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Carcinogenicity - Crossref

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Last Updated: 10 August 2022

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Carcinogenicity of Psychotropic Drugs

The majority of prescriptions for psychotropic drugs in the United States occur at the primary care level, usually for anxiety and depressive symptoms and their physical correlates. Based on animal research, certain psychotropic drugs have some evidence of carcinogenicity. Here are the animal studies, and available human records are also investigated.

Source link: https://doi.org/10.1093/med/9780199995486.003.0025


A combined COMPACT and HazardExpert study of 40 chemicals for which information on mutagenicity and carcinogenicity is known, including the results of human epidemiological studies

The finding that the majority of procarcinogens that require metabolic activation by P450s are lipophilic in nature, highlights the importance of using the log P value to determine the likelihood of a potentially lethal substance reaching the site of activation.

Source link: https://doi.org/10.1177/096032719801701009


Abstract 5002: Intermittent hypoxia selects for increased carcinogenicity in breast epithelial cells.

Abstract The hypoxic regions of solid tumors are hotbeds of drug resistance and selection. Because cells within a solid tumor do not get a constant supply of oxygen, cycles of acute hypoxia and reoxygenation occur, a phenomenon known as intermittent hypoxia. We expect that this will result in widespread unrepaired DNA damage that consistently selects for populations that are adapted to survive in complex tumor microenvironmental environments. After multiple cycles of IH, we tested three breast cell lines - one aggressive carcinoma, one DCIS line, and one non-transformed epithelial cell line for DNA damage and transformation. Multiple clones of each cell line isolated under IH conditions were then isolated. The MCF10A IH-selected clones show increased resistance to etoposide relative to unselected clones. These findings support our theories of why hypoxia causes more aggressive cancers and poorer prognoses, as well as how de novo drug resistance emerges.

Source link: https://doi.org/10.1158/1538-7445.am2013-5002


Abstract 4795: N-hydroxylation of 4-aminobiphenyl (ABP) and associated oxidative stress may influence ABP carcinogenicity in the mouse liver.

Abstract Liver cancer is the third most common cause of cancer death worldwide due to poor prognosis and a lack of treatment options. Even after accounting for recognized etiological causes, a significant sex difference is found in human liver cancer, with men having a 3 to 5 fold higher risk than women. In addition, female mice were also shielded from liver tumors relative to males, which is similar to the sex difference in human liver cancer. Because all key etiological risk factors for human liver cancer, including viral hepatitis, alcohol, obesity, and chemical carcinogens, have been shown to be linked to oxidative stress, oxidative stress has been shown to be connected to oxidative stress in human liver carcinogenesis. We first tested whether oxidative stress is involved in ABP-mediated carcinogenesis in the mouse, first determining whether oxidative stress is involved in ABP-mediated carcinogenesis in the mouse. More than one cytochrome P450 seems to be involved in the reaction, according to us, who characterized ABP N-hydroxylation by mouse liver microsomes. The high affinity ABP N-hydroxylation reaction is mediated by CYP1A2, according to a separate low affinity site belonging to an as yet unidentified CYP, although at least one other low affinity site within an ABP N-hydroxylation reaction is likely for significant ABP N-hydroxylation at higher concentrations of ABP in our tumor study.

Source link: https://doi.org/10.1158/1538-7445.am2013-4795


Abstract 4365: A Bhas 42 cell transformation assay sensitive to Ames-negative and Ames-discordant carcinogens: Its performance for the prediction of chemical carcinogenicity

Abstract: A cell transformation assay can determine the carcinogenicity of chemicals, but it is not limited to a genotoxicity assay, which has been used for the prediction of chemical carcinogenicity. The Bhas 42 cells were transplanted from the BALB/c 3T3 cells by transfection of the v-Has gene and described as initiated cells in the two-stage carcinogenesis model. In terms of cost and labor results, Bhas 42 CTA is superior to conventional CTAs in cost and labor results. We used this short-term CTA to 92 chemicals to test the assay and assess its results for chemical carcinogenicity prediction. Methods: The Bhas 42 cells were seeded on 6-well microplates, treated with test chemicals from Day 1, when the cells were sparse, to Day 4, and then cultured in normal medium until Day 21. The cells were seeded at a density of 7000 cells/mL from Day 4, when the cells were sub-confluent, to Day 14, and maintained in normal medium until Day 21. Bhas 42 CTA's findings were compared to recent genotoxicity studies, and we're discussing our findings. The promotion assay confirmed that the Bhas 42 cells behave as initiated cells in the CTA, with Ames-negative and Ames-discordant chemicals detecting Ames-negative and Ames-discordant chemicals assay evidenced most of them. We found that the reliability of prediction for chemical carcinogenicity would be enhanced by adding Bhas 42 CTA to the battery of in vitro assays based on these results.

Source link: https://doi.org/10.1158/1538-7445.am10-4365


Abstract 5553: Low-dose carcinogenicity of 2-amino-3-methylimidazo[4,5- f ]quinoline in rats: Evidence for the existence of no-effect levels and a mechanism involving p21Cip/WAF1

We discovered that IQ doses of 1 ppm and below did not cause preneoplastic lesions in either the liver or colon, nor did it cause preneoplastic lesions in both organs, while IQ doses of 10 and 100 ppm caused preneoplastic lesions in both these organs. These findings show that there are no effect levels of IQ for both liver and colon carcinogenicity in rats, as well as rats, and that the dose-response relationship for IQ carcinogenicity is nonlinear. In the finding that p21Cip/WAF1 was significantly stimulated in the liver at doses much lower than those required for IQ-mediated carcinogenic effects, suggests that the induction of p21Cip/WAF1 is one of the mechanisms responsible for the observed no-effect of low doses of IQ. Similarly, the IQ administration led to significant induction of CYP1A2 at doses of 0. 01 to ten ppm, but 100 ppm IQ produced CYP1A1 rather than CYP1A2.

Source link: https://doi.org/10.1158/1538-7445.am2011-5553

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions