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Biomedical subjects

L Tomatis

Publications and source records attributed to L Tomatis.

At least 19 recordsLinked to original sources
PubMed1997

Subcutaneous soft tissue tumours at the site of implanted microchips in mice.

An experiment using 4279 CBA/J mice of two generations was carried out to investigate the influence of parental preconceptual exposure to X-ray radiation or to chemical carcinogens. Microchips were implanted subcutaneously in the dorsolateral back for unique identification of each animal. The animals were kept for lifespan under standard laboratory conditions. In 36 mice a circumscribed neoplasm occurred in the area of the implanted microchip. Females were significantly more frequently affected than male mice. An influence of age or different treatment on the s.c. tumour incidence in two mice generations could not be observed. Macroscopically, firm, pale white nodules up to 25 mm in diameter with the microchip in its center were found. Microscopically, soft tissue tumours such as fibrosarcoma and malignant fibrous histiocytoma were detected.

Animal Identification Systems↗
PubMed1997

Avoided and avoidable risks of cancer.

Despite the considerable efforts and funds devoted to cancer research over several decades, cancer still remains a mainly lethal disease. Cancer incidence and mortality have not declined at the same rate as other major causes of death, indicating that primary prevention remains a most valuable approach to decrease mortality. There is general agreement that environmental exposures are variously involved in the causation of the majority of cancer cases and that at least half of all cancers could be avoided by applying existing etiologic knowledge. There is disagreement, however, regarding the proportion of cancer risks attributable to specific etiological factors, including diet, occupation and pollution. Estimates of attributable risks are largely based today on unverified assumptions and the calculation of attributable risks involves taking very unequal evidence of various types of factors and treating them equally. Effective primary prevention resulting in a reduction of cancer risk can be obtained by: (i) a reduction in the number of carcinogens to which humans are exposed; or (ii) a reduction of the exposure levels to carcinogens. Exposure levels that could be seen as sufficiently low when based on single agents, may actually not be safe in the context of the many other concomitant carcinogenic and mutagenic exposures. The list of human carcinogens and of their target organs might be quite different if: (i) epidemiological data were available for a larger proportion of human exposures for which there is experimental evidence of carcinogenicity; (ii) more attention was paid to epidemiological evidence that is suggestive of an exposure-cancer association, but is less than sufficient, particularly in identifying target organs; and (iii) experimental evidence of carcinogenicity, supported by mechanistic considerations, were more fully accepted as predictions of human risk.

Carcinogenicity Tests↗
PubMed1997

Poverty and cancer.

Despite the attraction of certain utopias and the convincing strength of some of the social and philosophical theories underlying attempts to change the social structure and to achieve a more egalitarian society, social inequalities have not disappeared and seem even to be increasing worldwide. Inequalities in health are part of the social inequalities present in our society and one of their most convincing indices. Sanitary conditions are worse, mortality higher, survival rates of cancer patients lower, and life expectancy shorter in developing countries than in industrialized countries. Similar if not identical differences can be seen within industrialized countries between socioeconomically less and more favoured population groups. In many areas of the industrialized countries social and environmental conditions comparable with those existing in the poorest countries last century have been recreated. Occupational risks are becoming a serious problem in developing countries, largely as a consequence of the transfer of hazardous industries from industrialized countries where certain industries are judged to be unacceptable. A similar double standard is applied to tobacco advertising and sales in the industrialized and developing countries. The projections of the total number of cancer cases in the next decades indicate a generalized increase, proportionally greater in developing than in industrialized countries.

Developed Countries↗
PubMed1996

Epithelial, possibly precancerous, lesions of the lung in relation to smoking, passive smoking, and socio-demographic variables.

We have undertaken an autopsy-based study to evaluate the etiologic importance of active and passive smoking, as well as socio-demographic variables, in the development of pathologic precursors of lung cancer. Lung specimens were taken at autopsy from 531 persons who had died within four hours from a cause other than respiratory or cancer in Athens (Greece) or the surrounding area. Specimens were examined blindly for basal cell hyperplasia, squamous cell metaplasia, cell atypia and mucous cell metaplasia, i.e., pathological entities considered as epithelial, possibly precancerous, lesions (EPPL). Interviews were conducted with next of kin of the deceased. Suitable autopsy specimens as well as completed interviews were eventually available for 275 subjects. EPPL score was regressed on the available independent variables. EPPL score was higher among active smokers than among nonsmokers, while ex-smokers occupied an intermediate position. Conditional on smoking habits, EPPL score was higher among women than among men and higher among manual than among non-manual workers, in agreement with the corresponding patterns with respect to lung cancer. Nonsmoking women married to ever smokers had significantly higher EPPL score than those married to never smokers. The overall findings of this study suggest that EPPL is a valuable indicator of lung cancer risk and that exposure to environmental tobacco smoke is associated with higher EPPL levels and therefore with higher lung cancer risk.

Adult↗
PubMed1995

Increased risk of cancer in the descendants of Syrian hamsters exposed prenatally to diethylnitrosamine (DEN).

Transmission of site-specific tumorigenicity (papillomas in larynx and trachea) of diethylnitrosamine (DEN) to the 2 subsequent generations (F1 and F2) was studied using an outbred strain (Han:AURA) of pregnant Syrian golden hamsters (P generation), which were treated i.p. with 10 mg/kg b.w. of DEN on day 12, 13 or 14 of gestation. Laryngotracheal papillomas were induced by DEN in the P and F1 generations only, while these tumours did not occur in the F2 generation. Spontaneously occurring tumours, including uterine adenocarcinomas, lymphomas, and laryngotracheal neuro-endocrine cell tumours, were observed at higher incidences among the F2 animals derived from the P generation hamsters treated with DEN only on day 13 or 14 of gestation. In the same animals, the ratio of malignant to benign tumours was considerably higher than in controls. In addition, the F2 hamsters derived from the DEN-treated P generation showed more frequent multiple organ involvement in tumorigenesis than the F2 controls. Several uncommon malignant tumours were detected in the F2 offspring, possibly the result of damage caused to germ cells by the prenatal exposure of F1 Syrian hamsters to DEN.

Animals↗
PubMed1995

Socioeconomic factors and human cancer.

In spite of the many attempts made at various periods of human history to arrive at an equalitarian society by reducing differences between the rich and the poor and by redistributing wealth, social inequalities have not disappeared and even seem to be increasing worldwide. Inequalities in health represent some of the social inequalities present in our society and are one of their most convincing indices. In industrialized countries, it has been consistently shown that total incidence of and mortality from cancer are higher in less favored socioeconomic groups, mainly due to increased rates at certain sites. The differences observed between socioeconomic groups within industrialized countries are similar, although not identical, to those prevailing between industrialized and developing countries. Occupational risks are becoming a very serious problem in developing countries, largely as a consequence of the transfer of hazardous industries from highly industrialized countries where certain industries are judged to be unacceptable. A similar double standard is applied toward tobacco advertising and sales in the industrialized and developing countries.

Developing Countries↗
PubMed1995

How much of the human disease burden is attributable to environmental chemicals?

According to the evaluations made by IARC, 66 agents or exposures have been recognised as human carcinogens. About 60% of all cancer cases occur in people over 65 years of age, which is indeed the most important risk factor for cancer, including both the duration of exposure to the variety of carcinogenic agents and allowing expression of genetically determined disorders. Diet as a source of mutagens as well as other environmental mutagens may affect blood pressure either directly or by favouring the development of arteriosclerosis: mutagens have been shown to accelerate arteriosclerotic plaque development. Some concern has also been expressed on the possible adverse effect that environmental chemicals may have on reproductive ability, on the basis of the decline in semen quality reported over the past decades. Better defining the role of aetiological agents would result in a more precise definition of attributable risks. Of particular interest to the latter goal are the studies of inter-individual variability in the susceptibility to carcinogens, which will hopefully contribute to define the role of low-level exposure to carcinogens.

Body Burden↗
PubMed1995

Ethical aspects of prevention.

Within the very large area of ethical concerns, the following issues are considered in this paper: (i) intellectual and career-oriented ambition, combined with the pressure that the competition for funds exerts, may push certain scientists to make dubious compromises with their conscience; (ii) exaggerated priority is sometimes given to the smooth running of a trial, even at the cost of ignoring some ethical requirements; (iii) it is questionable whether preventive intervention can adequately and systematically replace primary prevention based on the cessation of exposure to carcinogens; (iv) it is of the utmost importance to ensure that preventive treatment that is to be administered for long periods has no adverse effects or that the benefits by far outweigh the possible risks; (v) the informed consent of participants to the trials is essential and it should be obtained on the basis of correct, complete and clear information; (vi) a different type of informed consent is that of all citizens with regard to risks to which they may be exposed voluntarily or involuntarily; (vii) there is no justification for, and it is profoundly unethical to omit, delay, or hide information that may be relevant to the protection of health. Four examples were chosen to illustrate the preceding points.

Anticarcinogenic Agents↗
PubMed1994

Toward the development of an equitable cancer prevention.

The most reasonable and socially acceptable development of cancer prevention should be the blending of the population approach, that is the shifting of the distribution of risk factors across an entire population in a favourable direction, with the high risk approach aimed at the identification, surveillance and possibly early interventions on individuals with particularly high values of predisposition to cancer. Interventions aimed at reducing or eliminating genetically determined weaknesses with regard to interactions with the environment, will not make, therefore, in any way obsolete or redundant, interventions aimed at eliminating or reducing exposure to environmental carcinogens.

Animals↗
PubMed1994

Progress in the fight against cancer in EC countries: changes in mortality rates, 1970-90.

The question of how much effective progress against cancer is being made has been raised repeatedly during the last decade; one approach to evaluating such progress is represented by the analysis of mortality, which has been used by several researchers. Here we report mortality trends for 1970-90 for four age-groups, calculated for each 3-year period, and presented as the percentage change of the rate of the first period examined. Detailed graphs for each country and for the European Community as a whole are presented for 'all cancers', and for cancer of the colon-rectum, lung, breast and ovary. For other cancers (stomach, melanoma, uterus, testis and Hodgkin's disease), the graphs are presented only for the whole of the European Community. Variations in mortality are discussed, in terms of changes in incidence, efficacy and diffusion of prevention, as well as improvement in diagnosis and treatment.

Adolescent↗
PubMed1993

Cell proliferation and carcinogenesis: a brief history and current view based on an IARC workshop report. International Agency for Research on Cancer.

The International Agency for Research on Cancer recently convened a Working Group of Experts (June 11-18, 1991) to discuss the use of information on carcinogenesis mechanisms in carcinogenic risk identification. The role of cell proliferation in carcinogenesis was among the items discussed in detail. It was recognized that cell proliferation is an important mechanistic aspect for both genotoxic and nongenotoxic carcinogens. It may act at each stage of the carcinogenesis process, altering the size of the pool of cells at risk for a next event. Cell proliferation was considered to be important, especially as a) an integral part of the process of converting DNA adducts to mutation, b) an enhancing factor for the mutation frequency by inducing errors in replication, and c) an important factor in determining dose-response relationships for some carcinogens. It was also recognized that not all agents that induce cell proliferation are necessarily involved in carcinogenesis; for example, a) not all skin hyperplasia-inducing compounds are skin tumor promoters, b) agents that induce "regenerative" cell proliferation appear to have different effects on tumor induction from agents that have a direct mitogenic effect, and c) the carcinogenic activity of many nonmutagenic agents depends on the continuous administration of the agent. In addition, tissues with a high rate of cell proliferation do not have a higher risk of developing cancer. Thus, no simple relationship exists between cell proliferation and carcinogenesis.

Animals↗
PubMed1992

Active and passive smoking and pathological indicators of lung cancer risk in an autopsy study.

OBJECTIVE: The association between involuntary smoking and lung cancer has been supported by most epidemiologic studies, but a number of authors and interest groups claim that the possibility of bias has not been excluded. Few autopsy-based studies have explored the role of active smoking and other exposures in lung carcinogenesis, and none has been previously done to examine the role of passive smoking. We have undertaken such an autopsy-based study in Athens, Greece. DESIGN: Lung specimens were taken at autopsy from 400 persons 35 years of age or older, of both genders, who had died within 4 hours from a cause other than respiratory or cancer in Athens or the surrounding area. For each person at least seven tissue blocks were taken from the main and lobar bronchi and at least five blocks from the parenchyma, including an average of about 20 smaller cartilaginous bronchi and membranous bronchioles. The specimens were examined without knowledge of the exposures of the particular subject in Turin, Italy. For 283 (71%) of the subjects the preservation of the bronchial epithelium was satisfactory for pathological examination, and for 206 among them (73%) an interview could be arranged with their next of kin, focusing on smoking habits of the deceased and their spouses, as well as other variables. The interviewers were not aware of the results of the pathological examinations. MAIN OUTCOME MEASURE: Specimens were examined for basal cell hyperplasia, squamous cell metaplasia, cell atypia, and (in membranous bronchioles and bronchiolo-alveolar airways) mucous cell metaplasia, ie, pathological entities that may be lung cancer risk indicators or epithelial, possibly precancerous, lesions (EPPL). The gland and wall thicknesses were also measured and their ratio calculated (Reid Index). RESULTS: In comparison with nonsmokers, EPPL values were significantly higher among current smokers and higher, but not significantly so, among former smokers. Furthermore, EPPL values were significantly higher among deceased nonsmoking women married to smokers rather than to nonsmokers. In this set of data neither occupation nor residence was associated with EPPL, but this could be due to the poor correlation of residential history with exposure to air pollution and the lack of adequate standardization of contemporary Greek occupations. The Reid Index was higher among smokers and former smokers in comparison with nonsmokers, among subjects with mainly urban residence in comparison with those with mainly rural residence, and among nonsmoking women married to smokers in comparison with those married to nonsmokers, but none of these differences was statistically significant. CONCLUSION: These results provide support to the body of evidence linking passive smoking to lung cancer, even though they are based on a study methodologically different from those that have previously examined this association.

Adult↗