Tesis sobre el tema "Anthracyclines"
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Nedonchelle, Agnès. "Synthèse énantiospécifique et activité de nouvelles anthracyclines". Paris 5, 1988. http://www.theses.fr/1988PA05P603.
Texto completoHuguen, Thierry. "Analyse par chimiluminescence : application au dosage des anthracyclines". Paris 5, 1991. http://www.theses.fr/1991PA05P010.
Texto completoHEMAMOU, MOHCINE. "Analyse chromatographique des anthracyclines". Amiens, 1988. http://www.theses.fr/1988AMIEM080.
Texto completoKulkarni, A. D. "Synthesis of analogues of anthracyclines". Thesis(Ph.D.), CSIR-National Chemical Laboratory, Pune, 1986. http://dspace.ncl.res.in:8080/xmlui/handle/20.500.12252/3250.
Texto completoFrançois, Anne. "Toxicité comparative des anthracyclines et des anthracène-diones". Paris 5, 1993. http://www.theses.fr/1993PA05P001.
Texto completoYoung, Charlene Rebecca. "Rational drug design : an information driven approach to the design of an anthracycline analog /". [Boise, Idaho] : Boise State University, 2009. http://scholarworks.boisestate.edu/td/10/.
Texto completoGallois, Laurence. "Interaction des anthracyclines avec des membranes". Paris 13, 1996. http://www.theses.fr/1996PA132031.
Texto completoHarper, Mark F. "Studies on heterocyclic compounds related to anthracyclines". Thesis, Heriot-Watt University, 1985. http://hdl.handle.net/10399/1613.
Texto completoNicholson, J. R. "Redox inactive ring C - aglycones of anthracyclines". Thesis, Teesside University, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.383678.
Texto completoNOBILI, PIERI NATHALIE. "Les anthracyclines : administration intraveineuse en perfusion continue". Aix-Marseille 2, 1994. http://www.theses.fr/1994AIX20116.
Texto completoBaracco, Elisa. "Rôle du profile immunogénétique des patients dans la réponse à la chimiothérapie". Thesis, Université Paris-Saclay (ComUE), 2018. http://www.theses.fr/2018SACLS153.
Texto completoAntitumor immunity driven by intratumoral dendritic cells contributes to the efficacy of anthracycline-based chemotherapy in cancer. We identified a loss-of-function allele of the gene coding for formyl peptide receptor 1 (FPR1) that was associated with poor metastasis-free and overall survival in breast and colorectal cancer patients receiving adjuvant chemotherapy.The therapeutic effects of anthracyclines were abrogated in tumor-bearing Fpr1(-/-) mice due to impaired antitumor immunity. Fpr1-deficient dendritic cells failed to approach dying cancer cells and, as a result, could not elicit antitumor T cell immunity.Experiments performed in a microfluidic device confirmed that FPR1 and its ligand, annexin-1, promoted stable interactions between dying cancer cells and human or murine leukocytes.We investigated also the possible contribution of FPR1 to the efficacy of a combination of mitoxantrone (MTX) and cyclophosphamide (CTX) for the treatment of hormone-induced breast cancer.Breast cancer induced by a combination of medroxyprogesterone acetate (MPA) and 7,12-Dimethylbenz[a]anthracene (DMBA) could be successfully treated with MTX plus CTX in thus far that tumor growth was retarded and overall survival was extended (as compared to vehicle-only treated controls).However, the therapeutic efficacy of the combination therapy was completely abolished when FPR1 receptors were blocked by means of cyclosporin H (CsH). Future genetic studies on neoadjuvant chemotherapy-treated breast cancers are warranted to validate these findings at the clinical level.Altogether, these results highlight the importance of FPR1 in chemotherapy-induced anticancer immune responses
Ellenberger, William Paul. "Synthesis of DEF ring synthons to nogarol anthracyclines /". Full text open access at:, 1987. http://content.ohsu.edu/u?/etd,136.
Texto completoScalabrin, Matteo. "Analysis of cross-linking between DNA and anthracyclines". Doctoral thesis, Università degli studi di Padova, 2011. http://hdl.handle.net/11577/3422017.
Texto completoLe antracicline sono un’importante famiglia di chemioterapici, tra queste sono usate prevalentemente l’adriamicina (doxorubicina), la daunorubicina, l’idarubicina e l’epirubicina. Sono farmaci con un ampio spettro d’azione, in particolare l’adriamicina è usata nel trattamento del cancro al seno, del linfoma di Hodgkin, del cancro al polmone, del mieloma multiplo e del cancro ovarico recidivo. Nonostante l’ampio spettro d’azione la resistenza e la severa cardiotossicità limitano l'uso di questi importanti farmaci anticancro. La ricerca di migliori derivati ha dato luogo a più di 2000 analoghi dei quali solamente pochi di essi hanno raggiunto l’approvazione clinica. Anche se il meccanismo esatto con il quale l’adriamicina esercita l’attività anticancro è incerta, il meccanismo principale coinvolge un danno nei confronti dell’enzima topoisomerasi II, un meccanismo supportato dall’intercalazione nel DNA e dalla localizzazione nucleare. La ricerca di antracicline meno tossiche e più efficaci ha portato alla scoperta della nemorubicina, un derivato della doxorubicina in cui l'azoto amminico della daunosamina è incorporato in un anello metossimorfolinico. Le indagini precliniche hanno mostrato che la nemorubicina, diversamente dalle antracicline classiche non è cardiotossica e l'attività antitumorale è mantenuta nei vari modelli di tumore resistenti alla terapia. Risultati incoraggianti sono stati ottenuti in fase I/II dove il composto è stato somministrato attraverso l’arteria intraepatica. La nemorubicina è 80-120 più potente della doxorubicina in vivo, diversamente la sua attività in vitro è solamente otto volte rispetto alla doxorubicina verso culture cellulari tumorali sensibili alle antracicline. Un recente studio ha stabilito che la nemorubicina è convertita dall’enzima CYP3A in un metabolita estremamente più citotossico, il PNU-159682. Questo metabolita è risultato dalle 700 alle 2400 volte più potente rispetto al progenitore nemorubicina verso cellule cancerose umane in coltura e ha mostrato un’efficacia significativa in diversi modelli di tumore in vivo. Studi in corso finalizzati a definire il meccanismo molecolare di azione di PNU-159682 indicano differenti effetti sul ciclo cellulare e una differente interazione col DNA rispetto al progenitore nemorubicina e alla doxorubicina. Inoltre, dati recenti indicano che PNU-159682 mantiene la sua attività anche verso cellule aventi diversi meccanismi di resistenza rispetto a diversi agenti anticancro classici, inclusa la sovraespressione del gene MDR-1, la riduzione dell’attività di topoisomerasi II e mutazioni nel gene codificante per la topoisomerasi I: quest’ultima modifica genetica conferisce resistenza in vitro alla nemorubicina [1]. Noi abbiamo usato diversi approcci sperimentali per razionalizzare l’elevata attività di questo metabolita. Test condotti in vitro nel nostro laboratorio con kinetoplast DNA hanno confermato l'inattività del metabolita nei confronti della topoisomerasi II. L'assenza dell'attività verso la topoisomerasi ci suggerisce che l’alta citotossicità di questo metabolita è da ricercarsi altrove. Antracicline come doxorubicina e daunorubicina possono legare covalentemente il DNA quando attivate con formaldeide. Inoltre è stato trovato che antracicline che hanno un’intrinseca attività a formare cross-link col DNA come la cianomorfolino-doxorubicina o la barminomicina posseggono un’alta citotossicità comparabile col PNU. Quindi abbiamo considerato la possibilità che il PNU interagisca col DNA come una antraciclina preattivata. Il nostro lavoro ha evidenziato che il PNU si comporta in modo analogo alla doxorubicina attivata (doxorubicina con formaldeide) nelle analisi di melting del DNA. PNU reagisce velocemente con oligonucleotidi a doppio filamento per formare addotti visualizzati in DPAGE. Questi addotti sono sufficientemente stabili per essere isolati tramite HPLC. La caratterizzazione ottenuta tramite spettrometria di massa ha confermato che questi complessi sono formati da DNA a doppio filamento legato all’antraciclina. Questi studi suggeriscono che la reazione tra PNU e DNA non coinvolge la formazione di un classico cross-link, ma in relazione ai risultati elettroforetici, cromatografici e di spettrometria di massa questi addotti possono essere annoverati nella famiglia dei “virtual cross-link” (VXL). I coniugati antracicline-formaldeide o le antracicline in tampone contenente formaldeide hanno la specifica abilità di intercalarsi nel DNA formando legami covalenti; un ponte etilenico lega l’ammino gruppo dell’antraciclina col 2-amino gruppo della base guaninica nel solco minore, mentre l’ altra catena del DNA è stabilizzata tramite legami idrogeno. Questa particolare combinazione di intercalazione, legame covalente e legame ad idrogeno è chiamata virtual cross-link (VXL) [2], che porta alla formazione di complessi più stabili tra le antracicline e il DNA aumentando la tossicità cellulare delle antracicline. Tra i diversi meccanismi anticancro delle antracicline, la formazione di addotti DNA-antracicline ha suscitato notevole interesse riferito alla possibilità di trovare nuovi farmaci anticancro più sicuri e più efficaci. I coniugati antraciclina-formaldeide e le antracicline cross-linkanti esibiscono un’elevata citotossicità comparabile con i classici agenti cross-linkanti. Abbiamo usato differenti antracicline con lo scopo di razionalizzare il rapporto struttura attività nella formazione del VXL. Abbiamo confermato attraverso l’analisi elettroforetica e cromatografica che l’amminozucchero e l’azoto amminico sono assolutamente necessari per la formazione del “VXL” e abbiamo discusso il ruolo della posizione 4' nella daunosamina nella modulazione di questa attività. La presenza del ponte metilenico e la sua relazione con la guanina è stata confermata mediante spettrometria di massa.
Borate, H. B. "Studies directed towards the total synthesis of anthracyclines". Thesis(Ph.D.), CSIR-National Chemical Laboratory, Pune, 1985. http://dspace.ncl.res.in:8080/xmlui/handle/20.500.12252/3247.
Texto completoFourré, Nicolas. "Microenvironnement cellulaire et réponse de la cellule tumorale au médicament : impact du microenvironnement sur les propriétés anti-migratoires des anthracyclines". Reims, 2007. http://www.theses.fr/2007REIMP209.
Texto completoThe @aim of our study was to evaluate the role of the microenvironment on the anti-migratory abilities of doxorubicin on HT-1080 cell line. In this context, two models of cell culture have been used: one on a 2D-coated substrate with extracellular matrix proteins (type I collagen or fibronectin) and the other one in a 3D collagen matrix mimicking an in vivo environment. Control experiments on plastic showed that subtoxic doses of doxorubicin exhibit a significant anti-migratory effect by totally disorganizing actin stress fibers and by modifying vinculin distribution. However, the anti-migratory effect of the drug is totally inhibited in presence of matrix proteins. This protection could be due to the preservation of the activation states of RhoA GTPase, which are necessary for the formation of actin stress fibers, and of FAK, implicated in the formation of focal adhesions. The study carried out in a 3D matrix demonstrates that this type of microenvironment can act as a physical barrier by delaying the biodistribution of doxorubicin. Long-term incubations, avoiding the barrier effect, show that the protectory effect to doxorubicin anti-migratory effect is less important and is not followed by a modification of FAK activation. In conclusion, the microenvironment is able to protect the tumor cell from the anti-migratory effect of a drug. However, this effect is very dependent on culture conditions, which underlines the extreme adaptability of the cell to its environment. In comparison to previous work on the cytotoxic effect of drugs, our results demonstrate that the microenvironment should be taken into account in the study of pharmacological properties of anti-tumor drugs
Moustatih, Abderrahmane abderrahmane. "Synthèse et caractérisation de composés bifonctionnels à propriétés antitumorales : étude de leur mécanisme d'action". Paris 13, 1989. http://www.theses.fr/1989PA132017.
Texto completoCoburn, Charles E. "The synthetic studies of 6-deoxyanthracyclinones /". The Ohio State University, 1985. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487257452613312.
Texto completoFourré, Nicolas Jeannesson Pierre. "Microenvironnement cellulaire et réponse de la cellule tumorale au médicament impact du microenvironnement sur les propriétés anti-migratoires des anthracyclines /". S.n. : S.l, 2007. http://scdurca.univ-reims.fr/exl-doc/GED00000613.pdf.
Texto completoCOSTA, BRIGITTE. "La toxicite cardiaque des anthracyclines et des autres traitements anticancereux". Reims, 1994. http://www.theses.fr/1994REIMM009.
Texto completoDekleva, Michael Louis. "Intermediary metabolism of Anthracycline-producing Streptomycetes /". The Ohio State University, 1987. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487326511715642.
Texto completoBaghdanov, Vaceli M. "Synthetic studies of naturally occurring hydroxylated polycyclic compounds : daunomycinone and pillaromycinone /". Full text open access at:, 1987. http://content.ohsu.edu/u?/etd,142.
Texto completoMancini, Michael. "Approaches to the synthesis of xanthone analogs of the anthracycline class of anticancer agents". Thesis, McGill University, 1985. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=72059.
Texto completoThe condensation of tetralin 2-acetyl-5,8-dimethoxy-1,2,3,4-tetrahydro-2-naphthol with o-methoxybenzoic acid was investigated and useful large-scale syntheses of important 1,4-dimethoxy-substituted xanthone intermediates were developed.
Diels-Alder cycloaddition reaction between a xanthone-derived o-quinodimethane intermediate and an olefin afforded a low yield of adduct. On the other hand, excellent yields of isolable but labile adducts were obtained in the cycloaddition reaction between xanthoquinone (and also thioxanthoquinone) and Danishefsky's dienes. The formation of linear vs internal adducts was rationalized on the grounds of resonance and FMO theory. Efforts to induce unactivated dienes to cycloadd using catalysts as well as annulation studies on model compounds using the novel reagent (E)-N-vinylpyrrolidine-(beta)-(2-lithio-1,3-dithian-2-yl) (as a synthon of the (alpha),(beta)-dianion of acetaldehyde) are discussed.
The synthesis of daunomycin and xanthodaunomycin analogs carrying a carbon substituent at position 7 were not accessible using the Diels-Alder cycloaddition reaction as diene 1-carbomethoxy-3-triethylsilyloxy-1,3-butadiene failed to react with either quinizarinquinone or xanthoquinone even at elevated temperatures.
The compound 4-hydroxy-1- 2- (2-hydroxyethyl)amino ethyl amino xanthone and the 4-methoxy derivative were prepared and found to be inactive in the in vivo P-388 mouse leukemia model system.
Bozak, Karen Aline 1960. "ANTHRACYCLINE CARDIOTOXICITY MODELING USING INTRACELLULAR ATP LEVELS IN NEONATAL RAT HEART CELL CULTURES (CHEMOTHERAPY, DOXORUBICIN, MYOCYTES)". Thesis, The University of Arizona, 1986. http://hdl.handle.net/10150/276748.
Texto completoBour, Dill Corinne. "Distribution intracellulaire des anthracyclines : implication dans le processus de mort cellulaire induite et le phénotype de résistance pléiotrope". Nancy 1, 2001. http://docnum.univ-lorraine.fr/public/SCD_T_2001_0275_BOUR-DILL.pdf.
Texto completoBel, Haj-Tayeb Hayet. "Interaction d'anthracyclines et de cyclopropylpyrrolindoles et de cyclopropylpyrrolindoles avec les cations métalliques : études spectroscopiques". Paris 13, 1996. http://www.theses.fr/1996PA132022.
Texto completoWedge, Stephen Robert. "Mechanism of action of polymer-anthracyclines : potential to overcome multidrug resistance". Thesis, Keele University, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.293794.
Texto completoBennani, Fatima-Zahra. "Nouvelle voie d’accès aux déméthoxy-4 anthracyclines à partir d’acides sacchariniques". Paris 11, 1985. http://www.theses.fr/1985PA112055.
Texto completoA seven steps synthesis of (+)-4-déméthoxy-9-déacétyl-9-hydroxyméthyl daunomycinone is described with an overall yield of ~20 to 30%. The strategy of the tetracyclic ring construction required two successive aldol condensation reactions (inter and intramolecular) under Lewis or Marschalk conditions between leucoquinizarine (DCB ring) and an aldehyde derived from the α-D-isosaccharino-1,4 lactone (precursor of ring A). The use of this highly functionalized carbohydrate avoids the incorporation of the hydroxyl groups at C-7 and/or C-9 at the last stage. Two noteworthy aspects of the synthesis were the stereocontrolled sequence and the stereospecific cyclization leading exclusively to the natural configuration 7(s), 9(s) cis of anthracyclinones. The anthracycline resulting from the coupling with 2-déoxy-L-fucose chloride is great interest since the first cytotoxicity tests show a similar activity in vitro to that of doxorubicin
WALLET, FRANCE. "Etude de la sensibilite aux anthracyclines de l'epithelium mammaire humain tumoral". Aix-Marseille 2, 1993. http://www.theses.fr/1993AIX20056.
Texto completoDonatiello, Cosima. "La toxicité cardiaque des anthracyclines dans le traitement des tumeurs de l'enfant /". Genève : [s.n.], 2002. http://www.unige.ch/cyberdocuments/theses2002/DonatielloC/these.pdf.
Texto completoEng, Jamei Raena. "Localization of anthracyclines in drug resistant human MCF-7 breast cancer cells". Thesis, University of Ottawa (Canada), 2007. http://hdl.handle.net/10393/27841.
Texto completoGARDELLE, FRANCOIS. "Cardiomyopathie aux anthracyclines et transplantations cardiaques : a propos de 2 observations pediatriques". Clermont-Ferrand 1, 1994. http://www.theses.fr/1994CLF1M025.
Texto completoAszodi, Attila. "Études synthétiques dans le domaine des antibiotiques : les anthracyclines et les aminoglycosides". Paris 11, 1988. http://www.theses.fr/1988PA112160.
Texto completoTwo types of antibiotics were studied in this thesis: anthracyclines and aminoglycosides. The first chapter deals with anthracyclines in which the synthesis of new classes of anthracyclines, hopefully with reduced cardiotoxicity, were attempted. Two approaches were explored:1- Substitution of the benzylic group at position 7 by different alcoholates,2- DIELS-ALDER cycloaddition of a dienophile (epoxytetrone) to a diene bearing chiral cyclohexane substituant. This leads essantially in one step ta the tetracyclic skeleton with a good asymetrie induction. The second chapter deals with the preparation of 1,4-diaminocyclitol which based on a Ferrier rearrangement. The second amine is introduced by oximation follow by reduction
Labroille, Gilles. "Etude de mécanismes de résistance de cellules leucémiques traitées par les anthracyclines". Bordeaux 2, 2000. http://www.theses.fr/2000BOR28744.
Texto completoAszodi, Bernadette. "Etudes synthétiques dans le domaine des antibiotiques les anthracyclines et les aminoglycosides /". Grenoble 2 : ANRT, 1988. http://catalogue.bnf.fr/ark:/12148/cb376114703.
Texto completoSultana, Azmiri. "Mechanistic insights into the biosynthesis of polyketide antibiotics /". Stockholm, 2006. http://diss.kib.ki.se/2006/91-7357-010-9/.
Texto completoXu, Xiangcong. "THE MOLECULAR MECHANISMS OF IRON AND FERRITIN METABOLISM IN NORMAL AND NEOPLASTIC CELLS". Thesis, The University of Sydney, 2008. http://hdl.handle.net/2123/3535.
Texto completoCottin, Yves. "Cardiotoxicité des anthracyclines : incidences fonctionnelles et métaboliques chez le rat. Apport de l'angioscintigraphie". Dijon, 1998. http://www.theses.fr/1998DIJOMU06.
Texto completoRibeiro, Maxance. "EPAC1 : une nouvelle cible thérapeutique pour limiter la cardiotoxicité induite par les Anthracyclines". Thesis, Université Paris-Saclay (ComUE), 2018. http://www.theses.fr/2018SACLS509/document.
Texto completoDoxorubicin (Dox) is an Anthracycline commonly used to treat many types of cancer; unfortunately this chemotherapeutic agent often induces side effects such as cardiotoxicity leading to cardiomyocyte death and dilated cardiomyopathy (DCM). This cardiotoxicity has been related to reactive oxygen species generation, DNA intercalation, topoisomerase II inhibition and bioenergetics alterations resulting in DNA damages and ultimately in cardiomyocyte death. Nevertheless, complete molecular mechanisms are not yet identified. Therefore, there is a need for new treatment options and strategies aiming at reducing Dox side effects in the heart. Among these mechanisms, EPAC1 (Exchange Protein directly Activated by cAMP) signaling could be worth investigating as EPAC1 indirectly activates small G proteins (Rac1 and Rho A), which are known to be involved in Dox-induced cardiotoxicity. Therefore, we have investigated the effect of Dox on EPAC1 signaling in both in vivo mice model (C57BL/6 vs EPAC1 KO mice, iv injections, 12mg/kg) and in vitro model (primary culture of neonatal rat cardiomyocytes (NRVM), Dox 1μM). In vivo, Dox-treated mice developed a DCM associated with Ca2+ homeostasis dysfunction. In vitro, Dox induced DNA damages and cell death associated with huge mitochondrial disorders, characterized by a decrease in mitochondrial biogenesis and respiratory chain activity. This cell death is associated with apoptotic features including mitochondrial membrane permeabilization, caspase activation, cell size reduction and relative plasma membrane integrity. We also observed that Dox led to a modification of the protein level and the activity of EPAC1 in the same manner to the cAMP level. By contrast, the inhibition of EPAC1, prevented DNA/TopIIβ complexes, decreased Dox-induced DNA damages, loss of mitochondrial membrane potential, apoptosis and finally cardiomyocyte death. Mitochondrial biogenesis and respiratory chain activity operated normally when EPAC1 was inhibited. These results were confirmed in vivo since Dox-induced cardiotoxicity was prevented in EPAC1 KO mice as evidenced by unaltered cardiac function (no DCM) at 15 weeks post-treatment. Interestingly, the protection conferred by EPAC1 inhibition was not transferred in human cancer cell lines treated by Dox. Inhibition of EPAC1 could thus be a valuable therapeutic strategy to limit Dox-induced cardiomyopathy during cancer chemotherapy
Ghirmai, Senait. "Synthesis of Organic Compounds for Nuclide Therapy : Derivatives of Carboranes, 9-Aminoacridine and Anthracyclines". Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2004. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-4264.
Texto completoFiallo, Maria Lorenzo. "Une Nouvelle classe d'antitumoraux : les complexes metal-anthracyclines, synthèse, caractéristiques physicochimiques et propriétés tumorales". Paris 13, 1986. http://www.theses.fr/1986PA132003.
Texto completoSavatier, Julien. "Chimiothérapie et oxygénothérapie : étude de la potentialisation de la chimiothérapie en milieu hyperoxygéné". Perpignan, 2004. http://www.theses.fr/2004PERP0581.
Texto completoHypoxia of tumor cells limits the effectiveness of treatments which can be improved by an increase of available oxygen at tumor level. However, modes of action of hyperoxygenation at cellular level are still poorly understood. We used videomicrofluorometry and triple labeling on living cells to measure nuclear dna (hoechst 33342), mitochondrias energetic state (rhodamine 123) and plasma membrane properties (nile red). The morphological and functional parameters obtained for each cell allowed us, using typology and discriminant factorial analysis, to define a reference population of ccrf-cem lymphoblatsic cells. We determined their distribution in cell cycle phases (g0-g1, s, g2+m and polyploid cells gn). This population enabled us to analyze the effects of adriamycin (adr) on ccrf-cem. At 200 ng. Ml-1 cells were stopped in gn phase, while at 1000 ng. Ml-1 dna denaturation froze cellular populations. Apoptosis was also highlighted. We compared adr with idarubicine (ida), an anthracycline which is kown to generate few free radicals. Results obtained under different oxygenation conditions (20 to 95%) revealed only a few effects of oxygen and no difference between adr and ida. The increase of partial pressure of oxygene does not seem to modify the modes of actions of these drugs. We can put forward the hypothesis that the gain of efficiency linked to hyperoxygenation is already obtained for cells under normoxic conditions (20%) compared to tumor hypoxia (~5%)
LE, BOT MARIE-ANNICK. "Contribution a l'etude analytique, metabolique in vitro et pharmacocinetique d'agents anticancereux de la famille des anthracyclines". Rennes 1, 1990. http://www.theses.fr/1990REN1B010.
Texto completoGuenancia, Charles. "Implications du stress oxydant et du fer dans la cardiotoxicité des anthracyclines et du trastuzumab". Thesis, Dijon, 2015. http://www.theses.fr/2015DIJOMU03/document.
Texto completoCancer treatment has advanced considerably in recent years, allowing a reduction in mortality. Longer life expectancy of patients has helped to highlight the delayed onset of cardiovascular toxicity induced by these chemotherapies. The pathophysiological mechanisms responsible for these cardiac dysfunctions are complex, entangled and remain partially unknown. A better understanding of the phenomena involved in these cardiotoxicities is needed to prevent their occurrence. Therefore, we have developed two different experimental approaches to understand the pathophysiological mechanisms involved in the cardiac toxicity of anthracyclines and trastuzumab.A first experimental study aimed to clarify the role of iron in heart failure induced by anthracyclines. We have demonstrated that a tissular iron overload in mice prior to doxorubicin injection does not increase the cardiotoxicity of chemotherapy. On the contrary, the involvement of anti-radical defenses following the iron load could reduce cardiac oxidative damage generated by doxorubicin. In view of these data, the role of iron chelators in cardioprotection against anthracyclines has to be questioned.Our second experimental work was to elucidate the role of overweight in the development of anthracycline and trastuzumab cardiotoxicity. Using a mouse model of moderate overweight and of increased risk of cardiometabolic induced postnatal programming, we have highlighted the role of overweight on the development of anthracycline cardiotoxicity; whereas trastuzumab cardiotoxicity did not appear to be increased by overweight. Our work also clarified the conditions in which there are cumulative cardiac alterations when doxorubicin and trastuzumab are associated
Praet, Michel. "Etude du mécanisme moléculaire responsable de la toxicité mitochondriale des anthracyclines-rôle des radicaux libres". Doctoral thesis, Universite Libre de Bruxelles, 1991. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/212994.
Texto completoBedja, Djahida Graduate School of Biomedical Engineering Faculty of Engineering UNSW. "Anthracyclines used in the treatment of cancer: their harmful effects on the Reno-cardiovascular connection". Publisher:University of New South Wales. Graduate School of Biomedical Engineering, 2008. http://handle.unsw.edu.au/1959.4/41501.
Texto completoRharass, Tareck. "Potentialisation de la chimiothérapie en milieu oxygéné : implication des radicaux libres dans l'effet des anthracyclines". Perpignan, 2007. http://www.theses.fr/2007PERP0815.
Texto completoTumour hypoxia is causally related with resistance to adriamycin (ADR) treatment. However, how hyperbaric oxygen therapy leads to therapeutic gain of the drug is unclear. We investigated the relation of reactive oxygen species (ROS) generation with anti-tumoural effect of ADR on human lymphoblastic CCRF-CEM cells under hypoxic (2% O2) and normoxic (21% O2) conditions. A new method was used to measure intracellular ROS variations through the fluorescence lifetime of 1-pyrenebutyric acid. Numerical image analysis of cell populations labelled with different vital stains allowed to collect morphometric (cellular and nuclear sizes) and physiological (mitochondrial activity, DNA content) informations used to (i) quantify apoptosis induction, and (ii) determine the cell cycle distribution through multiparametric analysis of collected data. We observed that oxygen level has no effect on the cell cycle arrest induced by ADR, whereas apoptosis induction and ROS production resulting from treatment are higher under oxygenated conditions (i. E. Normoxia). Considering normoxia as a hyperoxygenated condition compared to in vivo hypoxic tumour level, we suggested that improvement of anti-cancerous effect of ADR due to hyperbaric oxygen therapy results from higher intracellular ROS generation by the drug, leading to a greater induction of apoptosis
Goette-Di, Marco Paola. "Effets protecteurs du brain natriuretic peptide (BNP) sur la toxicité cardiaque et musculaire des anthracyclines". Strasbourg, 2011. http://www.theses.fr/2011STRA6274.
Texto completoThe purpose of this research was to study the protective effects of brain natriuretic peptide (BNP), a hormone synthesized by cardiomyocytes, on the acute and chronic toxicity of doxorubicine, which is widely used in cancer treatment. These studies were carried out on live animals on various types of muscle, on cultured muscular cells, and subsequently on fragments of human heart appendages. During acute treatments doxorubicine modifies the mitochondrial function of the cardiomyocytes and the muscular cell structure by an increase in oxidative stress. The injection of BNP provides protection by opening the mKATP channels, by increasing the mitochondrial respiratory chain complex activity , the antioxidant systems, and participle in the maintenance of mitochondrial membrane potential. Chronic treatment with doxorubicine reduces the oxydatives capacities of the I, II and III complexes activities of respiratory chain and increase oxidative stress. Pre-treatment by BNP protects both heart and skeletal muscles from this deterioration
Jansson, Anna. "Structural enzymology of the biosynthesis of polyketide antibiotics /". Stockholm, 2004. http://diss.kib.ki.se/2004/91-7349-916-1/.
Texto completoMontaigne, David. "Pathologie du métabolisme énergétique cardiaque induite par la doxorubicine". Lille 2, 2010. http://www.theses.fr/2010LIL2S018.
Texto completoDuffy, Peter Martin. "Intravesical chemotherapy for superficial bladder cancer : an in vitro study of anthracyclines, pH and multidrug resistance". Thesis, University of Southampton, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.326586.
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