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Aetiology<br />
The uncontrolled cell growth characterising cancer can be initiated by the interaction of human cells<br />
with specifi c agents, on the basis of an individual genetic predisposition. Despite great advances in the<br />
understanding of these interactions, our ability to treat tumours remains very low: this is a clear sign<br />
that much remains to be learnt.<br />
Human carcinogenesis related knowledge has shown a dramatic increase in its width and complexity<br />
over the last few years. In fact, the availability of enhanced and more powerful tools along with a more<br />
functional translational approach including valuable proof-of-principle feedback from the clinical perspective<br />
have created the opportunity to look more closely into the regulatory processes of the cell<br />
growth and, once initiated, cancer behaviour (including tissue invasion and metastatic potential).<br />
Not only it is now clear that diff erent regulatory pathways are to be altered in order to create a predisposition<br />
for cancer initiation: environmental external factors (biological, chemical and physical agents)<br />
seem to have diff erent activities when they act on the cell alone or in combination. The striking evidence<br />
that diff erent patterns of gene-to-environment interactions can develop when a population with<br />
certain genetic characteristics move from an area of the world to another (as like as the incidence of<br />
breast cancer of Japanese people levelling the one of Northern Americans when the former move from<br />
Japan to US) add as well a further degree of complexity to the overall.<br />
A quick and reliable identifi cation of agents capable to induce carcinogenesis, along with a better understanding<br />
of the genetic substrate on which these environmental factors express their action is ideally<br />
coupled with epidemiological and molecular pathology state of the art validated information and preliminary<br />
results from clinical experiences. These processes of gathering multidisciplinary enhanced knowledge<br />
benefi t from a look forward perspective towards cancer prevention and treatment strategies.<br />
EU funded projects aimed to better understand cancer aetiology clearly shift towards a pragmatic application<br />
of the basic knowledge generated so far and do exploit the whole range of foreseen funding instruments:<br />
from the Specifi c Support Action –SSA- ‘AIDIT’ aimed at extending the clinical platform of another EU funded<br />
initiative (IMPACT) to the Framework Programme Associated and Candidate Countries for the targeted<br />
screening of prostate cancer in men with genetic predisposition; to the Specifi c Targeted <strong>Research</strong> Project<br />
(STREP) ‘POLYGENE’ aimed at identifying novel key determinants underlying breast and prostate cancer<br />
and fi nally to the large Integrated Project ‘CARCINOGENOMICS’ aimed at creating a validated high-throughput<br />
genomic based test for assessing genotoxic and carcinogenic properties of chemical compounds<br />
in vitro; the Network of Excellence ‘GENOMEL’ aimed at understanding the genetic causes (susceptibility)<br />
of melanoma and the gene-to-environment interaction, predominantly with the exposition to the sun<br />
light and the ‘Integrated Project INCA’ focused on the role of biological agents capable of inducing chronic<br />
infections in the pathogenesis of infection-associated cancers.<br />
Alfredo Cesario