Academic literature on the topic 'DNA Damage; Drug effects; Genetics'

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Journal articles on the topic "DNA Damage; Drug effects; Genetics"

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Araújo, Maria Cristina P., Francisca da Luz Dias, Andréa O. Cecchi, Lusânia M. G. Antunes, and Catarina S. Takahashi. "Chromosome damage induced by DNA topoisomerase II inhibitors combined with g-radiation in vitro." Genetics and Molecular Biology 21, no. 3 (1998): 407–17. http://dx.doi.org/10.1590/s1415-47571998000300021.

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Combined radiation and antineoplastic drug treatment have important applications in cancer therapy. In the present work, an evaluation was made of two known topoisomerase II inhibitors, doxorubicin (DXR) and mitoxantrone (MXN), with g-radiation. The effects of DXR or MXN on g-radiation-induced chromosome aberrations in Chinese hamster ovary (CHO) cells were analyzed. Two concentrations of each drug, 0.5 and 1.0 µg/ml DXR, and 0.02 and 0.04 µg/ml MXN, were applied in combination with two doses of g-radiation (20 and 40 cGy). A significant potentiating effect on chromosomal aberrations was obser
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Błasiak, J., and J. Kowalik. "Protective action of vitamin C against DNA damage induced by selenium-cisplatin conjugate." Acta Biochimica Polonica 48, no. 1 (2001): 233–40. http://dx.doi.org/10.18388/abp.2001_5131.

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Genotoxicity of anticancer drugs is of a special interest due to the risk of inducing secondary malignancies. Vitamin C (ascorbic acid) is a recognized antioxidant and, since human diet can be easily supplemented with vitamin C, it seems reasonable to check whether it can protect against DNA-damaging effects of antitumor drugs. In the present work the ability of vitamin C to modulate cytotoxic and genotoxic effects of a cisplatin analog, conjugate (NH3)2Pt(SeO3), in terms of cell viability, DNA damage and repair in human lymphocytes was examined using the trypan blue exclusion test and the alk
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Tempel, Karlheinz, Hannelore Kortenbeutel, and Christina von Zallinger. "Bleomycin - Induced DNA Damage and DNA Repair in Chicken Embryo Cells as Compared to X-Irradiation." Zeitschrift für Naturforschung C 54, no. 12 (1999): 1068–74. http://dx.doi.org/10.1515/znc-1999-1211.

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Following in vitro- and in ovo-exposure of chicken embryo cells, the level of bleomycin (BM) - induced damage was evaluated by using DNA synthesis, nucleoid sedimentation (SED), and viscometry of alkaline cell lysates (VISC). This damage was compared to Xirradiation, using 5.9-378 nM BM in vitro, 1.5-116 μg BM/egg in ovo, and 2-32 Gy, respectively, in vitro as well as in ovo. With respect to BM. the most notable result is the increase in DNA synthesis and VISC at the lowest concentrations of the drug. A decrease in both parameters was observed at high BM concentrations and following exposure t
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Nemeth, Margit A., T. C. Hsu, and S. Pathak. "Chromosome instability in the murine melanoma cell line K-1735 is due to drug-specific mechanisms." Genetics and Molecular Biology 23, no. 4 (2000): 763–69. http://dx.doi.org/10.1590/s1415-47572000000400010.

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The purpose of the present study was to investigate chromosomal instability and DNA repair by exposing clones from the murine melanoma cell line K-1735 to the radiomimetic drug bleomycin and to the DNA polymerase a inhibitor aphidicolin. Results from previous experiments conducted with human lymphocytes have suggested synergistic chromosomal damage after simultaneous exposure to these two agents. However, in the murine cell line studied here, there was no direct correlation between the effects of these two agents. Indeed, the extensive variation in the responses to aphidicolin and bleomycin su
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Blasiak, Janusz, Kinga Widera, and Tomasz Pertyński. "Hyperthermia can differentially modulate the repair of doxorubicin-damaged DNA in normal and cancer cells." Acta Biochimica Polonica 50, no. 1 (2003): 191–95. http://dx.doi.org/10.18388/abp.2003_3726.

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Hyperthermia can modulate the action of many anticancer drugs, and DNA repair processes are temperature-dependent, but the character of this dependence in cancer and normal cells is largely unknown. This subject seems to be worth studying, because hyperthermia can assist cancer therapy. A 1-h incubation at 37 degrees C of normal human peripheral blood lymphocytes and human myelogenous leukemia cell line K562 with 0.5 microM doxorubicin gave significant level of DNA damage as assessed by the alkaline comet assay. The cells were then incubated in doxorubicin-free repair medium at 37 degrees C or
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Szikriszt, Bernadett, Ádám Póti, Eszter Németh, Nnennaya Kanu, Charles Swanton, and Dávid Szüts. "A comparative analysis of the mutagenicity of platinum-containing chemotherapeutic agents reveals direct and indirect mutagenic mechanisms." Mutagenesis 36, no. 1 (2021): 75–86. http://dx.doi.org/10.1093/mutage/geab005.

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Abstract Platinum-based drugs are a mainstay of cancer chemotherapy. However, their mutagenic effect can increase tumour heterogeneity, contribute to the evolution of treatment resistance and also induce secondary malignancies. We coupled whole genome sequencing with phenotypic investigations on two cell line models to compare the magnitude and examine the mechanism of mutagenicity of cisplatin, carboplatin and oxaliplatin. Cisplatin induced significantly more base substitution mutations than carboplatin or oxaliplatin when used at equitoxic concentrations on human TK6 or chicken DT40 cells, a
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Gloc, Ewa, Mariusz Warszawski, Wojciech Młynarski, et al. "TEL/JAK2 tyrosine kinase inhibits DNA repair in the presence of amifostine." Acta Biochimica Polonica 49, no. 1 (2002): 121–28. http://dx.doi.org/10.18388/abp.2002_3828.

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The TEL/JAK2 chromosomal translocation (t(9;12)(p24;p13)) is associated with T cell childhood acute lymphoblastic leukemia. The TEL/JAK2 fusion protein contains the JAK2 catalytic domain and the TEL-specific oligomerization domain. TEL-mediated oligomerization of the TEL/JAK2 proteins results in the constitutive activation of the tyrosine kinase activity. Leukemia cells expressing TEL/JAK2 tyrosine kinase become resistant to anti-neoplastic drugs. Amifostine is a pro-drug which can selectively protect normal tissues against the toxicity of anticancer drugs and radiation. We investigated the ef
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Donmez-Altuntas, Hamiyet, Fahri Bayram, Ayse N. Coskun-Demirkalp, Osman Baspınar, Derya Kocer, and Peter P. Toth. "Therapeutic effects of statins on chromosomal DNA damage of dyslipidemic patients." Experimental Biology and Medicine 244, no. 13 (2019): 1089–95. http://dx.doi.org/10.1177/1535370219871895.

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Statins are a group of cholesterol lowering drugs and frequently used in the therapy of dyslipidemia. Our knowledge of the impact of statin therapy on DNA damage is as yet rudimentary. In this study, we aimed to assess the possible (1) genotoxic, cytostatic, and cytotoxic effects of statins in peripheral blood lymphocytes by using the cytokinesis-block micronucleus cytome (CBMN-cyt) assay, and (2) oxidative DNA damage by measuring plasma 8-hydroxy-2′-deoxyguanosine (8-OHdG) levels in response to statin therapy. Thirty patients with dyslipidemia who had no chronic diseases and did not use any m
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Mollazadeh, Samaneh, Maryam M. Matin, Ahmad Reza Bahrami, et al. "Feselol Enhances the Cytotoxicity and DNA Damage Induced by Cisplatin in 5637 Cells." Zeitschrift für Naturforschung C 66, no. 11-12 (2011): 555–61. http://dx.doi.org/10.1515/znc-2011-11-1204.

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Transitional cell carcinoma (TCC), which is the most common type of bladder cancer, shows resistance to chemotherapeutic agents due to the overexpression of drug efflux pumps. In this study, the effects of feselol, a sesquiterpene coumarin extracted from Ferula badrakema, on cisplatin cytotoxicity were investigated in 5637 cells, a TCC subline. Cell viability and DNA lesion were evaluated by thiazolyl blue tetrazolium bromide and comet assays, respectively. Feselol had no significant cytotoxic effect in 5637 cells but at 32 μg/mL it increased the cytotoxicity of 1 μg/mL cisplatin by 37% after
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Chen, Ling, Ting Zhang, Qiuli Liu, et al. "Buformin increases radiosensitivity in cervical cancer cells via cell-cycle arrest and delayed DNA-damage repair." Experimental Biology and Medicine 243, no. 14 (2018): 1133–40. http://dx.doi.org/10.1177/1535370218813320.

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Buformin is a commonly used hypoglycemic agent, and numerous studies have shown that buformin has potent antitumor effects in several malignancies. In this study, we aimed to assess the cytotoxic effect of buformin combined with ionizing radiation (IR) on two human cervical cancer cell lines (Hela and Siha). Cytotoxicity was detected by colony formation assays; impacts on the cell cycle and apoptosis were detected by flow cytometric analyses. Changes in histone H2AX (γ-H2AX) phosphorylation and impacts on the AMPK/S6 pathway were also explored. Our data show that the combination of buformin an
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Dissertations / Theses on the topic "DNA Damage; Drug effects; Genetics"

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Ditzel, Mark Clifford. "Modulation of the p53 response : effects of DNA damage and MDM-2 overexpression." Thesis, University College London (University of London), 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.322581.

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Nadkarni, Aditi A. "Functional analysis of the Rad51d (E233G) breast cancer associated polymorphism and a pharmacogenetic evaluation of RAD51D status." Connect to full text in OhioLINK ETD Center, 2008. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=mco1222877984.

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Dissertation (Ph.D.)--University of Toledo, 2008.<br>"In partial fulfillment of the requirements for the degree of Doctor of Philosophy in Biomedical Sciences." Title from title page of PDF document. Bibliography: pages 73-77, 93-95, 109-111, 145-172.
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Zauri, Melania. "Tet2 and relevant potential intervention in cancer." Thesis, University of Oxford, 2014. http://ora.ox.ac.uk/objects/uuid:09208267-5766-47b6-b9f4-5c97a6e6b5a2.

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Laubenthal, Julian, O. Zlobinskaya, Krzysztof Poterlowicz, et al. "Cigarette smoke-induced transgenerational alterations in genome stability in cord blood of human F1 offspring." 2012. http://hdl.handle.net/10454/6063.

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The relevance of preconceptional and prenatal toxicant exposures for genomic stability in offspring is difficult to analyze in human populations, because gestational exposures usually cannot be separated from preconceptional exposures. To analyze the roles of exposures during gestation and conception on genomic stability in the offspring, stability was assessed via the Comet assay and highly sensitive, semiautomated confocal laser scans of gammaH2AX foci in cord, maternal, and paternal blood as well as spermatozoa from 39 families in Crete, Greece, and the United Kingdom. With use of multivari
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Travica, S., Klaus Pors, Paul M. Loadman, et al. "Colon cancer-specific cytochrome P450 2W1 converts duocarmycin analogues into potent tumor cytotoxins." 2013. http://hdl.handle.net/10454/6217.

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PURPOSE: Cytochrome P450 2W1 (CYP2W1) is a monooxygenase detected in 30% of colon cancers, whereas its expression in nontransformed adult tissues is absent, rendering it a tumor-specific drug target for development of novel colon cancer chemotherapy. Previously, we have identified duocarmycin synthetic derivatives as CYP2W1 substrates. In this study, we investigated whether two of these compounds, ICT2705 and ICT2706, could be activated by CYP2W1 into potent antitumor agents. EXPERIMENTAL DESIGN: The cytotoxic activity of ICT2705 and ICT2706 in vitro was tested in colon cancer cell lines expre
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"Novel traditional Chinese medicine-platinum compound that bypasses mitotic DNA damage checkpoints in cancer cells." Thesis, 2010. http://library.cuhk.edu.hk/record=b6074932.

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Aim: Cisplatin is the first platinum drug that shows promising anti-tumor effect clinically. Oxaliplatin, a third-generation platinum drug that incorporates a diaminocyclohexane (DACH) structural entity, can overcome cisplatin resistance. R,R-5, a novel platinum compound that integrates the DACH entity with a demethylcantharidin (DMC) component that is derived from a traditional Chinese medicine (TCM) , can also overcome cisplatin resistance. The principal objectives of this study was to investigate in detail, the effect of these compounds at the antephase and G2 checkpoints of the cell cycle,
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Osman, I. F., A. Baumgartner, E. Cemeli, J. N. Fletcher, and D. Anderson. "Genotoxicity and cytotoxicity of zinc oxide and titanium dioxide in HEp-2 cells." 2010. http://hdl.handle.net/10454/6119.

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AIMS: The rapidly growing industrial and medical use of nanomaterials, especially zinc oxide and titanium dioxide, has led to growing concerns about their toxicity. Accordingly, the intrinsic genotoxic and cytotoxic potential of these nanoparticles have been evaluated. MATERIALS & METHODS: Using a HEp-2 cell line, cytotoxicity was tested along with mitochondrial activity and neutral red uptake assays. The genotoxic potential was determined using the Comet and the cytokinesis-blocked micronucleus assays. In addition, tyrosine phosphorylation events were investigated. RESULTS & CONCLUSION: We fo
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Salem, Mohamed M. A., Mohammad Shalbaf, Nick C. Gibbons, Bhavan Chavan, M. Julie Thornton, and Karin U. Schallreuter. "Enhanced DNA binding capacity on up-regulated epidermal wild-type p53 in vitiligo by H2O2-mediated oxidation: a possible repair mechanism for DNA damage." 2009. http://hdl.handle.net/10454/6168.

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Vitiligo is characterized by a patchy loss of inherited skin color affecting approximately 0.5% of individuals of all races. Despite the absence of the protecting pigment and the overwhelming evidence for hydrogen peroxide (H(2)O(2))-induced oxidative stress in the entire epidermis of these patients, there is neither increased photodamage/skin aging nor a higher incidence for sun-induced nonmelanoma skin cancer. Here we demonstrate for the first time increased DNA damage via 8-oxoguanine in the skin and plasma in association with epidermal up-regulated phosphorylated/acetylated p53 and high le
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Books on the topic "DNA Damage; Drug effects; Genetics"

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European Environmental Mutagen Society. Meeting. Workshop on chromosome instability and cell cycle control: Istituto Superiore di Sanità, Rome, September 3-7, 1996 : abstract book. L'Istituto, 1996.

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Dhawan, Alok. The comet assay in toxicology. RSC Pub., 2009.

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Snapka, Robert M. The SV40 replicon model for analysis of anticancer drugs. R.G. Landes, 1996.

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The SV40 replicon model for analysis of anticancer drugs. Academic Press, 1996.

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Genes and the environment. Taylor & Francis, 1999.

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Madhusudan, Srinivasan, and David M. Wilson III. DNA Repair and Cancer: From Bench to Clinic. Taylor & Francis Group, 2013.

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Madhusudan, Srinivasan, and David M. Wilson III. DNA Repair and Cancer: From Bench to Clinic. Taylor & Francis Group, 2013.

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Madhusudan, Srinivasan, and David M. Wilson III. DNA Repair and Cancer: From Bench to Clinic. Taylor & Francis Group, 2013.

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D, Bloom Arthur, Poskitt Paula K. F, March of Dimes Birth Defects Foundation., and Environmental Health Institute (Pittsfield, Mass.), eds. Genetic risk assessment. March of Dimes Birth Defects Foundation, 1988.

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(Editor), Gilbert de Murcia, and Sydney Shall (Editor), eds. From DNA Damage & Stress Signalling to Cell Death Poly ADP-Ribosylation Reaction. Oxford University Press, USA, 2000.

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Book chapters on the topic "DNA Damage; Drug effects; Genetics"

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Sapse, Anne-Marie. "Ab Initio Studies of Anti-Cancer Drugs." In Molecular Orbital Calculations for Biological Systems. Oxford University Press, 1998. http://dx.doi.org/10.1093/oso/9780195098730.003.0011.

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Cancer is an extraordinarily complicated group of diseases which are characterized by the loss of normal control of the maintenance of cellular organization in the tissues. It is still not completely understood how much of the disease is of genetic, viral, or environmental origin. The result, however, is that cancer cells possess growth advantages over normal cells, a reality which damages the host by local pressure effects, destruction of tissues, and secondary systemic effects. As such, a goal of cancer therapy is the destruction of cancer cells via chemotherapeutic agents or radiation. Since the late 1940s, when Farber treated leukemia with methotrexate, cancer therapy with cytotoxic drugs made enormous progress. Chemotherapy is usually integrated with other treatments such as surgery, radiotherapy, and immunotherapy, and it is clear that post-surgery, it is effective with solid tumors. This is due to the fact that only systemic therapy can attack micrometastases. The rationale for using chemotherapy is the control of tumor-cell populations via a killing mechanism. The major problem in this approach is the lack of selectivity of chemotherapeutic agents. Some agents indeed preferentially kill cancer cells, but no agents have been synthesized yet which kill only cancer cells and do not affect normal cells. Unfortunately, normal tissues are affected, giving rise to a multitude of side effects. In addition to drugs exhibiting cytotoxic activity, antiproliferative drugs are also formulated. According to their mode of action, anti-cancer drugs are divided into several classes. . . . alkylating agents antimetabolites DNA intercalators mitotic inhibitors lexitropsins drugs which bind covalently to DNA . . . Experimental studies of these molecules are complemented and enhanced by theoretical studies. Some of the theoretical studies use molecular mechanics methods while others apply ab initio or semi-empirical quantum-chemistry methods. Most of these molecules are large and besides their structures and properties it is important to investigate their interaction with DNA fragments (themselves large molecules). Ab initio calculations cannot always be applied to the whole system. Therefore, models are used and through a judicious choice of the entities investigated, the calculations can shed light on the problem and provide enough information to complement the experimental studies.
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Conference papers on the topic "DNA Damage; Drug effects; Genetics"

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Haque, Ainul, Ameeya Kumar Nayak, and Bernhard Weigand. "Electrokinetic Transport of Power Law Fluid Through a Micro-Channel With Hydrodynamic Slippage." In ASME-JSME-KSME 2019 8th Joint Fluids Engineering Conference. American Society of Mechanical Engineers, 2019. http://dx.doi.org/10.1115/ajkfluids2019-4848.

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Abstract A pressure driven electroosmotic flow (EOF) is numerically studied in a slit micro-channel with alternating hydrodynamic slip patches. The coupled Poisson-Boltzman-Navier Stokes equations dealt with external electric potential are solved for the flow enhancement of non-Newtonian fluids in microfluidic domain, which is a big challenge in the transportation and mixing of fluids in BioMEMS devices as the drag effect is very strong along the walls. This effect can be minimized with the use of slip boundary conditions by the coupling effects of liquid-liquid or gas-liquid interface positio
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