Mutagenesis, 2015, 30, 167–168
doi:10.1093/mutage/geu085
Commentary
Commentary
Les Entretiens Jacques Cartier Symposium 4—
targeted cancer therapies: stakes and prospects
for patients
David G. Cox* and Alain Puisieux; on behalf of the organizing committee
Université de Lyon, 28 rue Laënnec, 69008 Lyon, France
*To whom correspondence should be addressed. Tel: +33 4 78 78 59 12; Fax: +33 4 78 78 27 20;
Email: [email protected]
Received October 22 2014; Accepted November 17 2014.
The Centre Jacques Cartier is named after the French captain Jacques
Cartier (1491–1557), who explored the Saint Laurence River to
modern-day Montreal in 1535–36. Charles Mérieux and Alain
Bideau initiated the Centre Jacques Cartier in 1984, with the aim of
fostering cultural and scientific exchanges between the Rhône-Alpes
region of France and the province of Quebec in Canada. Due in large
part to the success of this initiative, the annual seminar series organised by the Centre Jacques Cartier draws speakers and participants
from around the globe, notably from North America and Europe.
In 2013, the 26th ‘Entretiens Jacques Cartier’ was held in France,
with seminar series particularly in the city of Lyon. This symposium
covered diverse topics, such as reducing school dropout rates, multimodal transportation and urbanism and various topics related to
health and technology. Researchers at the Cancer Research Centre
of Lyon (CRCL) led the organisation of Symposium 4, focusing on
targeted cancer therapies. The CRCL is composed of over 400 scientists and staff, all dedicated to carrying out basic, translational
and clinical research in oncology. This symposium was held at
the International Agency for Research on Cancer, a World Health
Organization research institute in Lyon. These two major institutions highlight the importance of cancer research in Lyon and the
surrounding area.
It is well known that cancer is a major public health concern,
and the impact of cancer on health systems will only grow in the
coming years. In 2010, there were 11 million new cancer cases, with
7 million cancer deaths worldwide. The World Health Organization
estimates that in 2030, these numbers will be 27 million new cases
per year with 17 million cancer deaths. In France, for the period
of 1980–2005, cancer incidence increased by 93% among men and
84% among women. In the same period, cancer deaths increased
by 13%.
Despite these staggering figures, advances in our understanding
of the biological mechanisms behind cancer initiation and development, particularly with respect to targeted therapies, have led to drastic increases in 5-year survival for cancer patients. In 1920, 5-year
survival rates were only 8% for all types of cancer. In 1950, only 44%
of breast cancer patients could hope to live 5 years beyond their diagnosis. Today, 5-year survival is at roughly 55% for all cancer types,
with 86% five-year survival among breast cancer patients.
The colloquium held in Lyon, November 25–26, 2013, in the
context of the Entretiens Jacques Cartier focused on methods of
development and application of targeted therapies from a basic and
clinical science aspect. These presentations, touching on aspects from
fundamental science to bioinformatics to transferring advances to
patients, involved researchers from both Europe and North America.
A subset of these presentations, summarised here, showcase the
potential for further improving our capacity to cure cancer.
In terms of fundamental research, Roux and colleagues (1)
explored the potential of targeting the mammalian target of rapamycin pathway, which is important in the regulation of cell growth
by promoting the biosynthesis of proteins, lipids and nucleic acids.
Another potential target was presented by Morettin et al. (2), who
review knowledge of the protein arginine methyltransferases, a family of catalytic enzymes that are deregulated in breast cancer, potentially altering their activity with respect to transcription, DNA repair,
RNA metabolism, signal transduction, protein–protein interactions
and subcellular localisation. These are only two examples of the large
increase of knowledge regarding the biology of cancer gleaned over
the last decades.
In order to make sense of this wealth of data, Barillot and colleagues
(3) have developed the Atlas of Cancer Signaling Networks. This tool is
developed to help researchers in the interpretation of data in the context of biological networks through the use of high-throughput data
such as mutation profiles, gene expression or siRNA screening.
Finally, in terms of translating results to clinical practice, two
paradigm shifts were presented. Marabell and colleagues (4) present
their work with respect to tumour-targeted therapies based on targeting immune rather than cancer cells, and Cox et al. (5) present
their approach of exploring the impact of germline genetic variability on risk of breast cancer progression.
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As a whole, this colloquium offered a rich panel of experts from
diverse fields, all working towards improving targeted therapies for
cancer patients.
Conflict of interest statement: Les Entretiens Jacques Cartier
Symposium 4 was made possible by funding from the Jacques Cartier
Foundation and the Cancer Research Center of Lyon.
References
1. Cargnello, M., Tcherkezian, J. and Roux, P. P. (2015) The expanding
role of mTOR in cancer cell growth and proliferation. Mutagenesis,
30, 169–176.
D. G. Cox et al., 2015, Vol. 30, No. 2
2. Morettin, A., Baldwin, R. M. and Côté, J. (2015) Arginine methyltransferases as novel therapeutic targets for breast cancer. Mutagenesis, 30,
177–189.
3. Kuperstein, I., Grieco, L., Cohen, D., Thieffry, D., Zinovyev, A. and
Barillot, E. (2015) The shortest path is not the one you know: application
of biological network resources in precision oncology research. Mutagenesis, 30, 191–204.
4. Shekarian, T., Wittmann, S., Caux, C. and Marabell, A. (2015) Paradigm
shift in oncology: targeting the immune system rather than cancer cells.
Mutagenesis, 30, 205–211.
5. Cox, D. G., Heudel, P.-E., Trédan, O. and Bachelot, T. (2015) Therogenetics: transferring GWAS technology to the clinic. Mutagenesis, 30,
213–215.