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An atypical t(12;15) translocation of chromosomes found in murine plasmacytomas and activation of the c‐myc oncogene
Author(s) -
Ohno Shinsuke,
Takahashi Rei,
Mihara KohIchiro,
Chen HuiLing,
Migita Shunsuke,
Sugiyama Taketoshi
Publication year - 1988
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.2910410420
Subject(s) - chromosomal translocation , chromosome , biology , microbiology and biotechnology , fluorescence in situ hybridization , karyotype , gene , genetics
Cells from murine plasmacytomas (MPC) consistently exhibit either the 12;15 or the 6;15 translocation. Recently, we found that cells from 2 MPC (ABPC 45 and ABPC 26) did not exhibit any known translocation. However, these MPC contained one chromosome 15 (15q ‐ ) that was shorter than its normal homologue and one 12 (12q + ) that was longer than its normal 12 counterpart. Chromosome 15q ‐ contained only one thin D band, corresponding in size to either D1 or D3 band. A minor light band D2 was apparently deleted. Chromosome 12q + contained a light F1 band that was longer than the normal 12F1. In ABPC 45, the c‐myc gene was assigned by in situ hybridization to the F1 region of 12q + as well as to its original site of 15D2. Moreover, the in situ hybridization experiment assigned the Sα gene to the F1 regions of both chromosomes 12 and 12q + . These findings indicate that a minor light band D2 of chromosome 15 carrying the c‐myc gene was translocated into the major light band F1 of 12, resulting in a longer chromosome 12q + and a correspondingly shorter chromosome 15q ‐ . This type of chromosomal translocation suggests that ABPC 45 developed through a cytogenetic mechanism different from that of MPC with the typical t(12;15) translocation.