfirio, B., Nicoletti, B. (1989). Chromosome breakage induced by bleomycin in an ataxia telangiectasia lymphoblastoid line: correlation with fragile sites and Epstein-Barr virus DNA localization. CYTOGENETICS AND CELL GENETICS, 52(3-4), 180-185.
Chromosome breakage induced by bleomycin in an ataxia telangiectasia lymphoblastoid line: correlation with fragile sites and Epstein-Barr virus DNA localization
VERNOLE, PATRIZIA;
1989-01-01
Abstract
We have analyzed the distribution of bleomycin-induced breaks in a subline of the ATL9 lymphoblastoid line, derived from peripheral lymphocytes of an ataxia telangiectasia patient, transformed in vitro by Epstein-Barr virus (EBV). As reported elsewhere (Caporossi et al., 1988), the major feature of this subline, ATL9/g, is a stable achromatic gap at 1p32 in one of the chromosomes 1, overlapping a preferential site of EBV localization. The results of this paper show that this gap is highly sensitive to bleomycin-induced damage. In addition, the breaks induced by bleomycin in ATL9 cells are distributed nonrandomly and are preferentially localized in bands where fragile sites have been mapped.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
