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Viral Induced Skin Tumors in Mice
Published in John P. Sundberg, Handbook of Mouse Mutations with Skin and Hair Abnormalities, 2020
John P. Sundberg, Hendrick G. Bedigian, Roderick Bronson
Papillomaviruses have been considered to be potential cocarcinogens in UV light or chemical carcinogen-induced cutaneous papillomas or squamous cell carcinomas in inbred and outbred laboratory mice, since the earliest lesions induced by these methods are morphologically similar to those induced by papillomaviruses. No conclusive evidence for a cocarcinogenic role was obtained in recent studies, however. Investigations of 30 strains and stocks of mice have failed to demonstrate papillomavirus structural antigens or genomic sequences in tumors induced with DMBA and promoted with TPA.40 However, integrated fragments that hybridized with several well-characterized cloned papillomavirus genomes have been identified in UV-induced skin tumors.21,22 A 2000-kb fragment was cloned, sequenced, and found to have some homology to the rodent papillomavirus genomes but was not collinear.21,22 These results suggest that the signals observed in Southern blots were due to hybridization with cellular genes, not viral integration events.41 Recently, several sequences of the normal mouse genome have been found to have a high degree of homology to sequences in the E5 gene of human papillomavirus type 18.23 These are intriguing observations that may ultimately be important for understanding carcinogenic mechanisms in mouse skin.
Liver Diseases
Published in George Feuer, Felix A. de la Iglesia, Molecular Biochemistry of Human Disease, 2020
George Feuer, Felix A. de la Iglesia
Liver cancer is fairly common and associated with cirrhosis in alcoholics.103,278 Hepatocellular carcinoma also occurs in noncirrhotic alcoholics. Alcohol is considered as a cocarcinogen. In addition to the direct effects of ethanol, indirect consequences of malnutrition are associated with carcinogenesis. These include deficient intake of vitamins, riboflavin, pyridoxine, pantothenic acid, and essential trace metals. The effect of malnutrition in promoting cancer is very common. It is associated with oral, head, and neck cancer.314,387,606 In these cases, deficiencies are reported in iron, zinc, thiamin, riboflavin, ascorbic acid, and vitamin A. Alcohol may cause malnutrition and influence the absorption, distribution, metabolism, storage, and elimination of various essential nutrients.
Experimental Oral Carcinogenesis
Published in Samuel Dreizen, Barnet M. Levy, Handbook of Experimental Stomatology, 2020
Samuel Dreizen, Barnet M. Levy
The results of these experiments indicated that the local effects of calcium hydroxide served to prepare or condition the buccal mucosa for the enhancement of carcinoma evolvement, using tobacco as the weak carcinogen. The severe caustic action of calcium hydroxide affected both the epithelium and the underlying connective tissue. The covering epithelium was initially lost by ulceration, and the subjacent connective tissue became markedly inflamed. Fibroblastic proliferation, foreign body giant cell formation, and capillary budding occurred as granulation healing transpired in the damaged subepithelial area. The tobacco exerted a definite carcinogenic effect on the epithelial tissues, already damaged and rendered hyperplastic or atrophic by calcium hydroxide. The hypothesis that these two substances do possess the capacity to act together in a cocarcinogenic fashion was substantiated by the findings. Hamner pointed out that the experimental evidence supported the concept of a complex etiology for cancer rather than multiple etiologies. He claimed that such agents as Indian tobacco, along with the proper accessory factors such as calcium hydroxide or protein deficiency, acted in an appropriate combination or sequence to lead to malignant transformation.
Cell cycle dysregulation on prenatal and postnatal arsenic exposure in skin of Wistar rat neonates
Published in Xenobiotica, 2023
Navneet Kumar, Astha Mathur, Suresh Kumar Bunker, Placheril J. John
Arsenic is a transplacental carcinogen, thus prenatal arsenic exposure causes serious health impacts including cancer and other diseases (Rager et al. 2014; Liu et al. 2020). Several epidemiological and laboratory studies indicate that early life exposure to arsenic is a key factor in its detrimental consequences. These data are significant considering a general lack of cancer causing response by arsenic in rodent models (Rossman et al. 2001; Burns et al. 2004; Garry et al. 2015). A series of studies conducted by Waalkes group suggests that arsenic upon prenatal exposure can act as a complete carcinogen in rodents (Waalkes et al. 2003, 2004a, 2004b, 2004c). Interestingly, to adult mice similar doses were comparatively tolerable and were completely carcinogenic to them only in the presence of a cocarcinogen, confirming that early developmental period is specifically sensitive to arsenic (Waalkes et al. 2000, 2007). These studies show similar results as were obtained in ecological studies associated with arsenic induced carcinogenesis and use several strains of wild type mice, providing a direct indication that prenatal arsenic exposure alone can elevate the risk of cancer in exposed offspring (Farzan et al. 2013). Despite all these compelling studies, still it is not possible to conclude that in-utero only exposure of arsenic to humans would lead to tumorigenesis in later life, hence, more research in this direction is required (Garry et al. 2015). Thus, in the current study we evaluated the toxic effects of arsenic exposure during prenatal as well as post natal period on epidermal keratinocytes of Wistar rat neonates.
An update on cutaneous complications of permanent tattooing
Published in Expert Review of Clinical Immunology, 2019
Tattoo inks are a mix of organic or inorganic pigments dispersed in water as well as additives to obtain ready-to-use tattooing products [14–17]. There is a high diversity of pigments used in tattoo inks. According to a recent US study, 44 different pigments were identified. They contain azo, diketopyrrolopyrrole, quinacridone, anthraquinone, dioxazine, or quinophthalone dyes. Metallic pigments are mainly iron, barium, zinc, copper, molybdenum, and titanium. Tattoo inks may contain several pigments [16]. Additives include binders (which bind the pigments particles to each other and the tattooing needle for easier injections into the skin), solvents and surfactants, preservative, and thickening agents [15]. Manufacturers in Europe have reinforced their inks following the resolution (ResAP(2008)1) on requirements and criteria for the safety of tattoos and permanent make-up (PMU) adopted by the council of Europe [18]. Lack of harmonized analytical methods, of guidelines for risk assessment and of guidelines for good manufacturing practice are still an issue for manufacturers [19]. In 2017, the European Chemicals Agency (ECHA) was asked by the European Commission to assess the chemical-related risks associated with the inks, the need for Union-wide action, and the relevant socio-economic impacts. In 2019, ECHA’s Committee for socio-economic analysis has adopted a restriction proposal on hazardous substances in tattoo inks and permanent make-up. The proposal has been forwarded to the European Commission for a draft regulation and possible amendment of Annex XVII to REACH [20]. Regarding cancer, in vivo tattooed mice models are currently showing no or only a weak cocarcinogenic effect, which is reassuring [21,22]. In the first model, immunocompetent hairless mice were tattooed with a black ink known to contain benzo(a)pyrene and then exposed to UV radiation (UVR). The development of UVR-induced squamous cell carcinoma was delayed on the tattooed areas compared to nontattooed areas [21]. In the second model, somewhat similar, immunocompetent hairless mice were tattoo with a red tattoo ink banned because of it contains 2-anisidine, a potential carcinogen. In this case, the time to the onset of the first and second tumor was identical in the red-tattooed group compared with the control group and only the third tumor appeared slightly faster in the red-tattooed group than in the controls [22]. In this late case, there seem indeed to be a cocarcinogenic effect that remains weak. The results give also insights regarding cases of keratoacanthomas on red tattoos as presented later in the article.