Chromosome 16q loss--a genetic key to the understanding of breast carcinogenesis.

摘要: In the last decade concepts of breast cancer dedifferentiation and progression have undergone a significant substantial change. past it was widely believed that detailed associations between genetic morphological changes defined in Vogelstein model colorectal pathogenesis could be transferred to carcinogenesis. A multitude studies seemed verify this priori hypothesis. However, with introduction global screening techniques, predominantly at DNA level, became obvious linear might oversimplified for cancer. It is now accepted losses chromosomal 16q characterize in-situ invasive tumours low tumour grade estrogen receptor (ER) positivity (luminal cancers). contrast, high cancers HER2, basal or non expressor phenotype 16q-losses are rarely seen consequence concept multiple, parallel pathways precursor lesions emerged. As consequence, hunt oncogenes/tumour suppressor genes pathway specific. Whereas been relatively well characterized by several recurrent located on various regions (e.g. egfr, p53, HER2), characterization 16q-specific gene ER-positive still tremendous challenge. This review will focus role aims give insights into actual research efforts, e.g. alternative explanations order unravel central