The progression of normal breast epithelial cells from a normal state toward one
characterized by uncontrolled growth and metastatic behavior is caused by the
deregulation of key cellular processes and signaling pathways. These alterations
in normal cellular behavior are rooted in the accumulation of genomic and
epigenomic lesions that impact hallmarks of cancer, such as the ability of the cell
to control proliferation, undergo apoptosis, increase motility leading to invasion,
and alter angiogenesis. A suite of technologies has now been developed to assess
genomic and epigenomic aberrations that contribute to cancer progression. The
application of these has shown that genome copy number abnormalities (CNAs)
are among the most frequent genomic aberrations. Remarkably, these studies
have revealed that 10% to 15% of the genes in a typical carcinoma tumor may be
deregulated by recurrent genome CNAs and regions. Some of these genes
influence disease progress and so may be assessed to facilitate prognosis. Others
influence response to therapy and so may be assessed as predictive markers.
Some of these enable oncogenic processes, on which tumors depend for survival,
and so are candidate therapeutic targets. In most cases, array comparative
genomic hybridization (CGH) is the method of choice for their discovery and
may be used in some setting for clinical assessments of these abnormalities.
Accordingly, we review here several of the current array CGH technologies
available and the considerations needed when determining the technology most
applicable to a given study.