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This article is part of the supplement: Beyond the Genome: The true gene count, human evolution and disease genomics

Invited speaker presentation

Personalized oncogenomics

Steven JM Jones1*, Janessa Laskin2, Yvonne Y Li1, Obi L Griffith1, Jianghong An1, Mikhail Bilenky1, Yaron S Butterfield1, Eric Chuah1, Richard Corbett1, Anthony Fejes1, Simon Chan1, Nancy Liao1, Katayoon Kasaian1, Malachi Griffith1, John Yee3, Montgomery Martin4, Michael Mayo1, Nataliya Melnyk5, Ryan D Morin1, Trevor J Pugh1, Tesa Severson1, Sohrab P Shah5, Margaret Sutcliffe6, Angela Tam1, Jefferson Terry7, Nina Thiessen1, Thomas Thomson7, Richard Varhol1, Thomas Zeng1, Yongjun Zhao1, Richard A Moore1, David G Huntsman7, Inanc Birol1, Martin Hirst1, Robert A Holt1 and Marco A Marra1

  • * Corresponding author: Steven JM Jones

Author Affiliations

1 Genome Sciences Centre, BC Cancer Agency, Vancouver, BC, V5Z 4S6, Canada

2 Medical Oncology, BC Cancer Agency, Vancouver, BC, V5Z 4E6, Canada

3 Division of Thoracic Surgery, University of British Columbia, Vancouver, BC, V5Z 4E3, Canada

4 Diagnostic Imaging, BC Cancer Agency, Vancouver, BC, V5Z 4E6, Canada

5 Molecular Oncology, BC Cancer Agency, Vancouver, BC, V5Z 1L3, Canada

6 Experimental Therapeutics, BC Cancer Agency, Vancouver, BC, V5Z 1L3, Canada

7 Pathology and Laboratory Medicine, BC Cancer Agency, Vancouver, BC, V5Z 4E6, Canada

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Genome Biology 2010, 11(Suppl 1):I5  doi:10.1186/gb-2010-11-s1-i5

The electronic version of this article is the complete one and can be found online at: http://genomebiology.com/2010/11/S1/I5


Published:11 October 2010

© 2010 Jones et al; licensee BioMed Central Ltd.

Invited speaker presentation

The comprehensive genetic characterisation of human tumours promises to contribute a profound understanding of the changes that contribute to and drive the oncogenic process. In one study, we have been able to determine the oncogenic mechanisms driving a rare adenocarcinoma of the tongue and provide clinically useful information to aid in its treatment, through the determination that the cancer was driven primarily by activation of the RET pathway. The administration of RET targeting kinase inhibitors, sunitinib and sorafenib, provided tumour stabilisation for several months, after which time therapeutic resistant tumours arose. This provided us with the opportunity to identify the genetic changes associated with drug resistance allowing the observation that resistance is correlated with an apparent up-regulation of the parallel proliferative AKT pathway.

However, the complete and comprehensive analysis of a genome using this technology is still nascent and many of the software tools required to achieve this are still in development. In the analysis of tumour normal pairs, it is not clear that current levels of sampling are sufficient to identify somatic changes accurately without further validation. Likewise, the level of false negatives that confound our analyses is unclear. Such considerations will be important if this technology is to be adopted in the routine provision of personalized medicine.