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<dc:dc xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:invenio="http://invenio-software.org/elements/1.0" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd"><dc:identifier>doi:10.1016/j.mrgentox.2024.503753</dc:identifier><dc:language>eng</dc:language><dc:creator>Catalán, Julia</dc:creator><dc:creator>Järventaus, Hilkka</dc:creator><dc:creator>Falck, Ghita C.-M.</dc:creator><dc:creator>Moreno, Carlos</dc:creator><dc:creator>Norppa, Hannu</dc:creator><dc:title>Chromosome-specific induction of micronuclei and chromosomal aberrations by mitomycin C: Involvement of human chromosomes 9, 1 and 16</dc:title><dc:identifier>ART-2024-138120</dc:identifier><dc:description>Cytogenetic studies have shown that human chromosomes 1, 9, and 16, with a large heterochromatic region of highly methylated classical satellite DNA, are prone to induction of chromatid breaks and interchanges by mitomycin C (MMC). A couple of studies have indicated that material from chromosome 9, and possibly also from chromosomes 1 and 16, are preferentially micronucleated by MMC. Here, we further examined the chromosome-specific induction of micronuclei (MN; with and without cytochalasin B) and chromosomal aberrations (CAs) by MMC. Cultures of isolated human lymphocytes from two male donors were treated (at 48 h of culture, for 24 h) with MMC (500 ng/ml), and the induced MN were examined by a pancentromeric DNA probe and paint probe for chromosome 9, and by paint probes for chromosomes 1 and 16. MMC increased the total frequency of MN by 6–8-fold but the frequency of chromosome 9 -positive (9+) MN by 29–30-fold and the frequency of chromosome 1 -positive (1+) MN and chromosome 16 -positive (16+) MN by 12–16-fold and 10–17-fold, respectively. After treatment with MMC, 34–47 % of all MN were 9+, 17–20 % 1+, and 3–4 % 16+. The majority (94–96 %) of the 9+ MN contained no centromere and thus harboured acentric fragments. When MMC-induced CAs aberrations were characterized by using the pancentromeric DNA probe and probes for the classical satellite region and long- and short- arm telomeres of chromosome 9, a high proportion of chromosomal breaks (31 %) and interchanges (41 %) concerned chromosome 9. In 83 % of cases, the breakpoint in chromosome 9 was just below the region (9cen-q12) labelled by the classical satellite probe. Our results indicate that MMC specifically induces MN harbouring fragments of chromosome 9, 1, and 16. CAs of chromosome 9 are highly overrepresented in metaphases of MMC-treated lymphocytes. The preferential breakpoint is below the region 9q12.</dc:description><dc:date>2024</dc:date><dc:source>http://zaguan.unizar.es/record/133442</dc:source><dc:doi>10.1016/j.mrgentox.2024.503753</dc:doi><dc:identifier>http://zaguan.unizar.es/record/133442</dc:identifier><dc:identifier>oai:zaguan.unizar.es:133442</dc:identifier><dc:identifier.citation>MUTATION RESEARCH-GENETIC TOXICOLOGY AND ENVIRONMENTAL MUTAGENESIS 896 (2024), 503753 [9 pp.]</dc:identifier.citation><dc:rights>by</dc:rights><dc:rights>https://creativecommons.org/licenses/by/4.0/deed.es</dc:rights><dc:rights>info:eu-repo/semantics/openAccess</dc:rights></dc:dc>

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