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Jeff Sutherland

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Revolution in Cancer Genetics

The (r)evolution of cancer genetics
Francesca D Ciccarelli
Department of Experimental Oncology, European Institute of Oncology, IFOM-IEO Campus, Via Adamello 16, 20139 Milan, Italy

BMC Biology 2010, 8:74doi:10.1186/1741-7007-8-74
The electronic version of this article is the complete one and can be found online at:

Recent advances in sequencing technologies and the launching of massive resequencing projects such as the Cancer Genome Project [1] have boosted the production of cancer genomics data. In the past few years, the entire repertoire of human exons has been sequenced in glioblastoma [2], pancreatic [3], breast and colorectal [4] cancers, and somatic mutations in selected genes have been mapped in multiple samples of renal [5] and lung [6] adenocarcinomas. In addition, the whole genomes of individuals affected by leukemia [7,8], melanoma [9], glioma [10], breast [11,12], and lung [13] cancers have been fully resequenced. All these studies have led to the identification of more than 1,000 potential cancer genes, and the list is likely to grow in the near future.

This massive amount of information will have a huge impact on our understanding of cancer genetics, even more so considering that the biological role of most mutations is still obscure. These first unbiased screenings have led to the identification of novel and unsuspected determinants of cancer, such as the isocitrate dehydrogenase enzyme genes IDH1 and IDH2, which have been found mutated in glioblastoma multiforme [2]. They have also started to question some cornerstones of cancer biology, such as the description of cancer as a unique disease driven by the somatic modification of a few key regulators. The progressive identification of novel mutated genes is expanding the ‘cast of actors’ [14] whose mutations might be causally involved in driving cancer. Moreover, given the high heterogeneity of genes mutated in different cancer types (Figure 1), the overall ‘plot’ is becoming more intricate. The emerging picture suggests that there may be distinct genetic routes to reach the common aftermath of all tumorigenic processes, which is uncontrolled cell proliferation. For example, as many as 12 core pathways are disrupted in the majority of pancreatic cancers through multiple somatic mutations [3]. This opens up an intriguing scenario where the deregulation of key pathways for tumorigenesis represents only the final step of a more general perturbation of cellular activity. The cell is seen as an integrated system in which all processes form a tightly interconnected network more than as an ensemble of independent pathways. In this context, the effect of somatic mutations occurring in the cancer genome should be interpreted in the light of their broader impact on the system’s equilibrium…

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