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Dissertations / Theses on the topic 'PARP1 Inhibitors'

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Published: 6 September 2023

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1

Alkhateeb, Hebah, Gregory A. Ordway, W. Drew Gill, et al. "PARP1 inhibition produces unique antidepressant effects in an animal model of treatment-resistant depression." Digital Commons @ East Tennessee State University, 2019. https://dc.etsu.edu/asrf/2019/schedule/49.

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Major depressive disorder (MDD) is a prevalent and enervating mental illness affecting millions globally. Unfortunately, a significant proportion of patients do not receive clinical benefit from existing antidepressant medications. The limited effectiveness of currently available antidepressant drugs emphasizes the need to identify more effective medications for individuals who are treatment-resistant. We have previously reported abnormally elevated poly (ADP-ribose) polymerase-1 (PARP1) gene expression levels in the postmortem brain from MDD brain donors. PARP1 is a DNA damage repair enzyme t

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2

D'Angeli, Floriana. "Biomolecular effects and bioclinical applications of PARPs inhibitors." Doctoral thesis, Università di Catania, 2017. http://hdl.handle.net/10761/3832.

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Abstract Section I Inhibitors of PARP-1(Poly(ADP-ribose) polymerase-1) act by competing with NAD+, the enzyme physiological substrate, which play a protective role in many pathological conditions characterized by PARP-1 overactivation. It has been shown that PARP-1 also promotes tumor growth and progression through its DNA repair activity. Since angiogenesis is an essential requirement for these activities, we sought to determine whether PARP inhibition might affect rat brain microvascular endothelial cells (GP8.3) migration, stimulated by C6-glioma conditioned medium (CM). Through wound-heali

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3

Geraets, Liesbeth. "Dietary PARP-1 inhibitors as anti-inflammatory compounds." Maastricht : Maastricht : Universitaire Pers ; University Library, Universiteit Maastricht [host], 2008. http://arno.unimaas.nl/show.cgi?fid=14252.

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4

Kumpan, Katerina. "Structure-activity studies on inhibitors of the tankyrases." Thesis, University of Bath, 2014. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.619223.

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Tankyrases-1 and -2 (TNKS-1 and -2) are members of the poly(ADP-ribose)polymerase (PARP) enzyme superfamily, which modify and regulate target proteins by addition of multiple (ADP-ribose) units from the substrate NAD+. TNKS-1 and -2 have many cellular roles, including regulation of elongation of telomeres, activation of nuclear mitotic apparatus protein (NuMA) in mitosis and regulation of the Wnt signalling pathway. This makes the tankyrases attractive new targets for design and development of new anti-cancer drugs. 2-(4-Trifluoromethylphenyl)-7,8-dihydro-3H-thiopyranopyrimidin-4-one (XAV939)

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5

Ahmed, Zina. "Poly-ADP ribos polymeras (PARP) inhibitorers effekt på bröstcancer : Poly-ADP ribos polymeras (PARP) inhibitorers effekt på bröstcancer." Thesis, Umeå universitet, Kemiska institutionen, 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-103397.

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6

Almeida, Gilberto Serrano de. "Pre-clinical imaging evaluation of the PARP inhibitor rucaparib." Thesis, University of Newcastle upon Tyne, 2013. http://hdl.handle.net/10443/2033.

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Poly(ADP-ribose) polymerase 1 (PARP1) is a DNA-binding enzyme involved in DNA repair by the base-excision pathway. The inhibition of PARP1 is being investigated as a cancer treatment. Rucaparib (CO338) is a potent PARP 31 inhibitor currently in Phase II clinical development. In this thesis P in vivo MR Spectroscopy (MRS) and Dynamic Contrast Enhanced (DCE) MRI were used to study acute effects of rucaparib on energy metabolism and tumour vasculature. 1 31 18 18 Ex vivo H and P-MRS, and in vivo [ F]FLT and [ F]FDG-PET, were used to study effects of treatment with rucaparib on tumour metabolism a

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7

Hukkanen, M. (Mikko). "DNA damage sensitization of breast cancer cells with PARP10/ARTD10 inhibitor." Master's thesis, University of Oulu, 2019. http://jultika.oulu.fi/Record/nbnfioulu-201909062843.

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Abstract. In this thesis, I studied the DNA damage sensitization of breast cancer cells with PARP10/ARTD10 inhibitor. As the ARTD10 inhibition field is relatively fresh, tests with breast cancer cell lines combined with clinically used chemotherapeutics will elucidate the potential future uses of the inhibitors in a clinically relevant context, directing the future research efforts in the field. To study the link between OUL35 and DNA damage sensitization, cell proliferation experiments were conducted, and to determine whether ARTD10 translocation from cytoplasm into nucleus is enhanced und

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8

Castroviejo, Bermejo Marta. "RAD51 as functional biomarker to select tumors for PARP inhibitor treatment." Doctoral thesis, Universitat Autònoma de Barcelona, 2019. http://hdl.handle.net/10803/667273.

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Los inhibidores de la enzima Poly (ADP-ribosa) polimerasa (PARPi) son efectivos en el tratamiento de cánceres que presentan defectos en la reparación del ADN por recombinación homóloga (HRR), incluyendo aquellos con mutaciones en BRCA1 y BRCA2 (BRCA1/2). Se han descrito distintos mecanismos de resistencia a PARPi en tumores con mutaciones germinales en BRCA1/2 (gBRCA), y existen otros tumores sin mutaciones en BRCA1/2 (no-BRCA) que responden a PARPi. Existe la necesidad de desarrollar un biomarcador robusto para una mejor selección de tumores deficientes en HRR y extender el uso de PARPi

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9

Löser, Dana A. "Investigating the mechanisms by which PARP inhibitors increase sensitivity to DNA damaging agents." Thesis, University of Sussex, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.505912.

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Damage induced by ionising radiation (IR) is mainly repaired by classical non homologous end joining (D-NHEJ), but a small subset of DSBs is repaired with slow kinetics in an ATM (Ataxia telangiectasia mutated) and Artemis dependent manner. In addition, a PARP-1 dependent NHEJ backup pathway (B-NHEJ) was described, which is thought to function in the absence of D-NHEJ. Using ATM, Artemis or DNA ligase IV deficient mouse embryonic fibroblasts (MEFs) as a model system, the effect of the potent and specific PARP-1/-2 inhibitor KU-0059436 upon clonogenic survival after various types of damage that

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10

Guillot, Clément. "Potentiel des inhibiteurs de poly(ADP-ribose) polymérases seuls ou en combinaison avec la radiothérapie comme nouvelle option thérapeutique pour le carcinome hépatocellulaire." Thesis, Lyon 1, 2013. http://www.theses.fr/2013LYO10281.

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Le carcinome hépatocellulaire est l'un des cancers les plus fréquents et des plus sévères à travers le monde. Le diagnostic est souvent tardif et les traitements curatifs ne peuvent être proposés qu'à un nombre limité de patients. Les technologies modernes ont permis le développement de nouvelles méthodes de radiothérapie qui montrent aujourd'hui de bons résultats. Par ailleurs, bien que des déficiences dans les voies de réparation de l'ADN soient associées à une instabilité génomique et une susceptibilité au cancer, une inhibition de ces voies sensibilise les cellules cancéreuses à la chimiot

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11

Michels, Judith. "Les Inhibiteurs de PARP dans le Traitement des Cancers Chimio-Résistants. Etude pré-clinique sur la Dépendance à PARP." Phd thesis, Université Paris Sud - Paris XI, 2013. http://tel.archives-ouvertes.fr/tel-01063796.

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Introduction Le cancer bronchique est un problème de santé publique en étant la première cause de décès par cancer dans le monde. Il reste de mauvais pronostic avec une résistance au Cisplatine qui est inéluctable dans l'histoire naturelle de la maladie. Nous nous sommes intéressés à l'association du CDDP aux inhibiteurs de la Poly(ADP-ribose) polymérase. Les inhibiteurs pharmacologiques de PARP sont source d'optimisme en oncologie clinique en monothérapie pour des tumeurs déficientes pour une voie de réparation de l'ADN et en association aux cytotoxiques classiques.Matériel et méthodes Nous a

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12

Michels, Judith. "Les inhibiteurs de PARP dans le traitement des cancers chimio-résistants : étude pré-clinique sur la dépendance à PARP." Thesis, Paris 11, 2013. http://www.theses.fr/2013PA11T049/document.

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Introduction Le cancer bronchique est un problème de santé publique en étant la première cause de décès par cancer dans le monde. Il reste de mauvais pronostic avec une résistance au Cisplatine qui est inéluctable dans l’histoire naturelle de la maladie. Nous nous sommes intéressés à l’association du CDDP aux inhibiteurs de la Poly(ADP-ribose) polymérase. Les inhibiteurs pharmacologiques de PARP sont source d’optimisme en oncologie clinique en monothérapie pour des tumeurs déficientes pour une voie de réparation de l’ADN et en association aux cytotoxiques classiques.Matériel et méthodes Nous a

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13

Raithel, Kerstin. "Effekt von S-Lost in HaCaT-Zellkulturen : Induktion der Apoptose und Effekt eines PARP-Inhibitors /." München, 2008. http://opac.nebis.ch/cgi-bin/showAbstract.pl?sys=000254372.

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14

Ordway, Gregory A., W. D. Gill, J. B. Coleman, Hui Wang-Heaton, and Russell W. Brown. "Anti-Inflammatory PARP Inhibitor Demonstrates Antidepressant Activity in Animal Model of Treatment Resistant Depression." Digital Commons @ East Tennessee State University, 2019. https://dc.etsu.edu/etsu-works/8643.

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Background: Major depressive disorder is associated with elevated levels of DNA oxidation, DNA damage, and gene expression of DNA repair enzymes including poly (ADP-ribose) polymerase-1 (PARP1). Elevated PARP1 activity is directly linked to neuroinflammation and PARP inhibitors are anti-inflammatory and neuroprotective. We previously showed that PARP inhibitors produce antidepressant-like effects equivalent to fluoxetine in rodent models. Here, we examined whether the PARP inhibitor 3-aminobenzamide (3AB) is effective in a rat model of treatment-resistant depression. Methods: Treatment-resis

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15

Maier, Christian. "Auswirkungen des PARP-1 Inhibitors INO-1001 auf Ischämie-Reperfusionsbedingte Organschädigungen nach thorakalem Aortencrossclamping am Schwein." [S.l. : s.n.], 2008. http://nbn-resolving.de/urn:nbn:de:bsz:289-vts-64137.

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16

Ordway, Gregory A., Attila Szebeni, Liza J. Hernandez, et al. "Antidepressant-Like Actions of Inhibitors of Poly(ADP-Ribose) Polymerase in Rodent Models." Digital Commons @ East Tennessee State University, 2017. https://dc.etsu.edu/etsu-works/2768.

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Many patients suffering from depressive disorders are refractory to treatment with currently available antidepressant medications, while many more exhibit only a partial response. These factors drive research to discover new pharmacological approaches to treat depression. Numerous studies demonstrate evidence of inflammation and elevated oxidative stress in major depression. Recently, major depression has been shown to be associated with elevated levels of DNA oxidation in brain cells, accompanied by increased gene expression of the nuclear base excision repair enzyme, poly(ADP-ribose) polymer

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17

Morel, Daphné. "Identifying Synthetic Lethal and Selective Approaches to Target PBRM1-Deficiency in Clear Cell Renal Cell Carcinoma PBRM1 Deficiency in Cancer is Synthetic Lethal with DNA Repair Inhibitors Exploiting Epigenetic Vulnerabilities in Solid Tumors: Novel Therapeutic Opportunities in the Treatment of SWI/SNF-Defective Cancers Combining Epigenetic Drugs with other Therapies for Solid Tumours — Past Lessons and Future Promise Targeting Chromatin Defects in Selected Solid Tumors Based on Oncogene Addiction, Synthetic Lethality and Epigenetic Antagonism." Thesis, université Paris-Saclay, 2020. http://www.theses.fr/2020UPASL017.

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L’inactivation de polybromo-1 (PBRM1) est un évènement fréquent dans de nombreux cancers. En particulier, les carcinomes rénaux à cellules claires présentent une déficience en PBRM1 dans 40 à 50% des cas. A ce jour, il n’existe pas d’approche de médecine précision connue capable de cibler spécifiquement les cellules tumorales déficientes en PBRM1.Pour identifier des cibles de létalité synthétique associées à la perte de PBRM1, nous avons (i) réalisé un criblage pharmacologique à haut débit évaluant la sensibilité à 167 molécules dans un modèle cellulaire isogénique pour PBRM1, et (ii) étudié l

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18

Block, Katherine M. "Design of Novel Cancer Therapeutics Through The Validation of PARG as a Therapeutic Target and the Evaluation of Small Molecule Inhibitors of Hypoxia-Induced Transcription." Diss., The University of Arizona, 2010. http://hdl.handle.net/10150/194826.

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Because of the severe toxicity and limiting side effects of traditional chemotherapy, there exists a critical need to develop better-tolerated, safer drugs to treat cancer. Recent advances in our understanding of the molecular mechanisms governing carcinogenesis have ushered in a new age in drug discovery and have enabled the design of much more sophisticated agents to treat cancer. This work describes two approaches to the development of novel, specifically targeted cancer therapeutics.The first approach involves the synthesis of a class of a new class of small molecules called epidithiodike

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19

Cherry, K. E. "The poly (ADP-ribose) polymerase (PARP) inhibitors AG14361 and AG014699 : mechanisms of action and implications for clinical application." Thesis, Queen's University Belfast, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.546027.

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20

Chabanon, Roman. "Exploiting DNA Repair Vulnerabilities to Modulate Anti-Cancer Immunity : a Study of the Immunological Potential of PARP inhibitors." Thesis, Université Paris-Saclay (ComUE), 2019. http://www.theses.fr/2019SACLS007.

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Les inhibiteurs de poly(ADP-ribose) polymérase (PARPi) ciblent sélectivement les cellules porteuses de défauts des voies de réparation de l’ADN tels que les mutations de BRCA1/2 et les défauts d’ERCC1. Sur le plan clinique, plusieurs PARPi ont été approuvés pour le traitement des cancers BRCA-mutés ou platine-sensibles du sein et de l’ovaire, et des essais cliniques sont en cours pour évaluer l’efficacité des PARPi dans le cancer bronchique non-à-petites cellules (CBNPC) platine-sensible. Alors que les PARPi ont un fort potentiel thérapeutique dans les cancers comportant des défauts de réparat

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21

Kohl, Vanessa [Verfasser], and Alice [Akademischer Betreuer] Fabarius. "Synthetische Letalität von PARP- und APE1-Inhibitoren bei hämatologischen Neoplasien / Vanessa Kohl ; Betreuer: Alice Fabarius." Heidelberg : Universitätsbibliothek Heidelberg, 2021. http://d-nb.info/1237750598/34.

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22

Harand, Kristina Marie. "Assessment of Acrolein-induced Toxicity Using In-vitro Modeling to Evaluate the Role of PARP Inhibitors in Reducing Cytotoxicity." Scholar Commons, 2016. http://scholarcommons.usf.edu/etd/6091.

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Acrolein is an electrophilic α, β-unsaturated aldehyde. Additionally, acrolein is a metabolite of the antineoplastic alkylating agent cyclophosphamide and is implicated in off-target effects, including to bladder hemorrhagic cystitis and cyclophosphamide-induced cardiotoxicity, both of which have led to serious secondary iatrogenic injury during and following chemotherapy. At low concentrations acrolein inhibits cell proliferation without inducing apoptosis, while at high concentrations may result in secondary apoptosis promotion. This investigation assessed the role of the enzyme poly (ADP-ri

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23

Drew, Yvette Claire. "The potential of the PARP-1 inhibitor, AGO14699, in human cancers defective in homologous recombination DNA repair." Thesis, University of Newcastle upon Tyne, 2012. http://hdl.handle.net/10443/1551.

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The aims of this study were to undertake the first comprehensive in vitro, in vivo and clinical investigation into the effects of the PARP-1 inhibitor, AG014699, in human cancers defective in homologous recombination (HR) DNA double strand break (DSB) repair. HR deficient cells were 9-fold more sensitive to AG014699 than HR proficient cells (mean LC50 = 3.26 μM vs. 29.68; P < 0.0001), confirming the theory of synthetic lethality. BRCA1 methylated UACC3199 breast cancer cells were also sensitive to AG014699 with mean LC50 significantly lower than the HR proficient cells (7.6 μM vs. 29.68; P = 0

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Jdey, Wael. "Mécanismes de sensibilité/résistance des cellules tumorales aux inhibiteurs de réparation de l'ADN Dbait." Thesis, Université Paris-Saclay (ComUE), 2016. http://www.theses.fr/2016SACLS463/document.

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Les défauts dans les voies de réparation de l’ADN sont aujourd’hui largement exploités pour le traitement du cancer. En effet, la capacité des tumeurs à réparer les lésions induites par les traitements génotoxiques (chimio- et radiothérapie) leur confère une résistance intrinsèque ou acquise à ces traitements. Développer des inhibiteurs de réparation de l’ADN permettrait de contrecarrer cette résistance et de sensibiliser les tumeurs à ces thérapies conventionnelles. Les inhibiteurs de la Poly(ADP-ribose) polymérase (PARPi), premiers candidats de cette famille d’inhibiteurs de réparation de l’

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Coleman, Joshua B., Wesley Drew Gill, Allee C. Maxwell, and Russell W. Brown. "Analysis of a Poly(ADP-ribose) Polymerase (PARP) Inhibitor in a Treatment-resistant Depression Model in the Rat." Digital Commons @ East Tennessee State University, 2020. https://dc.etsu.edu/asrf/2020/presentations/53.

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Over 16 million people in the US suffer from major depressive disorder (MDD) each year. Approximately 1/3rd of MDD patients (~5 million) obtain only partial remission or no benefit after trials with multiple drugs or drug combinations. Recently, Ordway and colleagues have reportedelevated levels of DNA oxidation and upregulated gene expression of the base excision repair enzyme poly(ADP-ribose) polymerase-1 (PARP1) in postmortem brain from donors who had MDD at the time of death, as compared to age-matched psychiatrically normal control donors. This study was designed to test whether an inhibi

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Jewett, Benjamin E., Merry N. Miller, Libby A. Ligon, Zachary Carter, Ibrahim Mohammad, and Gregory A. Ordway. "Rapid and Temporary Improvement of Depression and Anxiety Observed Following Niraparib Administration: A Case Report." Digital Commons @ East Tennessee State University, 2020. https://dc.etsu.edu/etsu-works/8592.

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Background: Cancer patients are disproportionately affected by generalized anxiety and major depression. For many, current treatments for these conditions are ineffective. In this case report, we present a serendipitous case of anxiety and depression improvement following administration of the poly (ADP-ribose) polymerase (PARP) inhibitor niraparib. Case presentation: A 61-year old woman with a 20-year history of mild depression developed recurrent ovarian carcinoma and was placed on niraparib for maintenance chemotherapy. With the original onset of ovarian cancer, she experienced an episode

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27

Cartwright, Luke. "The potential of poly (ADP-ribose) polymerase (PARP) inhibitors to improve plant growth and yield : novel crop protection agents under stressed conditions." Thesis, University of Sheffield, 2017. http://etheses.whiterose.ac.uk/19289/.

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Chemical inhibition of the activity of poly (ADP-ribose) polymerases (PARPs) is associated with enhanced stress tolerance and growth in response to a broad range of abiotic plant stressors. This led to the suggestion that PARP inhibitors might have application in future crop protection strategies. However, the vast majority of studies to date have involved short-term, in vitro assays which are not representative of the conditions crop plants experience in the field. This work aimed to quantify the impact of chemical PARP inhibitor application on photosynthesis, growth and yield in planta, unde

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Burckel, Hélène. "Synthèse et évaluation de molécules bifonctionnelles alkylantes de l’ADN et inhibitrices de la PARP pour la radiochimiothérapie concomitante." Thesis, Strasbourg, 2012. http://www.theses.fr/2012STRAJ092.

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Cette étude a consisté en le développement et l’évaluation de nouvelles molécules pour la radiochimiothérapie concomitante. Ce travail a abouti à la conception de nouveaux agents chimiothérapeutiques duaux basés sur la combinaison covalente de deux radiosensibilisateurs: un inhibiteur de la PARP d’une part, et un alkylant de l’ADN (complexe de platine ou témozolomide) d’autre part. Les évaluations biologiques ont permis de mettre en évidence l’intérêt d’une molécule duale inhibiteur de la PARP/platine. Parallèlement à ce projet, le développement d’outils moléculaires pour l’étude d’inhibiteurs

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Weigert, Verena [Verfasser], Rainer [Akademischer Betreuer] Fietkau, and Luitpold [Gutachter] Distel. "PARP inhibitors combined with ionizing radiation induce different effects in melanoma cells and healthy fibroblasts / Verena Weigert ; Gutachter: Luitpold Distel ; Betreuer: Rainer Fietkau." Erlangen : Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU), 2021. http://d-nb.info/1231077956/34.

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Morice, Pierre-Marie. "Evaluation de la déficience de la recombinaison homologue et de la réponse des tumeurs ovariennes aux inhibiteurs de PARP grâce à l'utilisation de modèles de culture 3D en vue du développement d'un test prédictif Identifying eligible patients to PARP inhibitors: from NGS-based tests to promising 3D functional assays Automated scoring for assessment of RAD51-mediated homologous recombination in patient-derived tumor organoids of ovarian cancers Risk of myelodysplastic syndrome and acute myeloid leukemia related to PARP inhibitors: a combined approach using a safety meta-analysis of placebo randomized controlled trials and the World Health Organization's pharmacovigilance database The long non-coding RNA ‘UCA1’ modulates the response to chemotherapy of ovarian cancer through direct binding to miR-27a-5p and control of UBE2N levels." Thesis, Normandie, 2020. http://www.theses.fr/2020NORMC414.

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Chaque année, plus de 150 000 décès sont associés aux cancers épithéliaux de l’ovaire dans le monde, notamment en raison du développement d’une résistance à la chimiothérapie. Environ la moitié de ces cancers présentent des altérations moléculaires provoquant une déficience de la réparation de l’ADN par recombinaison homologue (HRD) qui les sensibilise à l’action des inhibiteurs de la protéine PARP (PARPi). A ce jour, il n’existe pas de test capable d’appréhender le phénotype HRD dans sa globalité, limitant ainsi l’accès à ces traitements. Dans ce contexte, nous avons entrepris de mettre au po

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Sulier, Kiaya Minh-Li. "Developing 1,2,3,4-tetrahydro-5H-aryl[1,4]diazepin-5-ones and Related Scaffolds as Poly-(ADP-ribosyl) Polymerase (PARP) Inhibitors and Exploring Their Targeted Polypharmacology with Kinases." Thesis, Virginia Tech, 2017. http://hdl.handle.net/10919/86200.

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Poly-(ADP-ribsoyl) Polymerases (PARPs) are a superfamily of enzymes comprised of 17 known isoforms. PARP inhibitors (PARPi) have shown success in clinical trials for the treatment of homologous recombination-deficient cancers. Though proven effective initially, tumors treated with PARPi eventually develop resistance. Combinatorial therapeutics targeting PARP and other pathways that may re-sensitize tumors to PARP inhibition, including PI3K/AKT/mTor pathway, and cell-cycle checkpoints (such as CDKs, CHK, and Wee) are being tested. In this context, the synthetic lethality of cyclin-dependent kin

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Chuang, Hsiao-Ching. "Mechanistic Validation of Potential Anti-Breast Cancer Therapeutics." The Ohio State University, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=osu1338213365.

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Grivas, Paul Christopher. "The role of poly (ADP-ribose) polymerase-1 inhibitors : prevention of non glutathione-dependent carbon tetrachloride-induced hepatotoxicity." [Tampa, Fla] : University of South Florida, 2007. http://purl.fcla.edu/usf/dc/et/SFE0001953.

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Engert, Florian [Verfasser], Volker Gutachter] Dötsch, and Simone [Gutachter] [Fulda. "PARP inhibitors in combination with chemotherapeutics target the underlying genetic phenotype of Ewing’s sarcoma and osteosarcoma to induce cell death or synthetic lethality / Florian Engert. Gutachter: Volker Dötsch ; Simone Fulda." Frankfurt am Main : Universitätsbibliothek Johann Christian Senckenberg, 2016. http://d-nb.info/1112601538/34.

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Engert, Florian Verfasser], Volker [Gutachter] Dötsch, and Simone [Gutachter] [Fulda. "PARP inhibitors in combination with chemotherapeutics target the underlying genetic phenotype of Ewing’s sarcoma and osteosarcoma to induce cell death or synthetic lethality / Florian Engert. Gutachter: Volker Dötsch ; Simone Fulda." Frankfurt am Main : Universitätsbibliothek Johann Christian Senckenberg, 2016. http://d-nb.info/1112601538/34.

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Steinbichler, Teresa Bernadette [Verfasser], Heinz Karl [Akademischer Betreuer] Höfler, and Irene [Akademischer Betreuer] Esposito. "Der Einfluss des PARP Inhibitors AZD2281 (Olaparib) auf das Wachstum von Mantelzelllymphomen in Abhängigkeit vom ATM und p53 Mutationsstatus / Teresa Bernadette Steinbichler. Gutachter: Irene Esposito ; Heinz Karl Höfler. Betreuer: Heinz Karl Höfler." München : Universitätsbibliothek der TU München, 2015. http://d-nb.info/1070624195/34.

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Kwan, Jair Chau Clinical School St Vincent's Hospital Faculty of Medicine UNSW. "Pharmacological activation of pro-survival pathways as a strategy for improving donor heart preservation." Awarded by:University of New South Wales. Clinical School - St Vincent's Hospital, 2009. http://handle.unsw.edu.au/1959.4/44663.

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Despite the development and use of specialised cardiac preservation solutions, the quality of the donor heart may still be compromised by its obligatory exposure to periods of ischaemia (both cold and warm) followed by reperfusion upon reintroduction of the recipient circulation. This is reflected in Transplant Registry data showing increased primary allograft failure as a function of increasing ischaemic time. The research described in this thesis is designed to further the understanding of the mechanisms by which the donor heart may be adapted to these prolonged periods of ischaemia and repe

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Croset, Amélie. "Identification et caractérisation des mécanismes d'action des molécules appats, les SiDNA, dans l'inhibition des voies de réparation des cassures simple-brin." Thesis, Paris 11, 2013. http://www.theses.fr/2013PA11T018.

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La plupart des traitements anticancéreux, comme la chimiothérapie ou la radiothérapie, sont cytotoxiques et causent des dommages à l'ADN dans le but d’induire la mort des cellules tumorales. Cependant, l’efficacité d’activité de réparation de l'ADN des tumeurs entraine des résistances intrinsèques et acquises aux traitements. L'une des étapes précoces de la réparation de l’ADN est le recrutement de protéines au niveau du site de dommage. Ce recrutement est coordonné par une cascade de modifications et est contrôlé par des protéines senseurs telles que la protéine kinase ADN dépendante (DNA-PK)

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Billaud, Amandine. "Analyse moléculaire, enjeux et limites des thérapies ciblées en oncologie : extension des sensibilités aux anti-PARP dans les cancers ovariens par caractérisation de variants non annotés et nouveaux mécanismes de résistance dans les cancers bronchiques. Caractérisation moléculaire de l’EGFR dans les cancers bronchiques non à petites cellules : étude prospective comparative des technologies NGS et automate Idylla Somatic mRNA analysis of BRCA1 splice variants provides a direct theranostic impact on PARP inhibitors." Thesis, Angers, 2020. http://www.theses.fr/2020ANGE0003.

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Malgré les bénéficies cliniques considérables de la prise en considération du contexte moléculaire tumoral, les thérapies ciblées présentent certaines limitations majeures. La première partie de ces travaux se concentre sur l’étude des inhibiteurs de tyrosine kinase ciblant l’EGFR dans les cancers bronchiques non à petites cellules. L’amélioration des méthodes de détection des biomarqueurs a été complétée par la caractérisation in vitro d’un mécanisme de résistance acquise non précédemment identifié. L’exposition de cellules pulmonaires à un agent mutagène puis une pression de sélection a ains

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Martin, Nadine. "Rôle de la SUMO E3 ligase PIASy dans les mécanismes de contrôle de la prolifération cellulaire et de réponse aux dommages." Paris 6, 2007. http://www.theses.fr/2007PA066243.

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La modification des protéines par SUMO joue un rôle important dans de nombreuses fonctions cellulaires. Le travail présenté dans cette thèse vise à analyser l'action des protéines PIAS, régulateurs transcriptionnels et SUMO E3 ligases, et en particulier de PIASy dans le contexte de l'oncogenèse. Nous avons montré que PIASy induit la sénescence des fibroblastes primaires, en activant les voies Rb et p53, ou l'apoptose si la voie Rb est déficiente. Nous avons parallèlement identifié de nouveaux partenaires protéiques de PIASy. PIASy induit l'accumulation de FIP200 dans le noyau, ce qui inhibe l'

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Hassanein, Mohamed. "Facteurs prédictifs de mutation germinale BRCA1 dans le cancer du sein héréditaire." Thesis, Aix-Marseille 2, 2010. http://www.theses.fr/2010AIX20714.

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En France, le cancer de sein héréditaire représente environ 2500 nouveaux cas par an, dont prés de la moitié est attribuée à la mutation du gène BRCA1.La recherche de la mutation par biologie moléculaire est un travail fastidieux, coûteux et long (8 mois d’attente environ actuellement).Pour trouver une solution à ce délai, nous avons étudié en immunohistochimie une série initiale de 21 anticorps répartis en 5 groupes : anticorps antiBrca1 du commerce, liés à la perte de l’inactivation de l’X, liés à la signature basale ou myoépithéliale, anticorps dits classiques du cancer de sein et finalemen

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Magro, Tatiana Natália Tavares. "Testing the combinatory use of PARP1 and RPA inhibitors in breast cancer cell lines." Master's thesis, 2019. http://hdl.handle.net/10773/29527.

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Loss of tumor suppressor BRCA2 is strongly associated to breast cancer. BRCA2 is essential to homologous recombination (HR), which is a DNA repair pathway crucial to genomic stability. When cells become mutant for BRCA2, they cannot repair DNA damage through homologous recombination, which is an accurate repair pathway, and instead, rely on alternative error-prone pathways for DNA repair. Tumor cells mutant for BRCA2 become therefore dependent on these alternative repair pathways for survival. The most recent generation of targeted therapies for breast cancer is PARP1 inhibitors. PARP1 is a p

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Dziaková, Lucia. "Studium interakcí PARP inhibitorů s ABC lékovými efluxními transportéry." Master's thesis, 2020. http://www.nusl.cz/ntk/nusl-411910.

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Charles University Faculty of Pharmacy in Hradec Králové Department of Pharmacology & Toxicology Student: Lucia Dziaková Supervisor: RNDr. Jakub Hofman, Ph.D. Title of diploma thesis: Study on interactions of PARP inhibitors with ABC drug efflux transporters. ATP-binding cassette (ABC) transporters are integral membrane proteins that use the energy obtained from ATP to carry transport of numerous endogenous substrances out of the cells, but attention is drawn primarily to the fact that they transfer also xenobiotics. Their overexpression in tumor tissue contributes to multidrug resistance (MDR

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Aubert-Jürgens, Ana. "STAT3 inhibitors for cancer treatment." Phd thesis, 2005. https://tuprints.ulb.tu-darmstadt.de/563/1/aubert-jurgens-part1.pdf.

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The critical role of the activation of signal transducer and activator of transcription 3 (STAT3) in the growth and survival of human tumor cells was one of the subjects of this thesis. It was found that the stable incorporation of v-Src into MCF10A cells, a human immortalized breast epithelial cell line, induced constitutive phosphorylation of STAT3 in these cells. MCF10A-v-Src cells displayed growth factor independence for proliferation and survival, and anchorage independence. However, these cells did not form tumors in nude mice, indicating that they were not fully transformed. Furthermore

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Sohail, Honeah. "PARP inhibitor ABT-888 as potentiating agent for topoisomerase inhibitor SN-38." 2009. http://hdl.rutgers.edu/1782.2/rucore10001600001.ETD.000051407.

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Allison, Simon J., Maria Sadiq, Efstathia Baronou, et al. "Preclinical anti-cancer activity and multiple mechanisms of action of a cationic silver complex bearing N-heterocyclic carbene ligands." 2017. http://hdl.handle.net/10454/11960.

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Yes<br>Organometallic complexes offer the prospect of targeting multiple pathways that are important in cancer biology. Here, the preclinical activity and mechanism(s) of action of a silver-bis(N-heterocyclic carbine) complex (Ag8) were evaluated. Ag8 induced DNA damage via several mechanisms including topoisomerase I/II and thioredoxin reductase inhibition and induction of reactive oxygen species. DNA damage induction was consistent with cytotoxicity observed against proliferating cells and Ag8 induced cell death by apoptosis. Ag8 also inhibited DNA repair enzyme PARP1, showed preferent

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Nikoloska, Irena. "Towards the Synthesis of Novel PARP Inhibitors through Diels-Alder Chemistry." Thesis, 2012. http://hdl.handle.net/10214/3561.

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Poly(ADP-ribose) polymerase (PARP) represents a large family of enzymes that are activated upon DNA breakage, which are then involved in a cascade of reactions that eventually lead to cell death. PARPs, known to cause a variety of damage to the human body, are targets of many researches’ investigating potential inhibition mechanisms. To this point, plenty of PARP inhibitors have been synthesized and tested for potency against many diseases. Some have great potency against particular diseases, while others are already being used as drugs. The current research suggests a potential synthesis of n

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Mishra, Anup. "Targeting RAD51C Pathological Mutants by Synthetic Lethality and Extended Functions of RAD51C/XRCC3 in Mitochondrial Genome Maintenance." Thesis, 2017. http://etd.iisc.ac.in/handle/2005/4155.

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To counteract the potentially calamitous effects of genomic instability in the form of double-strand breaks (DSBs), cells have evolved with two major mechanisms. First, DNA non¬homologous end joining (NHEJ) which requires no significant homology, and second, homologous recombination (HR) that uses intact sequences on the sister chromatid or homologous chromosome as a template to repair the broken DNA. Although NHEJ repairs DSBs in all stages of cell cycle; it is generally error-prone due to insertions or deletions of few nucleotides at the breakpoint. In contrast, DSBs that are generated durin

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Wang, Wei-Jie, and 王為婕. "Mechanisms of SAHA and PARP Inhibitors Induced Cell Death in Cancer Cells." Thesis, 2015. http://ndltd.ncl.edu.tw/handle/34790258374946152730.

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碩士<br>國立陽明大學<br>生命科學系暨基因體科學研究所<br>103<br>I. Combination therapy of SAHA and PARP inhibitors in HCC treatment Genomic instability is one of the cancer hallmarks. Because severe DNA damage results in cell death, inhibitors of the DNA repair system can be used as anticancer drugs. An inhibitor of histone deacetylases (HDACs) - suberoylanilide hydroxamic acid (SAHA), is being evaluated for phase2/3 clinical trial to treat several types of cancers. Mechanism of SAHA-induced cell death is not totally clear, but reactive oxygen species (ROS) release and double strand break (DSB) may play a role in ap

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Meyer, Stephanie C. "Synergistic effects of combining PARP inhibitor (AZD2281) and ATR inhibitor (AZD6738) in Ewing Sarcoma cell lines." Thesis, 2018. https://hdl.handle.net/2144/30818.

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Ewing Sarcoma (ES) is an aggressive pediatric solid tumor. Even though overall-survival for localized patients is approximately 70%, the overall-survival for high risk ES patients has not improved in the last 20 years. Therefore, there is a need for exploration of new therapeutic agents in ES. Recent evidence has demonstrated that ES cells behave like BRCA-deficient tumor types which renders them sensitive to PARP inhibitors in vitro and in vivo. However, a phase II study of the efficacy of single-agent PARP inhibition in patients with relapsed ES did not significantly improve outcome. As sing

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