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Alternative mechanisms of gene amplification in human cancers
Author(s) -
Kuwahara Yoshitaka,
Tanabe Chikako,
Ikeuchi Tatsuro,
Aoyagi Kazuhiko,
Nishigaki Michiko,
Sakamoto Hiromi,
Hoshinaga Kiyotaka,
Yoshida Teruhiko,
Sasaki Hiroki,
Terada Masaaki
Publication year - 2004
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.20075
Subject(s) - amplicon , biology , gene duplication , genetics , locus (genetics) , chromosomal fragile site , gene , tandem repeat , microbiology and biotechnology , chromosome , polymerase chain reaction , genome
Gene amplification is a common phenomenon in cancer. Cytogenetic analyses have indicated that breakage‐fusion‐bridge (BFB) cycles drive intrachromosomal amplification of some oncogenes in a head‐to‐head manner in human cancers. However, the complex structures of an amplified sequence found in cancers are not always explained by the BFB model. At the 17q21 locus, which is not linked to common fragile sites, we discovered a recombination hot spot harboring amplicon repeats in tandem in a head‐to‐tail orientation, with the interamplicon junctions in each cancer cell being homogeneous. These findings clearly show the presence of alternative mechanisms other than BFB cycles in oncogene amplification. © 2004 Wiley‐Liss, Inc.