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Non‐random duplication of chromosome 15 in murine T‐cell leukemias: Further studies on translocation heterozygotes
Author(s) -
Wiener F.,
Spira J.,
Babonits M.,
HaranGhera N.,
Klein G.
Publication year - 1980
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.2910260519
Subject(s) - chromosomal translocation , gene duplication , biology , chromosome , chromosome 21 , genetics , chromosome 17 (human) , chromosome 15 , microbiology and biotechnology , chromosome 22 , karyotype , chromosome 4 , gene
Abstract Four combinations of translocation heterozygotes with cytogenetically distinct chromosomes 15 were used to investigate whether the T‐cell leukemia‐associated duplication of chromosome 15 is a non‐random or a random event. In leukemias of AKR X CBAT6T6 F 1 (Group I) and C57BL X CBAT6T6 F 1 (Group IV) crosses the duplication was non‐random, affecting the AKR‐derived chromosome 15 (Group I) and CBAT6T6‐derived T (14;15) 6 chromosome (Group IV), respectively. In contrast, in leukemias induced in CBA X CBA T6T6 F 1 combinations (Group III) ‐ where both chromosomes 15 (normal and translocated) were CBA‐derived ‐ the duplication was random. Similarly, in the Rb6;15 X CBAT6T6 F 1 cross (group II) the duplication of chromosome 15 appeared to be random. The results supported the hypothesis that the genetic content of chromosome 15 rather than its translocated state is decisive for the preferential duplication of this chromosome in T‐cell leukemogenesis. However, the genetic background of the strain from which chromosome 15 is derived may also influence the duplication pattern of individual tumors.