Cancer induction

The incomplete (less differentiated) foci of metaplasia surround foci of cancer, suggesting progressive loss of differentiation (16, 19). High nitrite levels in the gastric cavity have been associated with acceleration of the gastric cancer induction with MNNG in experimental animals (26). Gastric cancer has been induced in experimental animals with products derived from nitro-sated fish (32). 

Lloyd RD, Miller SC, Taylor GN, et al. 1994a. Relative effectiveness of 239Pu and some other internal emitters for bone cancer induction in beagles. Health Phys 67 346-353. 

Taylor GN, Lloyd RD, Mays CW, et al. 1993b. Liver cancer induction by 239Pu, 241 Am, and Thorotrast in the grasshopper mouse, Onychomys leukogaster. Health Phys 64(2) 141-146. 

Cigarette smoking may act as a promotor for lung cancer induction. 

From the above it can be concluded that the risk for lung cancer induction from chronic indoor exposure to Rn-d is unlikely to be higher than 1.10 4/mSv. in order to understand the magnitude of this risk it has to be emphasized that man can be exposed to a multitude of different hazardous materials in the indoor atmosphere besides Rn-d, such as formaldehyde, nitrogen dioxide, carbon monoxide, nitrosamines, polyaromatic hydrocarbons, volatile organic compounds, asbestos and pesticides (Gammage and Kaye, 1985). 

Chameaud,J., and J. Lafuma, Experimental Study of Cancer Induction with Rn 222 Daughters, Rad Prot.Dosimetry 7 385 (1984). 

Martell, E. A., Bronchial cancer induction by alpha radiation A new hypothesis, Paper C6-11 in Proceedings of the 7th International Congress of Radiation Research, (J. J. Broerse et al., eds), Martinus Nijhoff, Amsterdam (1983b). 

Hofmann, W., Lung Cancer Induction by Inhaled Radon Daughters-What is the Relevant Dose , in Radiation Protection Dosimetry, Indoor Exposure to Natural Radiation and Associated Risk Assessment, (Clemente, G., F. et al, eds), pp.367-370, Nuclear Technology... 

Data for PCP and terrestrial wildlife are incomplete and — in view of the large interspecies variations in sensitivity — need to be collected. Research is needed on reproductive effects in animals following inhalation exposure to PCP additional acute and intermediate toxicity testing chronic duration exposure studies on cancer induction, genotoxicity, and immunotoxicity and the development of alternate biomarkers of PCP exposure and antidotes (WHO 1987 USPHS 1994). Until the results of these studies become available, it seems reasonable to apply to wildlife the same levels recommended for human health protection. 

Urocanic acid (2-propanoic acid 3-[lH-imidazol-4-yl] is located superficially in the stratum comeum. Metabolism of epidermal UCA does not occur in situ due to the absence of urocanase, resulting in the accumulation of UCA in the epidermis. Upon UV exposure, naturally occurring trans-UCA converts to the d.s-isomer, in a dose dependent manner, until the photostationary state is reached, when equal quantities of trans- and m-UCA are found in the skin.15 Based on an analysis of the action spectrum for UV-induced immune suppression, and the fact that no immune suppression was observed in mice whose stratum comeum was previously removed by tape stripping, De Fabo and Noonan suggested that urocanic acid was the photoreceptor for UV-induced immune suppression.16 Since the initial experiments many others have documented, the ability of ris-UCA to initiate immune suppression, documented its presence in the serum of UV-irradiated mice, and demonstrated that m-UCA plays a role in UV-induced skin cancer induction. (For a more complete review of the role of m-UCA in immune suppression see two excellent reviews by Norval and colleagues.1718)... 

The use of information on the mode of action in the assessment of potential carcinogens is a main focus of the revised cancer guidelines because of the significant scientific advances that have developed concerning the causes of cancer induction. 

Taylor GN, Mays CW, Lloyd RD, et al. 1986. Liver cancer induction by Am and Thorotrast in deer mice and grasshopper mice. Strahlen Therapie 80(Suppl) 172-177. 

A long-term goal is to evaluate the correspondence between carbocation-derived structure/reactivity relationships and those derived from biological assays. Such comparisons could prove valuable toward predictability of cancer induction in various environmentally relevant classes of PAHs and hetero-PAHs. 

It is not known how chemicals cause cancer. A fascinating aspect of the story is that many "carcinogenic" chemicals are in fact, not the culprits responsible for cancer induction. The metabolic processes of the body change the chemicals from relatively innocuous substances into reactive intermediates which in as yet unknown fashion, trigger the chain of events which finally result in tumor formation. In other words, chemical carcinogenesis is an effect of "failed" detoxification. 

Tokiwa, H., N. Sera, K. Horikawa, Y. Nakanishi, and N. Shigematu, The Presence of Mutagens/Carcinogens in the Excised Lung and Analysis of Lung Cancer Induction, Carcinogenesis, 14, 1933-1938 (1993). 

As discussed in detail in Section 5, with chemical carcinogens, the route of exposure can be an important determinant of the site of cancer induction, particularly with direct-acting carcinogens which may act at the initial point of contact. For the majority of carcinogens, however, which require metabolic activation, the location in the body of activating enzymes is thought to be the major determinant of the site of carcinogenesis. 

Stage D Limited in vivo bioassays 1. altered foci induction in rodent liver 2. skin neoplasm induction in mice 3. pulmonary neoplasm induction in mice 4. breast cancer induction in female Sprague-Dawley rats... 

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