[Breast cancer screening : present situation and prospects]. / Dépistage du cancer du sein : actualité et perspectives.

Breast cancer screening is a public health challenge. Belgium has the worldwide highest age-standardized breast cancer incidence. It ranks third in terms of specific mortality. The causes are unclear and presumably multifactorial. Like most European countries, Belgium has set up a screening program since 2001. Despite coverage rates varying from one Region to another, the annual 2 % specific mortality decline (observed in the vast majority of European countries) is the same. The age-based screening programs recommended by the European Union are often debated for their questionable impact on mortality and on incidence of advanced tumors (stages II and beyond), and for the harms they may generates (over-diagnosis, false positives). A risk-stratified screening strategy considering other well-documented risk factors (family history, breast density, and genetic variants) could lead to better results while reducing the disadvantages. This hypothesis will be tested through the European My Personal Breast Screening (My PeBS) study, a multicenter randomized clinical trial involving 85,000 volunteers.

Le dépistage du cancer du sein est un enjeu de santé publique. La Belgique possède le record mondial d'incidence du cancer du sein standardisée pour l'âge. Elle se classe en troisième position pour la mortalité spécifique. Les causes ne sont pas claires et vraisemblable- ment multifactorielles. Comme la plupart des pays européens, la Belgique a mis en place un programme de dépistage dès 2001. Malgré des taux de couvertures très différents selon les régions du pays, la baisse de mortalité spécifique de 2 % par an (observée dans la grande majorité des pays européens), est la même. La stratégie de dépistage basée sur l'âge comme seul facteur de risque est recommandée par l'Union européenne. Elle est souvent débattue pour son impact relatif sur la mortalité et quasi nul sur l'incidence des tumeurs avancées (stades II et au-delà) et pour les inconvénients qu'elle génère (surdiagnostics, faux positifs). Une stratégie de dépistage prenant en compte d'autres facteurs de risque aujourd'hui bien documentés (antécédents familiaux, densité mammaire, variants génétiques) pourrait conduire à de meilleurs résultats tout en diminuant les inconvénients. C'est ce que l'étude européenne My Personal Breast Screening (My PeBS) se propose de tester dans le cadre d'un essai clinique multicentrique randomisé portant sur 85.000 femmes volontaires.

Tumor markers in serum, polyamines and modified nucleosides in urine, and cytogenetic aberrations in lymphocytes of workers exposed to polycyclic aromatic hydrocarbons.

Some polycyclic aromatic hydrocarbons (PAHs) such as benzo(a)pyrene and benzo(a)anthracene are well-established genotoxic agents. Long-term exposure to PAHs may lead to proliferative cell disorders in humans, predominantly in the skin, lung, and bladder. The concentration of several tumor markers in serum, of polyamines and modified nucleosides in urine, and of cytogenetic endpoints in peripheral lymphocytes (sister-chromatid exchanges, high frequency cells [HFC], and micronuclei) were measured in 149 male workers exposed to PAHs in two coke oven and one graphite electrode plants, and in 137 controls. We have assessed whether these biomarkers were related to several parameters reflecting exposure to PAHs, i.e., the sum of the airborne concentration of 13 PAHs, 1-hydroxypyrene (1-OHP) concentration in postshift urine, benzo(a)pyrene-diolepoxide adducts to hemoglobin (BPDE-Hb adducts), and duration of exposure, taking also into account several possible confounding factors. HFC was the biomarker most consistently associated with the intensity of current exposure to PAHs. Smoking exerts an independent effect on the same parameter. On the basis of the logistic regression between the prevalence of abnormal HFC values and PAHs in air and 1-OHP in postshift urine found in nonsmokers, it is suggested that the latter should be kept below 6.4 micrograms/m3 and 2.7 micrograms/g creatinine, respectively. No relationship was found between the cytogenetic effects and BPDE-Hb adducts although both parameters are statistically correlated with the airborne PAH level. Some tumor markers in serum (carcinoembryonic antigen, tissue polypeptide antigen, sialic acid) and the urinary concentration of some polyamines were correlated with either PAHs in air or 1-OHP in urine. The associations, however, were very weak which suggests that these biomarkers have limited practical value for the health surveillance of groups of workers exposed to genotoxic PAHs.

Determinants of urinary thioethers, D-glucaric acid and mutagenicity after exposure to polycyclic aromatic hydrocarbons assessed by air monitoring and measurement of 1-hydroxypyrene in urine: a cross-sectional study in workers of coke and graphite-electrode-producing plants.

A cross-sectional epidemiological study was performed on 286 workers from two coke oven and one graphite electrode plants. The aim was to evaluate the usefulness of monitoring 1-hydroxypyrene (1-HOP) in urine for assessing exposure to polycyclic aromatic hydrocarbons (PAHs), and that of the urinary excretion of thioethers and D-glucaric acid, and the mutagenic activity of urine as indicators or biological effects of PAHs. The results confirm that 1-HOP determination in urine probably reflects exposure to PAHs by all routes and is not significantly influenced by the smoking habit. In comparison with the total PAHs in the air and 1-hydroxypyrene in urine, taken as reference exposure parameters, the results indicate that urinary D-glucaric acid excretion is not positively influenced by PAHs exposure; thioethers determination in urine is of poor value, since the smoking habit is a strong confounding factor. The determination of urinary mutagenicity might contribute to the detection of groups of workers exposed to potentially genotoxic PAHs.