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Academic literature on the topic 'DNA-reactive entities'
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Journal articles on the topic "DNA-reactive entities"
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Sharma, Anmol, Pawan Gupta, and Pranav Kumar Prabhakar. "Endogenous Repair System of Oxidative Damage of DNA." Current Chemical Biology 13, no. 2 (July 12, 2019): 110–19. http://dx.doi.org/10.2174/2212796813666190221152908.
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DNA is one of the most important biomolecules of living cells which carries genetic information from generation to generation. Many endogenous and exogenous agents may disrupt the structure of DNA. Change in the cellular genome can lead to errors in replication, transcription and in protein synthesis. DNA damage occurs naturally or result from a metabolic and hydrolytic process which release some very active chemical entities like free radicals, Reactive Oxygen Species (ROS), Reactive Nitrogen Intermediate (RNI), Reactive Carbonyl Species (RCS), lipid peroxidation products and alkylating agents. Superoxide radical, hydroxyl radical and hydrogen peroxide cause a significant threat to cellular integrity by damaging the DNA, lipids, proteins and other biomolecules. Oxidative stress may be explained as a disturbance in the number of free radicals and our system’s ability to neutralize these free radicals. Imbalances in the normal redox potential can also lead to toxic effects via the generation of peroxides. Oxidation of DNA bases leads to the base damage, nick in the strand and break in the strand either single or double strand. Oxidative stress can also cause modifications in normal mechanisms of cell signaling. DNA mutation can result in a number of genetic abnormalities such as cancer, heart failure, Alzheimer’s disease, and depression. Human body has special protection in the form of antioxidant molecules and enzymes against these free radicals. Generation of ROS and its neutralization must be regulated to protect cells and signalling biomolecules from the deleterious effect of oxidative stress with the involvement of antioxidant systems, enzymes, and specific proteins. DNA repair system is a complex system which helps in the identification, removal of the wrong nucleotide and repairs them and as a result, the cell will produce correct and functional protein and active enzyme.
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Motherby, Helma, Mary Kube, Nikolaus Friedrichs, Bahram Nadjari, Kristiane Knops, Andreas Donner, Betty Baschiera, Peter Dalquen, and Alfred Böcking. "Immunocytochemistry and DNA-Image Cytometry in Diagnostic Effusion Cytology I. Prevalence of Markers in Tumour Cell Positive and Negative Smears." Analytical Cellular Pathology 19, no. 1 (1999): 7–20. http://dx.doi.org/10.1155/1999/459158.
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To determine the prevalence of immunocytochemical positivities for a panel of antibodies in benign and malignant cells in effusions with known follow‐up in order to use these as diagnostic markers. Besides their ability to identify malignant epithelial cells their contribution to the differential diagnosis between carcinomatoses and mesotheliomas was investigated. 101 tumour cell positive and 53 negative effusions were stained with 12 different antibodies. Results were scored semiquantitatively per cell type. Furthermore, DNA‐image cytometry was performed. While prevalence of Ber‐EP4 positivity was 95.4% in metastatic carcinoma cells, it was 0% in those from mesotheliomas. No cell type reacted with this marker in benign effusions (0%). Ber‐EP4 correctly differentiated between metastatic carcinoma and mesothelioma in 98.0%. Prevalence of DNA‐aneuploidy was 95.4% in metastatic carcinomas, 57.1% in mesotheliomas and 0% in reactive effusions. Combining immunocytochemistry (Ber‐EP4 positivity) and DNA‐image cytometry (aneuploidy) results in a 100% detection of metastatic carcinomatoses and 57.1% of mesotheliomas. Both markers furthermore allowed a correct differentiation of these entities in 98%.
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Centio, Anders, Montserrat Estruch, Kristian Reckzeh, Kumar Sanjiv, Camilla Vittori, Sophia Engelhard, Ulrika Warpman Berglund, Thomas Helleday, and Kim Theilgaard-Mönch. "Inhibition of Oxidized Nucleotide Sanitation By TH1579 and Conventional Chemotherapy Cooperatively Enhance Oxidative DNA Damage and Survival in AML." Molecular Cancer Therapeutics 21, no. 5 (February 28, 2022): 703–14. http://dx.doi.org/10.1158/1535-7163.mct-21-0185.
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Abstract Currently, the majority of patients with acute myeloid leukemia (AML) still die of their disease due to primary resistance or relapse toward conventional reactive oxygen species (ROS)- and DNA damage–inducing chemotherapy regimens. Herein, we explored the therapeutic potential to enhance chemotherapy response in AML, by targeting the ROS scavenger enzyme MutT homolog 1 (MTH1, NUDT1), which protects cellular integrity through prevention of fatal chemotherapy-induced oxidative DNA damage. We demonstrate that MTH1 is a potential druggable target expressed by the majority of patients with AML and the inv(16)/KITD816Y AML mouse model mimicking the genetics of patients with AML exhibiting poor response to standard chemotherapy (i.e., anthracycline & cytarabine). Strikingly, combinatorial treatment of inv(16)/KITD816Y AML cells with the MTH1 inhibitor TH1579 and ROS- and DNA damage-inducing standard chemotherapy induced growth arrest and incorporated oxidized nucleotides into DNA leading to significantly increased DNA damage. Consistently, TH1579 and chemotherapy synergistically inhibited growth of clonogenic inv(16)/KITD816Y AML cells without substantially inhibiting normal clonogenic bone marrow cells. In addition, combinatorial treatment of inv(16)/KITD816Y AML mice with TH1579 and chemotherapy significantly reduced AML burden and prolonged survival compared with untreated or single treated mice. In conclusion, our study provides a rationale for future clinical studies combining standard AML chemotherapy with TH1579 to boost standard chemotherapy response in patients with AML. Moreover, other cancer entities treated with ROS- and DNA damage–inducing chemo- or radiotherapies might benefit therapeutically from complementary treatment with TH1579.
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Dhir, Hardika, Monica Choudhury, Ketki Patil, Candice Cheung, Adriana Bodlak, Danny Pardo, Asana Adams, Stefano Travaglino, Jose Araque Rojas, and S. Balakrishna Pai. "Interception of Signaling Circuits of Esophageal Adenocarcinoma Cells by Resveratrol Reveals Molecular and Immunomodulatory Signatures." Cancers 13, no. 22 (November 19, 2021): 5811. http://dx.doi.org/10.3390/cancers13225811.
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Deregulation of signaling pathways due to mutations sets the cell on a path to neoplasia. Therefore, recent reports of increased mutations observed in esophageal tissue reflects the enhanced risk of tumor formation. In fact, adenocarcinoma of the esophagus has been on the rise lately. Increase in mortality due to a paucity of efficacious drugs for this cancer prompted us to discover molecular signatures to combat this malady. To this end, we chose resveratrol—a polyphenol with anticancer property—and studied its impact on three esophageal adenocarcinoma cell lines (OE33, OE19 and FLO-1) by multilevel profiling. Here, we show the impact of resveratrol on the viability of the three adenocarcinoma esophageal cell systems studied, at the cellular level. Furthermore, an analysis at the molecular level revealed that the action was through the programmed cell death pathway, resulting in an increase in apoptotic and caspase-positive cells. The impact on reactive oxygen species (ROS) and a decrease in Bcl2 levels were also observed. Moreover, proteomic profiling highlighted pivotal differentially regulated signaling molecules. The phenotypic effect observed in resveratrol-treated esophageal cells could be due to the stoichiometry per se of the fold changes observed in entities of key signaling pathways. Notably, the downregulation of Ku80 and other pivotal entities by resveratrol could be harnessed for chemo-radiation therapy to prevent DNA break repair after radiation therapy. Additionally, multilevel profiling has shed light on molecular and immune-modulatory signatures with implications for discovering novel treatments, including chemo-immunotherapy, for esophageal adenocarcinomas which are known to be aggressive cancers.
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Senoner, Thomas, and Wolfgang Dichtl. "Oxidative Stress in Cardiovascular Diseases: Still a Therapeutic Target?" Nutrients 11, no. 9 (September 4, 2019): 2090. http://dx.doi.org/10.3390/nu11092090.
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Cardiovascular diseases (CVD) are complex entities with heterogenous pathophysiologic mechanisms and increased oxidative stress has been viewed as one of the potential common etiologies. A fine balance between the presence of reactive oxygen species (ROS) and antioxidants is essential for the proper normal functioning of the cell. A basal concentration of ROS is indispensable for the manifestation of cellular functions, whereas excessive levels of ROS cause damage to cellular macromolecules such as DNA, lipids and proteins, eventually leading to necrosis and apoptotic cell death. CVD is the main cause of death worldwide with several conditions being affected by oxidative stress. Increased ROS lead to decreased nitric oxide availability and vasoconstriction, promoting arterial hypertension. ROS also negatively influence myocardial calcium handling, causing arrhythmia, and augment cardiac remodeling by inducing hypertrophic signaling and apoptosis. Finally, ROS have also been shown to promote atherosclerotic plaque formation. This review aims at giving an introduction into oxidative stress in CVD, with special focus on endothelial dysfunction, and then examining in detail the role of oxidative stress in the most prevalent of these diseases. Finally, potential nutraceuticals and diets that might be beneficial in diminishing the burden of oxidative stress in CVD are presented.
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Deaton, C. "Effects of airway inflammation, ozone and exercise on the pulmonary antioxidant capacity of the horse: A war of nutrition." BSAP Occasional Publication 32 (2004): 129–31. http://dx.doi.org/10.1017/s0263967x00041318.
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Within the body there is continual production of entities known as Reactive Oxygen Species (ROS). These include radical derivatives of oxygen that contain at least one unpaired electron and include species such as the superoxide and hydroxyl radicals. ROS also include nonradical derivatives of oxygen that are capable of oxidising biomolecules such as hydrogen peroxide, ozone and nitrogen dioxide. ROS are formed from processes such as the respiratory burst of phagocytes and from mitochondrial oxidative phosphorylation, so production is often increased by situations that elevate oxygen utilisation such as exercise. ROS may also act as “signalling” species within the body. Controlled production of ROS is therefore essential for normal cellular function and health, especially with respect to the functioning of the immune system. However, uncontrolled production of ROS can result in cell damage and death, the induction and propagation of inflammation and DNA damage. Thus, the body has evolved intricate and elaborate enzymatic and non–enzymatic antioxidant defences to control and buffer excess ROS production. In situations where the antioxidant defences are overwhelmed either due to their depletion, malfunction or simply due to excessive ROS bombardment, oxidative stress and oxidative damage are likely to occur.
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Gautam, Nandini, Anil K. Mantha, and Sunil Mittal. "Essential Oils and Their Constituents as Anticancer Agents: A Mechanistic View." BioMed Research International 2014 (2014): 1–23. http://dx.doi.org/10.1155/2014/154106.
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Exploring natural plant products as an option to find new chemical entities as anticancer agents is one of the fastest growing areas of research. Recently, in the last decade, essential oils (EOs) have been under study for their use in cancer therapy and the present review is an attempt to collect and document the available studies indicating EOs and their constituents as anticancer agents. This review enlists nearly 130 studies of EOs from various plant species and their constituents that have been studied so far for their anticancer potential and these studies have been classified asin vitroandin vivostudies for EOs and their constituents. This review also highlights in-depth various mechanisms of action of different EOs and their constituents reported in the treatment strategies for different types of cancer. The current review indicates that EOs and their constituents act by multiple pathways and mechanisms involving apoptosis, cell cycle arrest, antimetastatic and antiangiogenic, increased levels of reactive oxygen and nitrogen species (ROS/RNS), DNA repair modulation, and others to demonstrate their antiproliferative activity in the cancer cell. The effect of EOs and their constituents on tumour suppressor proteins (p53 and Akt), transcription factors (NF-κB and AP-1), MAPK-pathway, and detoxification enzymes like SOD, catalase, glutathione peroxidase, and glutathione reductase has also been discussed.
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Münch, A., D. Teichmann, P. Kuzman, D. Spille, E. Perez, S. May, W. Mueller, et al. "P05.05.B A new IDH-wildtype glioma subtype characterized by highly diffuse growth pattern, distinct epigenetic profile and relatively favorable prognosis." Neuro-Oncology 24, Supplement_2 (September 1, 2022): ii37. http://dx.doi.org/10.1093/neuonc/noac174.124.
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Abstract Background DNA methylation profiling has emerges as a powerful approach to CNS tumor classification and the discovery of novel, molecularly distinct entities. With the release of the 12.5 version of the Heidelberg Brain Tumor Classifier, some unclassifiable cases can be assigned to novel methylation classes. We retrospectively reviewed our databases and identified 16 previously unclassifiable cases, all of which belong to the provisional methylation class “adult-type diffuse high-grade glioma, IDH-wildtype, subtype F (HGG_F)”. Material and Methods We clinically, radiologically and morphologically characterized 16 HGG_F cases and compared them to 347 glioblastomas. We additionally analyzed copy-number alterations and performed DNA exome sequencing. Results Median age at diagnosis of the 12 males and 4 females was 65 years. Upon initial diagnostic workup, specimens were classified as CNS tissue with reactive changes (n=3) or suspicious for the infiltration zone of a diffuse glioma (n = 13). None of the cases demonstrated endothelial proliferation or necrosis and 10/16 tumors had flat copy number profiles. Radiological characteristics were reminiscent of gliomatosis cerebri in eight cases and 9/9 cases had normal FET-PET scans. Whole-exome sequencing revealed genetic alterations frequently found in IDH-wildtype glioblastomas, including TERT promoter mutations in 11/14 (78.6%) and PIK3 mutations (10/14, 71.4%). Outcome was significantly better compared to TCGA IDH-wildtype glioblastomas with a median progression-free survival of 58 months and overall survival of 73 months (both p<0.001). Conclusion We provide evidence that TERT promoter mutations in diffusely infiltrating gliomas without further morphological or molecular signs of high-grade glioma should be interpreted in the context of the clinico-radiological presentation as well as epigenetic prolife and may not be suitable as standalone diagnostic marker for glioblastoma, IDH wildtype.
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Kattoor, Jayasree, and Meherbano M. Kamal. "The gray zone squamous lesions: ASC-US / ASC-H." Cytojournal 19 (April 30, 2022): 30. http://dx.doi.org/10.25259/cmas_03_10_2021.
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The unequivocal and easily recognizable entities of LSIL and HSIL pose no diagnostic problems for a trained eye. However, when the defining morphologic features are either qualitatively or quantitatively insufficient, it is then that the borderline category of “Atypical Squamous cells” (ASC) may have to be used. Scant and suboptimal preparations (mainly in conventional smears) are the common causes that hinder confident decision-making. The binary classification of the ASC category has been retained in The Bethesda System 2014. It includes ASC of undetermined significance (ASC-US) when the atypia is seen in mature cells and ASC-cannot rule out high-grade lesion (ASC-H) when borderline changes are seen in less mature, smaller metaplastic cells or smaller basaloid cells. There are many criticisms of the ASC category. The major one is its subjective and inconsistent applications and the low interobserver and intraobserver reproducibility. However, studies have shown that if we eliminate ASC-US, the LSIL rate will increase. If ASC-H is eliminated, the chances of detecting true lesions are reduced. Hence, there are strong reasons to retain the ASC category. The usual problems leading to the categorization of such cells as atypical are hyperchromasia beyond that acceptable as reactive change; abnormal chromatin pattern that is not overt dyskaryosis; minor variations in nuclear shape; and membrane outlines. Qualifying the atypical cells precisely in one of the categories has bearing on the clinical management and follow-up of the patient. Surveillance of women under the ASC-US category is either by repeat smear at 6 months and 1 year or by reflex human papillomaviruses DNA testing. Women with a Pap smear interpretation of ASC-H are directed to undergo immediate colposcopy. This article describes in detail the morphologic features of the ASC category, doubts about the correct interpretation of the chromatin pattern of the cells in question, and the differential diagnosis between normal, reactive, or inflammatory conditions, and LSIL/HSIL.
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Kanakis, C. E., K. Gvozdjan, L. Sereseanu, D. Rodheim, and P. J. DeChristopher. "Fatal, Rapidly Progressive EBV-Associated Warm Autoantibody Hemolytic Anemia (WAIHA): A Rare Case Study." American Journal of Clinical Pathology 156, Supplement_1 (October 1, 2021): S158. http://dx.doi.org/10.1093/ajcp/aqab191.337.
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Abstract Introduction/Objective Separately WAIHA and Epstein-Barr Virus-infectious mononucleosis (EBV-IM) are well- studied clinical entities. EBV-IM cases are commonly linked with cold autoagglutinins (IgMs with anti-i specificity), but uncommonly associated with WAIHA. More rarely, EBV-IM can be associated with rapidly fatal AIHA. Prompt and appropriate diagnostic Blood Bank testing for WAIHA in EBV-infected patients should include work-ups to prevent missing the possibility of treating complicating WAIHA. Methods/Case Report A 24-year-old woman presented to the ED with a month of cough/cold symptoms, night sweats, cervical lymphadenopathy, and imaging showing diffuse thoracic lymphadenopathy. DNA/PCR testing was positive for active EBV infection and a lymph node biopsy was diagnostic for EBV lymphadenitis. Increasing respiratory distress developed, coupled with renal and liver insufficiency, hypotension, and possible DIC, and (suspected septic) shock. On hospital day (HD) 5, altered mental status worsened, cardiac arrest occurred requiring resuscitation and vasopressors, and acidosis trended rapidly higher. The patient rapidly decompensated and she was compassionately extubated, expiring on HD 6. There were significant laboratory interval changes in the final 20 hours of life. New positive DATs (with anti-IgG and - C3b/d), a pan-reactive warm autoantibody of broad specificity (in plasma & eluate), onset of acute hemolysis (nadir Hgb to 4.6 g/dL with net drop of 4.7 g/dL & LDH 23, 582 U/L), coagulopathy (peak PT 96.6 sec) and evidnece of organ failure. Blood Bank testing, received on HD 5 at 21:45, was resulted in the EMR on HD 6 at 00:30 and the patient expired at 05:15--further illustrating the rapid clinical course presented in this case. Results (if a Case Study enter NA) N/A Conclusion This patient died of complications directly associated with acute, immune-mediated intravascular hemolysis leading to high-output cardiac failure and resulting in multi-organ failure. With a relative paucity of published EBV-IM WAIHA associations, the rapidly evolving unexpected hematologic sequelae observed complicated the clinical recognition and treatment of severe WAIHA during the course of treatment for clinically suspected DIC. The rapid progression of this patients’ symptoms and laboratory values did not allow for adequate recognition of WAIHA-related pathogenesis and appropriate interventions.
Dissertations / Theses on the topic "DNA-reactive entities"
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(9874484), PJP Foley. "DNA bis-intercalators: Design, synthesis and DNA binding properties of potential anti-cancer agents based on rigid polynorbornyl molecular scaffolds." Thesis, 2001. https://figshare.com/articles/thesis/DNA_bis-intercalators_Design_synthesis_and_DNA_binding_properties_of_potential_anti-cancer_agents_based_on_rigid_polynorbornyl_molecular_scaffolds/13423973.
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DNA bis-intercalating agents constitute an important class of compounds for cancer chemotherapy. The work presented in this dissertation deals with the synthesis of a new class of DNA bis-intercalating agents of type I containing rigid polynorbomyl molecular frameworks. The highly rigid molecular framework is designed to place and orient the two intercalating chromophores (the DNA-reactive entities) optimally for specific binding to a known nucleotide sequence. The chromophores are attached to the rigid framework via short flexible tethers, allowing some degree of conformational mobility while maintaining well-defined maximum and minimum inter-chromophore separations. A modular approach to synthesis has been adopted to prepare the bis-intercalators that involved initial preparation of a series of complementary A-BLOCKs II and B-BLOCKIII (Scheme I), each of which contains one intercalating chromophore. These BLOCKs contain different end-functionality (A-BLOCK: alkene; B-BLOCK: epoxide) which react with each other stereospecifically, but not with themselves to produce the desired product IV. The wide range of topologically well defined products generated by this approach show variations which include spacer length, chromophore type and nature of the tether joining the chromophores to the rigid molecular framework. In particular, the BLOCK approach has permitted the preparation of the most comprehensive range of asymmetrical bis-intercalators containing rigid spacers yet described. Representative products derived from this methodology, include the bisacridine V and the acridine-naphthalimide mixed derivative VI. In addition, significant advances have been made to control the hydrophilicity of these drugs, thereby enhancing the bio-compatibility of these novel molecules. DNA binding experiments have been performed on the bis-intercalators prepared in this study. Polynucleotide structural selectivity was observed and sequence-selectivity was associated with the binding of two of the compounds with the highest affinity for DNA. Some features that enhance binding selectivity and affinity have been identified so that the synthesis of more selective compounds for effective gene targeting in chemotherapy can proceed in the future. The results which have helped to define more clearly the parameters of drug-DNA interaction represent a good example of how organic chemistry can be a useful tool to help elucidate and understand biological phenomena. The ground work has been completed providing a solid foundation from which the preparation of novel synthetic targets of medicinal interest using the BLOCK coupling concept can now be approached with less trepidation.