Comprehensive copy number profiles of breast cancer cell model genomes

Abstract

Introduction Breast cancer is the most commonly diagnosed cancer in women worldwide and consequently has been extensively investigated in terms of histopathology, immunochemistry and familial history. Advances in genomewide approaches have contributed to molecular classification with respect to genomic changes and their subsequent effects on gene expression. Cell lines have provided a renewable resource that is readily used as model systems for breast cancer cell biology. A thorough characterization of their genomes to identify regions of segmental DNA loss (potential tumorsuppressor-containing loci) and gain (potential oncogenic loci) would greatly facilitate the interpretation of biological data derived from such cells. In this study we characterized the genomes of seven of the most commonly used breast cancer model cell lines at unprecedented resolution using a newly developed whole-genome tiling path genomic DNA array.

Amplification of MPZL1/PZR promotes tumor cell migration through Src-mediated phosphorylation of cortactin in hepatocellular carcinoma

“…Moreover, amplification of 1q has frequently been detected in many other solid tumors, including breast, ovarian, prostate, and lung tumors [37][38][39][40]. In our previous study, a focal amplified region has been narrowed down to 1q24.1-24.2, suggesting the existence of a cancer gene at this amplicon.…”

The transcriptional induction of PIK3CA in tumor cells is dependent on the oncoprotein Y-box binding protein-1

“…The BLBC specimens and MDA-MB-231 were assayed using an SMRT aCGH platform as previously described (Shadeo and Lam, 2006;Stratford et al, 2007). To be classified as gain, there has to be a probability >80% (determined by Hidden Markov Model algorithm) and >0.15 log 2 ratio (determined by aCGH-Smooth software).…”

Profiling YB-1 target genes uncovers a new mechanism for MET receptor regulation in normal and malignant human mammary cells

“…One could argue that high levels of MET may be due to gene amplification. To begin to address this, we performed comparative genomic hybridization on MDA-MB-231 and reported that amplifications were not found in the 7q31.1 where the MET gene resides (Shadeo and Lam, 2006). Similarly, MET is not commonly amplified in primary BLBC based on the analysis of 10 tumors (Supplementary Figure 2).…”