Chromosome 6p amplification and cancer progression
Gilda C Santos 1, Maria Zielenska 2, Mona Prasad 1 and Jeremy A Squire 1*
1 Ontario Cancer Institute, Canada
2 University of Toronto, Canada
* To whom correspondence should be addressed. E-mail: jeremy.squire{at}utoronto.ca.
Accepted 18 May 2006
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Abstract |
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Chromosomal imbalances represent an important mechanism in cancer progression. A clear association between DNA copy-number aberrations and prognosis has been found in a variety of tumours. Comparative genomic hybridization studies have detected copy number increases affecting chromosome 6p in several types of cancer. Systematic analysis of large tumour cohorts is required to identify genomic imbalances of 6p that correlate with a distinct clinical feature of disease progression. Recent findings suggest that a central part of the short arm of chromosome 6p harbours one or more oncogenes directly involved in tumour progression. Gains at 6p have been associated with advanced or metastatic disease, poor prognosis, venous invasion in bladder, colorectal, ovarian and hepatocellular carcinomas. Copy number gains of 6p DNA have been described in a series of patients who presented initially with follicle centre lymphoma and subsequently transformed to diffuse large B-cell lymphoma. Melanoma cytogenetics has consistently identified aberrations of chromosome 6 and a correlation to lower overall survival has been described. Most of the alterations observed in tumours to date map to the 6p21-p23 region which encompasses about half of the genes on all of chromosome 6 and one third of the number of CpG island in this chromosome. Analyses of the genes that cluster to the commonly amplified regions of chromosome 6p have helped identify a small number of molecular pathways that become deregulated during tumour progression in diverse tumour types. Such pathways offer promise for new therapies in the future.
Key Words:
cancer progression, chromosomal imbalances, chromosome 6, comparative genomic hybridization
