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Translocation remodeling in the primary BALB/c plasmacytoma TEPC 3610. Genes Chromosomes Cancer 2001 Mar;30(3):283-91

Date

02/15/2001

Pubmed ID

11170286

DOI

10.1002/1098-2264(2000)9999:9999<::aid-gcc1094>3.0.co;2-i

Abstract

Myc-activating chromosomal 12;15 translocations, the hallmark mutations of inflammation-induced BALB/c plasmacytomas, have recently been shown to undergo remodeling by isotype switch-like genetic recombinations that remove approximately 180 kb of immunoglobulin heavy-chain sequence in the vicinity of the rearranged, expressed Myc gene. Here we combine cytogenetic data on the 12;15 translocation (SKY and FISH) with the molecular analysis of key junction sites (long-range PCR followed by DNA sequencing) to demonstrate that translocation remodeling occurred as an infrequent, stepwise, and disomic tumor progression event in the tetraploid, fully transformed, and transplantable plasmacytoma TEPC 3610. This result was used, in conjunction with previously obtained molecular data on five other primary plasmacytomas, to devise a hypothesis that predicts that the selective pressure to undergo translocation remodeling may be predetermined by the location of the break site in Myc. The pressure may be low if the break occurs 5' of the normal promoter region of Myc, but it may be considerably stronger if the break occurs 3' of the Myc promoter. Published 2001 Wiley-Liss, Inc.

Author List

Kovalchuk AL, Esa A, Coleman AE, Park SS, Ried T, Cremer CC, Janz S

Author

Siegfried Janz MD Professor in the Medicine department at Medical College of Wisconsin




MESH terms used to index this publication - Major topics in bold

Animals
Cell Transformation, Neoplastic
Chromosome Mapping
Genes, myc
Immunoglobulin Constant Regions
In Situ Hybridization, Fluorescence
Karyotyping
Mice
Mice, Inbred BALB C
Neoplasm Transplantation
Plasmacytoma
Ploidies
Translocation, Genetic
Tumor Cells, Cultured