Cancer Research - Europa

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