This study differs fundamentally from current approaches, which focus on human cancers only. The results of this study could have important implications for research to develop future diagnostic assays and treatments for the disease.

In recent years, increasing evidence for the contribution of copy number abnormalities to cancer development and progression has been reported. Copy number abnormalities are most easily detected using microarray-based comparative genomic hybridization (CGH), in which entire genomes of healthy and cancer samples are compared in a single experiment.

Because these changes can be numerous and complex in certain cancers, especially advanced-stage cancers, it is challenging to determine which copy number abnormalities are cancer-causing and which are non-causative changes.

To test the hypothesis that copy number abnormalities common in both human and dog colorectal cancer are most likely to be the direct cause of colorectal cancer, Dr Shaying Zhao’s team used NimbleGen CGH microarrays to characterize copy number abnormalities in human colorectal cancer and canine colorectal cancer samples.

‘The results have revealed for the first time a strong degree of genetic homology between sporadic canine and human colorectal cancer,’ said Dr Zhao. ‘The study provides the molecular evidence supporting that sporadic canine cancers are excellent models for the corresponding human cancers, and that comparison between dog and human cancers of similar types would be a powerful way to identify driver alterations.’

Colorectal cancer is one of the most common cancers affecting humans globally. Although early screening and risk factor modification is contributing to a downward trend in mortality rate for this disease, considerable research is still needed to identify the genomic cause of this cancer.

Further reading

Tang, J. et al. (2010) Copy number abnormalities in sporadic canine colorectal cancers. Genome Res. 20, 341–350