The dynamics of cancer chromosomes and genomesYe C.J.a · Liu G.a · Bremer S.W.a · Heng H.H.Q.a, b, c
aCenter for Molecular Medicine and Genetics, bDepartment of Pathology, cKarmanos Cancer Institute, Wayne State University School of Medicine, Detroit, MI (USA)
A key feature of cancer chromosomes and genomes is their high level of dynamics and the ability to constantly evolve. This unique characteristic forms the basis of genetic heterogeneity necessary for cancer formation, which presents major obstacles to current cancer diagnosis and treatment. It has been difficult to integrate such dynamics into traditional models of cancer progression. In this conceptual piece, we briefly discuss some of the recent exciting progress in the field of cancer genomics and genome research. In particular, a re-evaluation of the previously disregarded non-clonal chromosome aberrations (NCCAs) is reviewed, coupled with the progress of the detection of sub-chromosomal aberrations with array technologies. Clearly, the high level of genetic heterogeneity is directly caused by genome instability that is mediated by stochastic genomic changes, and genome variations defined by chromosome aberrations are the driving force of cancer progression. In addition to listing various types of non-recurrent chromosomal aberrations, we discuss the likely mechanism underlying cancer chromosome dynamics. Finally, we call for further examination of the features of dynamic genome diseases including cancer in the context of systems biology and the need to integrate this new knowledge into basic research and clinical applications. This genome centric concept will have a profound impact on the future of biological and medical research.
© 2007 S. Karger AG, Basel
Request reprints from Dr. Henry Heng
Center for Molecular Medicine and Genetics
Wayne State University School of Medicine
3226 Scott Hall, 540 E Canfield, Detroit, MI 48201 (USA)
telephone: +1 313 577 9544; fax: +1 313 577 5218
This work was supported by the fund from the Center for Molecular Medicine and Genetics; Wayne State University School of Medicine; Karmanos Cancer Institute and the Office of the Vice President for Research. Additional support came from the Susan Komen Breast Cancer Foundation and the R&D fund from SeeDNA Biotech Inc.
Manuscript received: 11 October 2006
Accepted in revised form for publication by L. Cannizzaro,: 8 December 2006.
Number of Print Pages : 10
Number of Figures : 1, Number of Tables : 0, Number of References : 68
Cytogenetic and Genome Research
Vol. 118, No. 2-4, Year 2007 (Cover Date: November 2007)
Journal Editor: Schmid, M. (Würzburg)
ISSN: 1424–8581 (print), 1424–859X (Online)
For additional information: http://www.karger.com/CGR