Premium
Genome‐wide search for loss of heterozygosity in Burkitt lymphoma cell lines
Author(s) -
Sobol Hagay,
Benziane Athmane,
Kerangueven Fabienne,
Yin Luo,
Noguchi Tetsuro,
Pauly Suzanne,
Eisinger François,
Longy Michel,
Romeo Giovanni,
Lenoir Gilbert,
Birnbaum Daniel
Publication year - 2002
Publication title -
genes, chromosomes and cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.754
H-Index - 119
eISSN - 1098-2264
pISSN - 1045-2257
DOI - 10.1002/gcc.10022
Subject(s) - loss of heterozygosity , biology , chromosomal translocation , lymphoma , gene , genome , chromosome , gene dosage , genetics , cancer research , virus , burkitt's lymphoma , epstein–barr virus , allele , cell culture , microbiology and biotechnology , gene expression , immunology
The molecular biological characteristics of Burkitt lymphoma (BL), in addition to the presence of the Epstein‐Barr virus (EBV) in some forms, relies on well‐characterized alterations, such as MYC translocations and TP53 inactivations. To ascertain the number and location of other genome alterations, we used 191 polymorphic markers in a genome‐wide search for loss of heterozygosity (LOH) in 31 Burkitt lymphoma cell lines and their normal counterparts. We were able to distinguish two types of altered allelic patterns: a bona fide LOH profile, indicative of deletion (LOH), and a profile indicative of increased dosage (ID). The former type was most frequent at chromosome arm 17p, most likely indicating TP53 gene inactivation. Increased dosage at 1q was found almost exclusively in non‐EBV cell lines ( P < 0.00004) and correlated well with karyotypic abnormalities affecting region 1q21‐25. Our results suggest that a gene important for BL pathogenesis is located in region 1q21‐25 and that the activation of this gene mimics the effects of EBV. © 2002 Wiley‐Liss, Inc.