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Biomedical subjects

L Tomatis

Publications and source records attributed to L Tomatis.

166 records · Page 10Linked to original sources
PubMedDate not supplied

[Transplacental and transgenerational carcinogenesis].

Effects of exposure to carcinogens at early stages of ontogenesis are considered. An increased cancer risk due to prenatal exposure may be related to: 1) exposure of the fetus during pregnancy to chemicals able to cross the placental barrier or to radiation; 2) exposure to a chemical or radiation of the parents or one parent prior to conception. In transplacental carcinogenesis, the effects observed after birth are a consequence of a direct interaction of the carcinogen with somatic cells of the fetus. DES and radiation were shown to increase cancer risk in humans following exposure during pregnancy, while in experimental animals a large variety of chemicals of quite different structure (including the widely used therapeutic agent cisplatin) were demonstrated to induce tumors in the progeny after administration during pregnancy. The experimental multigeneration effect of carcinogens is manifested in an increased incidence of tumors in several generations of untreated descendants of: a) females exposed to carcinogen during pregnancy; b) males exposed to carcinogen prior to mating with untreated females. The inherited change may be an initiating event revealed by the exposure during post-natal life to a promoting agent. In humans deleterious information inherited through the germ cells (occurring either following a spontaneous error in DNA replication and repair or as a consequence of a chemical or physical agent) can increase the risk of developing cancer in certain individuals by several orders of magnitude (retinoblastoma, familial polyposis of the colon and some others). The multigeneration transmission of carcinogenic risk is also demonstrated by cancer prone families that are probably more frequent than originally thought, with a risk that is one order of magnitude higher than in general population. Familial clusterings of cancer may also indicate germline mutations in one or more genes. Thus the inherited predisposition to cancer that is observed today may, at least in part, be explained by the exposure to environmental noxious agents in previous generation(s). Since humans are exposed throughout life to many environmental agents, either carcinogenic or capable to enhance the progression of cancer, an understanding of the contribution of prenatal exposure to carcinogens could improve the efficacy of prevention.

Adolescent↗
PubMedDate not supplied

[What priorities in prevention?].

The progress in knowledge on the etiology of tumours has not been matched by an adequate and effective practical application in prevention. Primary prevention shows its effects only in the long term; politicians and administrations therefore tend to neglect prevention in favour of other initiatives that reflect more directly on their possibilities of reelection. So one positive aspect of the new National Health Plan is that, for the first time, it officially recognizes the fundamental role of prevention in health preservation. Nevertheless, the problem remains of the financial dependence of most of biomedical research on direct or indirect funding by pharmaceutical corporations, plus the tendency, even by public funding sources or private donations, to prefer research projects where the economic investment is justified a priori. The research projects aimed at primary prevention do not lend themselves to a rapid or relatively easy quantitative evaluation. For these projects, in spite of their importance in the context of a public health plan, there is a risk of ever increasing difficulty in competing for founding.

Carcinogens, Environmental↗