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Introduction to Genomics
Published in Altuna Akalin, Computational Genomics with R, 2020
Mutations in the genome occur due to multiple reasons. First, DNA replication is not an error-free process. Before a cell division, the DNA is replicated with 1 mistake per 10^8 to 10^10 base-pairs. Second, mutagens such as UV light can induce mutations on the genome. The third factor that contributes to mutation is imperfect DNA repair. Every day, any human cell suffers multiple instances of DNA damage. DNA repair enzymes are there to cope with this damage but they are also not error-free, depending on which DNA repair mechanism is used (there are multiple), mistakes will be made at varying rates.
Radiation Hormesis in Immunity
Published in T. D. Luckey, Radiation Hormesis, 2020
Increased cell repair enzymes and enhanced immune competence are keys to understanding many physiologic effects of low doses of ionizing radiation. DNA repair enzymes are effective for exposures which are low enough to provide adequate time to repair one strand using the intact strand as a template; these function in most cells.297,478 Also important are repair of cell membranes, altered enzyme concentrations, and changed metabolic priorities. Specific mechanisms for important immunologic effects require modern methods for studying immune competence.
Causes Of Alzheimer’s Disease
Published in Zaven S. Khachaturian, Teresa S. Radebaugh, Alzheimer’s Disease, 2019
Considerable heterogeneity has already been identified in the susceptibility of individuals to toxins. Individuals have different kinds and amounts of liver enzymes to detoxify exogenous and endogenous toxins. Just as genetic mutations can lead to disease, normal genetic variation can lead to disease susceptiblity. Some of the best examples of this is susceptibility to cancer. DNA repair enzymes differ in their properties. If an individual is never under undue stress, no consequences of the genetic differences are apparent. If, however, the individuals are exposed to toxins, then those whose repair enzymes are not as active or efficient as others have a higher incidence of certain kinds of cancer such as colon cancer. Investigators are now looking furiously for such factors in neurodegenerative diseases such as Alzheimer’s and Parkinson’s disease. Variants for the gene for ApoE, for instance, appear to confer different degrees of susceptibility to Alzheimer’s disease.12 Whether this susceptibility arises from a differential sensitivity to an endogenous toxin is as yet unknown but it is certainly a likely possibility.
Influence of extremely low-frequency magnetic field on chemotherapy and electrochemotherapy efficacy in human Caco-2 colon cancer cells
Published in Electromagnetic Biology and Medicine, 2022
Mehmet Esref Alkis, Mehmet Zulkuf Akdag, Sevgi Irtegun Kandemir
In general, the present study revealed that the ELF-MF exposure before and after CT and ECT caused an increase in the cell viability compared to the treatments without ELF-MF. Our results suggest that ELF-MF exposure may cause a protective response. This may be explained by that the ELF-EMF exposure may produce a “triggering effect” that does not cause a significant increase in the genetic damage but stimulates the signal transduction pathways, resulting in the activation of cell defense mechanism and consequently providing protection from the genotoxic agent subsequently applied (Mansourian et al. 2020). The triggered cell defense may enable the cells to show a resistance against the high-level damage caused by ECT and CT. Resistance to ECT/CT might also be due to the ELF-MF-induced DNA repair. This resistance might develop in many ways. The change in cytosolic ion concentration (especially Ca++) significantly affects DNA repair, and this change might be caused by EMF (Blackman et al. 1980; Gafter et al. 1997; Mansourian et al. 2020). DNA repair enzymes fix the damage to the DNA molecules, caused by x- and gamma rays, endogenous ROS, plant toxins, ultraviolet radiation, mutagenic chemicals, and CT drugs. DNA repair is classified in two types: nucleotide excision repair and base excision repair, which can confer the resistance to chemo agents targeting DNA (Zheng 2017).
Ponatinib is a potential therapeutic approach for malignant pleural mesothelioma
Published in Experimental Lung Research, 2021
Yi-Wei Yang, Angelica Marrufo, Jillian Chase, Gavitt A. Woodard, David M. Jablons, Hassan Lemjabbar-Alaoui
DNA repair enzymes are critical for maintaining the genome,32 and defects in the repair process lead to genome instability and promote tumorigenesis.33,34 Conversely, good DNA repair provides resistance to therapeutic radiation and some cytotoxic chemotherapy.26 Moreover, combined impairment in different DNA repair systems results in gross genomic instability and death of tumor cells, a principle called “synthetic lethality.”35,36 Radiation therapy, as well as the majority of chemotherapy, weaken cancer cells by damaging DNA. Successful DNA repair is essential for the normal cells to surmount the therapy's adverse effects, but in the tumor can result in treatment resistance. cAbl inhibition has been recently shown to alter DNA damage response.30 DNA damage elicits cAbl activation, which then binds and activates DNA damage repair proteins, including ATM, ATR, Rad51, BRCA1, DNA-PK, RFX1, and p73.23 Moreover, activated cAbl increases the Rad51 gene.
Association of XRCC1 and XPD functional gene variants with nicotine dependence and/or schizophrenia: a case-control study and in silico analysis
Published in Psychiatry and Clinical Psychopharmacology, 2019
S. Pehlivan, N. Aydin, A. F. Nursal, M. A. Uysal, M. Pehlivan, A. Tekcan, F. K. Yavuz, U. Sever, H. Yavuzlar, S. Kurnaz, S. Uysal, P. C. Aydin
X-ray repair cross-complementing group 1 (XRCC1) gene, found at chromosome 19q13.2, is a major component of base excision repair (BER) and is necessary for genetic stability [6]. Xeroderma pigmentosum complementation group D (XPD) is among the crucial DNA repair genes [7]. This is also called as the excision repair cross-complementing complementation group 2 (ERCC2) gene and located in chromosome 19q13.2–13.3 and codes for an evolutionally conserved helicase which plays a key role in transcription and nucleotide excision repair (NER) [7]. Genetic variation in DNA repair genes can have an impact on the activity of DNA repair enzymes, thus modifying the DNA repair ability. This study aimed to find out whether functional SNP variants in the XRCC1 Arg399Gln (rs25487), XPD Lys751Gln (rs13181) variants play any role in both ND and Sch + ND etiopathogenesis in a Turkish population, which was followed up with an in silico analysis approach.