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Further studies on the asymmetry of chromosome 15 duplication in trisomic leukemias of heterozygous origin: Preferential status of the AKR chromosome
Author(s) -
Wirschubsky Zvi,
Wiener Francis,
Bregula Ursula,
Klein George
Publication year - 1984
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.2910340217
Subject(s) - gene duplication , biology , genetics , chromosome , chromosomal translocation , karyotype , leukemia , microbiology and biotechnology , gene
Abstract Four combinations of translocation heterozygotes with cytogenetically distinct chromosomes 15 were used to investigate whether the T‐cell leukemia‐associated preferential duplication of the AKR‐derived chromosome 15 (AKR‐15) is determined by factors within this chromosome, or is due to genes within the AKR genotype, but outside chromosome 15. Two of the four combinations were also used to determine whether the AKR‐15 duplication preference could be cancelled by MCF‐viremia in permissive F 1 hybrids. Chemically and virally induced 15‐trisomic leukemias showed the same AKR‐15 duplication preference, which was due to some autonomous property of AKR‐15 itself. It was maintained in (C57BL 6;15 × C57BL) F 1 leukemias, where 6;15 is the only AKR‐derived chromosome propagated on the C57BL/background. In the (C57BL 6;15 × AKR) F 1 hybrid cross where both chromosomes 15 are of AKR origin, duplication occurred at random. To approach the second question, MCF viremia was induced by neonatal virus inoculation into permissive (AKR 6;15 × B6Fv‐1 n ) F 1 hosts. The preferential duplication status of the AKR‐derived 6;15 remained unchanged.