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Cancer Biology and Genetics for Non-Biologists
Published in Trevor F. Cox, Medical Statistics for Cancer Studies, 2022
Cancer is not one disease but a collection of diseases. It occurs when the DNA of a cell is damaged, and as there are about 200 different types of cells in the body, there can be 200 types of cancer. DNA damage is caused by mutations (changes) of the genetic code. The mutation can affect a single gene or, more widely, a chromosome.
Plantago ovata (Isabgol) and Rauvolfia serpentina (Indian Snakeroot)
Published in Azamal Husen, Herbs, Shrubs, and Trees of Potential Medicinal Benefits, 2022
Ankur Anavkar, Nimisha Patel, Ahmad Ali, Hina Alim
Chromium (VI), naturally occurring in drinking water, is harmful when found above permissible limits. It has been known to cause DNA damage, resulting in cancers, reproductive damage, and respiratory and skin ailments. A study reported chromium (Ⅵ) toxicity causes oxidative stress in fish (Channa punctata). It further reported increased inactivity of liver enzymes, micronuclei formation, chromosomal aberrations, and decreases in the protein number of fish. When administered an ethanolic root extract of R. serpentina, improvement could be seen in toxicity symptoms, reduction in DNA damage, and restoration of mitochondrial damage due to its antioxidant properties. Thus, it could be useful for aquatic biodiversity against heavy metal toxicity (Trivedi et al., 2021).
Urothelial and Urethral Cancer
Published in Karl H. Pang, Nadir I. Osman, James W.F. Catto, Christopher R. Chapple, Basic Urological Sciences, 2021
Ibrahim Jubber, Karl H. Pang, James W.F. Catto
These compounds result in DNA damage:Double strand breaks.Base modifications.Bulky adduct formation.
IFN-γ activates the tumor cell-intrinsic STING pathway through the induction of DNA damage and cytosolic dsDNA formation
Published in OncoImmunology, 2022
Hui Xiong, Yu Xi, Zhiwei Yuan, Boyu Wang, Shaojie Hu, Can Fang, Yixin Cai, Xiangning Fu, Lequn Li
DNA damage and cellular responses to DNA damage are important determinants of cancer outcomes following radiation therapy, chemotherapy, and immune-directed therapies.7,50 Several studies have shown how radiation therapy and chemotherapy induce DNA damage and repair and revealed the biological consequences of the cellular response to DNA damage.50 The role of IFN-γ, which is the most important mediator involved in immune-directed therapies,51,52 in the induction of DNA damage in cancer cells and the subsequent cellular response to DNA damage have not been fully investigated. Hubackova et al. reported that IFN-γ could induce TGF-β/Smad signaling-dependent DNA damage and senescence in HeLa cells.32 IFN-γ did not activate TGF-β/Smad signaling in lung cancer cells (data not shown); instead, we showed that IFN-γ upregulated iNOS expression and resulted in the production of NO in lung adenocarcinoma cells. Inhibiting NO production resulted in the abrogation of IFN-γ-induced DNA damage. NO is the precursor of the highly reactive nitrogen species peroxynitrite (ONOO-), which is a required factor in oxidative DNA damage. High levels of iNOS-dependent DNA damage could cause DNA double-strand breaks and genomic instability.53
Evaluation of possible protective role of Chrysin against arsenic-induced nephrotoxicity in rats
Published in Toxin Reviews, 2022
Muhammad Umar Ijaz, Faryal Jabeen, Asma Ashraf, Muhammad Imran, Nazia Ehsan, Abdul Samad, Muhammad Kashif Saleemi, Javed Iqbal
DNA injury was observed in renal cells of arsenic intoxicated albino rats through comet assay. Comet assay is a simple method for measuring DNA damage (Azqueta et al. 2013). Many toxicity-mediators exert DNA damaging effects through ROS production, which break down its helical structures and also disturb the DNA integrity (Baş et al. 2016, Mujahid et al. 2021). In the current study considerable changes were observed in comet length, head length, tail length, tail moment, % DNA in tail in the kidney cells of rat, presenting a high level of damage followed by arsenic exposure. Free radicals triggers the metal ions to discharge reactive ions which can cause DNA damage (Dasheng et al. 2001). It is still unclear that arsenic reacts directly with DNA or not, but it has been proposed that arsenic induces DNA damage instigating single and double‐strand breaks (Hei et al. 1998, Guillamet 2004). Previous investigations have reported that arsenic causes biological dysfunctions by increasing DNA disruption and reducing antioxidant defence mechanism (Kligerman et al. 2010). Co-treatment with chrysin restored the comet parameters toward normal. Our results are in line with Manzolli et al. (2015), who reported that chrysin effectively protected methylmercury-induced genotoxicity in male rats.
Profiling and Integrated Analysis of the ERCC6-regulated circRNA-miRNA-mRNA Network in Lens Epithelial Cells
Published in Current Eye Research, 2021
Ying Wang, Guowei Zhang, Pengfei Li, Lihua Kang, Bai Qin, Yu Cao, Jiawei Luo, Xiaojuan Chen, Miaomiao Qin, Huaijin Guan
Age-related cataract (ARC) is a disease characterized by progressive opacification of the lens of the eye, and is a common cause of visual impairment and blindness in elderly patients.1,2 Lens epithelial cells (LECs) death appears to be a common cellular basis for non-congenital cataract development.3 Many studies have reported that LECs death is related to cataract formation and development.4–6 Oxidative stress triggers the death of LECs via apoptosis,6,7 autophagy,8 and pyroptosis.9,10 In addition, studies have suggested that oxidative stress which can cause DNA strand-breaks in LECs, contributes to the onset of ARC.11,12 DNA damage is routinely repaired by various DNA repair mechanisms, including nucleotide excision repair (NER).13 NER has been demonstrated to be a pivotal excision process that removes DNA lesions by a series of enzymatic activities.14 In one NER process, excision repair cross-complementation group 6 (ERCC6) recruits repair factors to the site of damaged DNA for repair.15,16 Our previous research demonstrated that the reduced expression of ERCC6 caused by epigenetic modification might be associated with the pathogenesis of cataracts.16 However, the mechanisms by which ERCC6 regulates oxidative damage repair and cell death are still unknown.