A reason why the <it>ERBB2 </it>gene is amplified and not mutated in breast cancer

Abstract

Abstract Alterations of receptor-type tyrosine kinases (RTK) are frequent in human cancers. They can result from translocation, mutation or amplification. The ERBB2 RTK is encoded by a gene that is amplified in about 20% breast cancers. The question is: why is this RTK specifically subjected to this type of alteration? We propose that ERBB2 gene amplification is used to overcome repression of its expression by sequence-specific transcription factors.