Bibliographies thématiques / Cisplatin analogues

Littérature scientifique sur le sujet « Cisplatin analogues »

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Publié le 10 mars 2023

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Articles de revues sur le sujet "Cisplatin analogues"

Fram, Robert j. « Cisplatin and platinum analogues ». Current Opinion in Oncology 4, n^o 6 (décembre 1992) : 1073–79. http://dx.doi.org/10.1097/00001622-199212000-00012.

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Weiss, Raymond B., et Michaele C. Christian. « New Cisplatin Analogues in Development ». Drugs 46, n^o 3 (septembre 1993) : 360–77. http://dx.doi.org/10.2165/00003495-199346030-00003.

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&NA;. « New cisplatin analogues attempt to supersede cisplatin and carboplatin ». Drugs & ; Therapy Perspectives 3, n^o 1 (janvier 1994) : 7–8. http://dx.doi.org/10.2165/00042310-199403010-00003.

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Bednarska-Szczepaniak, Katarzyna, Damian Krzyżanowski, Magdalena Klink et Marek Nowak. « Adenosine Analogues as Opposite Modulators of the Cisplatin Resistance of Ovarian Cancer Cells ». Anti-Cancer Agents in Medicinal Chemistry 19, n^o 4 (25 juin 2019) : 473–86. http://dx.doi.org/10.2174/1871520619666190118113201.

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Background: Adenosine released by cancer cells in high amounts in the tumour microenvironment is one of the main immunosuppressive agents responsible for the escape of cancer cells from immunological control. Blocking adenosine receptors with adenosine analogues and restoring immune cell activity is one of the methods considered to increase the effectiveness of anticancer therapy. However, their direct effects on cancer cell biology remain unclear. Here, we determined the effect of adenosine analogues on the response of cisplatinsensitive and cisplatin-resistant ovarian cancer cells to cisplatin treatment. Methods: The effects of PSB 36, DPCPX, SCH58261, ZM 241385, PSB603 and PSB 36 on cisplatin cytotoxicity were determined against A2780 and A2780cis cell lines. Quantification of the synergism/ antagonism of the compounds cytotoxicity was performed and their effects on the cell cycle, apoptosis/necrosis events and cisplatin incorporation in cancer cells were determined. Results: PSB 36, an A1 receptor antagonist, sensitized cisplatin-resistant ovarian cancer cells to cisplatin from low to high micromolar concentrations. In contrast to PSB 36, the A2AR antagonist ZM 241385 had the opposite effect and reduced the influence of cisplatin on cancer cells, increasing their resistance to cisplatin cytotoxicity, decreasing cisplatin uptake, inhibiting cisplatin-induced cell cycle arrest, and partly restoring mitochondrial and plasma membrane potentials that were disturbed by cisplatin. Conclusion: Adenosine analogues can modulate considerable sensitivity to cisplatin of ovarian cancer cells resistant to cisplatin. The possible direct beneficial or adverse effects of adenosine analogues on cancer cell biology should be considered in the context of supportive chemotherapy for ovarian cancer.

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Aggarwal, S. K. « A histochemical approach to the mechanism of action of cisplatin and its analogues. » Journal of Histochemistry & ; Cytochemistry 41, n^o 7 (juillet 1993) : 1053–73. http://dx.doi.org/10.1177/41.7.8515048.

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The effects of cisplatin (CDDP), a potent anti-cancer agent, and its various analogues were analyzed for any biochemical changes involving Ca2+ and lysosomal and membrane-associated transport enzymes in rat kidney, liver, serum, urine, tissue homogenates, and isolated mitochondria. Correlation was made with any morphological changes observed by light and electron microscopy to gain an insight into the mechanism of action of various platinum coordination complexes. CDDP in its hydrolyzed state under conditions of low chloride ion concentrations causes uncoupling of oxidative phosphorylation, calcium efflux from the mitochondria, inhibits ATP synthesis, lowers membrane-associated calcium and various membrane transport enzymes, and induces an increase in the number of lysosomes. Enzymes such as alkaline phosphatase are stripped from the brush borders of the proximal tubule cells and are discharged in the urine. However, daily IV injections of calcium (1.1 ml of 1.3% CaCl2) supplementation protect the membrane-associated enzymes from cisplatin action. Carboplatin (CBDCA), an analogue of CDDP and the least nephrotoxic of all its analogues, shows little effect on the membrane-associated transport enzymes. Therefore, cisplatin and its various analogues seem to affect the membrane transport enzymes to varying degrees with related nephrotoxicity. Calcium supplementation seems to protect these enzymes and preserve kidney function.

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Murray, Vincent, Heather M. Campbell et Annette M. Gero. « Plasmodium falciparum : DNA sequence specificity of cisplatin and cisplatin analogues ». Experimental Parasitology 128, n^o 4 (août 2011) : 396–400. http://dx.doi.org/10.1016/j.exppara.2011.05.002.

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Rodriguez-Fernandez, E., J. Manzano, A. Alonso, M. Almendral, M. Perez-Andres, A. Orfao et J. Criado. « Fluorescent Cisplatin Analogues and Cytotoxic Activity ». Current Medicinal Chemistry 16, n^o 32 (1 novembre 2009) : 4314–27. http://dx.doi.org/10.2174/092986709789578169.

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Neumann, Wilma, Brenda C. Crews, Menyhárt B. Sárosi, Cristina M. Daniel, Kebreab Ghebreselasie, Matthias S. Scholz, Lawrence J. Marnett et Evamarie Hey-Hawkins. « Conjugation of Cisplatin Analogues and Cyclooxygenase Inhibitors to Overcome Cisplatin Resistance ». ChemMedChem 10, n^o 1 (15 octobre 2014) : 183–92. http://dx.doi.org/10.1002/cmdc.201402353.

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Riley, Christopher M. « Bioanalysis of cisplatin analogues — a selective review ». Journal of Pharmaceutical and Biomedical Analysis 6, n^o 6-8 (janvier 1988) : 669–76. http://dx.doi.org/10.1016/0731-7085(88)80078-5.

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Amptoulach, Sousana, et Nicolas Tsavaris. « Neurotoxicity Caused by the Treatment with Platinum Analogues ». Chemotherapy Research and Practice 2011 (27 juin 2011) : 1–5. http://dx.doi.org/10.1155/2011/843019.

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Platinum agents (cisplatin, carboplatin, and oxaliplatin) are a class of chemotherapy agents that have a broad spectrum of activity against several solid tumors. Toxicity to the peripheral nervous system is the major dose-limiting toxicity of at least some of the platinum drugs of clinical interest. Among the platinum compounds in clinical use, cisplatin is the most neurotoxic, inducing mainly sensory neuropathy of the upper and lower extremities. Carboplatin is generally considered to be less neurotoxic than cisplatin, but it is associated with a higher risk of neurological dysfunction if administered at high dose or in combination with agents considered to be neurotoxic. Oxaliplatin induces two types of peripheral neuropathy, acute and chronic. The incidence of oxaliplatin-induced neuropathy is related to various risk factors such as treatment schedule, cumulative dose, and time of infusion. To date, several neuroprotective agents including thiol compounds, vitamin E, various anticonvulsants, calcium-magnesium infusions, and other nonpharmacological strategies have been tested for their ability to prevent platinum-induced neurotoxicity with controversial results. Further studies on the prevention and treatment of neurotoxicity of platinum analogues are warranted.

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Thèses sur le sujet "Cisplatin analogues"

Barnes, Katie R. 1978. « Mechanism-based rational design of cisplatin analogues ». Thesis, Massachusetts Institute of Technology, 2005. http://hdl.handle.net/1721.1/33647.

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Thesis (Ph. D.)--Massachusetts Institute of Technology, Dept. of Chemistry, 2005.
Vita.
Includes bibliographical references.
The success of cisplatin as an anticancer drug is attributed to the ability of the platinum compound to damage DNA and subsequently induce apoptosis. Details of the cellular processing of cisplatin-damaged DNA can provide invaluable insight into the rational design of cisplatin analogues or combination therapies. Chapter I provides a survey of recent developments in the understanding of the mechanism of cisplatin action and summarizes relevant platinum-based anticancer compounds. Chapter 2 describes a series of estrogen-tethered platinum(IV) complexes (BEPn, n=l -5) that were synthesized, evaluated for their ability to upregulate HMGB1 and screened for cytotoxicity against human breast cancer cell lines. All BEPn complexes induced the overexpression of HMGB I in ER(+) MCF-7 cells. BEP3 was nearly twice as cytotoxic in ER(+) MC'F-7 cells than in ER(-) HCC-1937 cells. This result suggests the possibility of using compounds in this class specifically to target ER(+) malignancies, such as breast and ovarian cancers. In addition, the series of BEPn compounds provide an example of a useful strategy in the development of platinum-containing anticancer agents, namely, using mechanistic insights to aid in the rational design of new complexes.
(cont.) The strategy of exploiting estrogen-induced HMGBI upregulation to sensitize ER(+) cells to platinum was further pursued in work described in chapters 3 and 4. Chapter 3 reports the synthesis and characterization of a series of platinum(IV)-estrogen conjugates derived from carboplatin. Although these BECPn complexes were moderately cytotoxic in ER(+) MCF-7 human breast cancer cells, no differential cytotoxicity was observed as compared to ER(-) HCC- 1937 cells. However, these compounds represent the first example of a biomolecule-tethered platinum(IV) complex that reduces to yield carboplatin in cells. The platinum estrogen conjugate described in chapter 4 was designed not only to induce upregulation of HMGB I but also to enter ER(+) cells selectively. Unlike the BEP and BECP compounds, BEEP was designed to maintain affinity for the estrogen receptor and by tethering platinum to estradiol through the 17c-position of the steroid ring. Compounds with affinity for the estrogen receptor, which is overexpressed in breast and ovarian cancers, are selectively taken up into ER(+) cells. Unexpectedly, BEEP had very low affinity for the estrogen receptor and was therefore equally cytotoxic in ER(+) and ER(-) human breast cancer cell lines.
(cont.) A common feature of many cancers is overexpression of the folate receptor, which is responsible for the uptake of folic acid. Therefore targeting the folic receptor is an attractive method for achieving selective uptake in cancer cells. Chapter 5 describes the synthesis and biological activity of a folic acid-tethered platinum(lV) compound, which demonstrates the validity of this premise. The nuclear protein HMGBI has recently been discovered to function as an extracellular signaling agent. Because of oxygen deprivation, the core of a solid tumor dies by necrosis and passively releases HMGB I into the extracellular environment. This characteristic of solid tumors leads to the hypothesis that extracellular HMGB I is taken up by surrounding viable tumor tissue and mediates cisplatin sensitivity. The final chapter investigates the capability of exogenously administered HMGB to modulate the cytotoxicity of cisplatin and trans-DDP in human cancer cells. The Appendix sections provide detailed experimental protocols for several useful laboratory methods. In Appendix A, a procedure for isolation of nuclei from cisplatin-treated cells is presented.
(cont.) The nuclei were subsequently used by our collaborators to examine the post- translational modifications of histones induced by cisplatin exposure. A protocol for isolation of protein extracts from formalin-fixed paraffin-embedded tissue is described in Appendix B. In addition, the extracts were probed by western blot analysis to examine the expression levels of HMGB1 in clinical testicular seminoma samples. Appendix C provides a solid-phase synthetic methodology for the preparation of peptide-conjugated platinum(IV) compounds.
by Katie R. Barnes.
Ph.D.

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Singh, Tanya N. « Ru(II) complexes as photoactivated cisplatin analogs ». Columbus, Ohio : Ohio State University, 2006. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1150391177.

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Bentefrit, Farida. « Analogues du cisplatine : quelques composes formes par le platine (ii) et (iv) ou palladium (ii) avec deux medicaments de la famille des biguanides (metformine et proguanil) ». Paris 11, 1996. http://www.theses.fr/1996PA114847.

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Jain, Avijita. « Tuning the Photophysical and Biological Properties of a Series of Ruthenium-Based Chromophores and Chromophore Coupled Cisplatin Analogs with Substituted Terpyridine Ligands ». Diss., Virginia Tech, 2008. http://hdl.handle.net/10919/77285.

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The goal of this research was to develop an understanding of the impact of component modifications on spectroscopic properties, DNA interaction, and bioactivity of tridentate, terpyridine containing ruthenium-based chromophores and chromophore coupled cisplatin analogs. The coupling of a light absorbing unit to a bioactive site offers the potential for developing supramolecules with multifunctional interactions with DNA and other biomolecules. A series of supramolecular complexes of the form [(TL)RuCl(dpp)](PF₆) and [(TL)RuCl(BL)PtCl₂](PF₆) with the BL (bridging ligand) = 2,3-bis(2-pyridyl)pyrazine (dpp) and varying TL (terminal ligand) (tpy = 2,2'':6'',2''-terpyridine, MePhtpy = 4''-(4-methylphenyl)- 2,2'':6'',2''- terpyridine, or tBu3tpy = 4,4'',4''-tri-tert-butyl-2,2'':6'',2''-terpyridine) have been designed and developed. The investigations described in this thesis were focused on the design and development of multifunctional supramolecules with improved DNA interaction and antibacterial properties. The impact of component modifications on photophysical and biological properties of the designed the supramolecular complexes was investigated. A series of supramolecular complexes of the type, [(TL)RuCl(dpp)](PF₆) and [(TL)RuCl(dpp)PtCl₂](PF₆), have been synthesized using a building block approach. Electronic absorption spectroscopy of these types of complexes displayed intense ligand-based transitions in the UV region and metal to ligand charge transfer (MLCT) transitions in the visible region. The Ru to dpp MLCT transitions in RuIIPtII bimetallic complexes were found to be red-shifted relative to the monometallic synthons. The MLCT transitions for [(TL)RuCl(dpp)](PF₆) and [(TL)RuCl(dpp)PtCl₂](PF₆) were centered at ca. 520 and 545 nm, in CH₃CN respectively. The RuIIPtII bimetallic complexes with (TL = tpy, MePhtpy, and tBu3tpy) displayed reversible RuII/III couples at 1.10, 1.10, and 1.01 V vs. Ag/AgCl, respectively. The tpy0/- reductions occurred for TL = tpy, MePhtpy, and tBu3tpy at -1.43, -1.44, and -1.59 V vs. Ag/AgCl, respectively. The RuIIPtII complexes displayed a more positive potential for the dpp0/- couples (-0.50 -0.55, -0.59 V for tpy, MePhtpy, and tBu3tpy, repectively) relative to their monometallic synthons (-1.15, -1.16, and -1.22 V), consistent with the coordination of electron deficient Pt(II) metal center. This research also presents first extensive DNA photocleavage studies of these relatively unexplored tridentate, tpy-containing chromophores. The DNA binding and photocleavage properties of a series of homoleptic and heteroleptic chromophores and RuIIPtII bimetallic complexes were investigated using agarose gel electrophoresis and equilibrium dialysis experiments. The heteroleptic complexes, [(MePhtpy)RuCl(dpp)](PF₆), [(tpy)RuCl(dpp)](PF6), and [(tBu3tpy)RuCl(dpp)](PF6), were found to photocleave DNA more efficiently than homoleptic complexes, [Ru(MePhtpy)2]2+, [Ru(tpy)2]2+, and [Ru(tBu₃tpy)2]2+, in the presence of oxygen. Coupling of [(TL)RuCl(BL)] subunit to a cis-PtIICl2 site provides for the application of typically shorter lived RuII(tpy) based chromophores in DNA photocleavage. The [(TL)RuCl(dpp)PtCl₂]+, complexes displayed covalent binding to DNA and photocleavage upon irradiation with visible light modulated by TL identity. The impact of component modifications on antibacterial properties of the designed molecules was explored for the first time. Both the RuIIPtII bimetallic complexes and their monometallic analogs displayed antibacterial properties. [(MePhtpy)RuCl(dpp)](PF₆) was found to be the most efficient antibacterial agent in the series of monometallic and RuIIPtII bimetallic complexes, displaying cell growth inhibition at 0.05 mM concentration compared to 0.1 mM concentration of [(MePhtpy)RuCl(dpp)PtCl₂](PF₆) needed to display the similar effect. A direct correlation was found to exist between the DNA interaction and bactericidal properties of the designed supramolecules. The effects of light on antibacterial properties of [(MePhtpy)RuCl(dpp)](PF₆) were also briefly examined. This complex represents the first inorganic chromophore-based photodynamic antibacterial agent.
Ph. D.

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Fjällskog, Marie-Louise. « Current Medical Treatment of Endocrine Pancreatic Tumors and Future Aspects ». Doctoral thesis, Uppsala University, Department of Medical Sciences, 2002. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-2709.

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We treated 16 patients with somatostatin analogs combined with α-interferon and achieved a biochemical and/or radiological response in 56% (median duration 22 months). We consider this treatment a good alternative for patients who fail during chemotherapy or who do not want to/cannot receive cytotoxic drugs.

Thirty-six patients with neuroendocrine tumors were treated with cisplatin combined with etoposide. Of 14 patients with evaluable EPTs, 50% responded radiologically and/or biochemically (median duration 9 months). We consider this treatment useful as first-line medical treatment in aggressive EPTs or in patients failing prior chemotherapy.

Twenty-eight tumor tissues from EPTs were examined with immunohistochemistry regarding expression of somatostatin receptors (ssts) 1 to 5 on tumor cells and in intratumoral vessels. We found that sst₂ and sst₄ were highly expressed on tumor cells and in vessels. However, sst₃ and sst₅ were lacking in half of the tumor tissues and in most of the vessels. Because of the variability in sst expression, we recommend analysis of each individual’s receptor expression before starting treatment.

Endocrine pancreatic tumors (EPTs) are rare with an incidence of 4 per million inhabitants. In the majority of cases they grow slowly, but there are exceptions with very rapidly progressing malignant carcinomas. First-line medical treatment is streptozotocin combined with 5-fluorouracil.

We examined 38 tumor samples regarding expression of tyrosine kinase receptors platelet-derived growth factor receptors (PDGFRs), c-kit and epidermal growth factor receptor (EGFR). We found that the receptors were expressed in more than half of the tumor tissues. Further studies will reveal if tyrosin kinase antagonists can be part of the future treatment arsenal.

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Burgess, Mark W. « Characterisation of the interactions and biological impacts of cisplatin analogues and metallo-drug complexes with DNA ». Thesis, 2013. http://handle.uws.edu.au:8081/1959.7/542443.

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The work described in this thesis develops and applies several methodologies to determine the potential of cisplatin analogues and novel metallo-drugs as anti-cancer compounds. These methodologies centred around three approaches that elucidate the DNA binding properties of these metallo-drugs. The first approach characterises the mode of DNA binding and measures the metallo-drug effect on modifying DNA structure. The second approach analysed both the ability of the metallo-drugs to inhibit DNA replication and determined the DNA binding sequence specificity. The third approach compared the binding affinity of metallo-drugs for GSH or DNA. The metallo-drugs tested include cisplatin, which served as a positive control since its interactions with DNA have been well studied. The cisplatin analogues tested included carboplatin, oxaliplatin, DCBP, DCRP, DACH, and metallo-intercalators 56MESS and 3478MEEN. Other metallo-drugs such as the copper(II) 56MESS analogue Cu56MESS and the ruthenium(II) compounds RuP1 and RuP2 were also studied. Finally, the well defined DNA strand breaker phleomycin was included to serve as a positive control in for compounds that may exhibit endonuclease activity. Data presented in this thesis demonstrated that the novel application of free solution CE-CC was effective to determine metallo-drug induced structure modifications on a linear dsDNA substrate. Furthermore, metallo-drugs were able to be differentiated into their DNA binding mode by combining CE-CC data with plasmid mobility data on a 2D scatter plot analysis. The 2D scatter plot analysis of metallo-drug/DNA structure modification showed that the ruthenium(II) groove binder RuP2, with is additional pyrrole ligand compared to the RuP1 analogue, could substantially increase the molecular weight of a linear dsDNA substrate. Furthermore, the 2D scatter plot DNA structure analysis revealed the platinum(II) metallo-intercalator 3478MEEN adopted exhibited duel covalent binding and π-π base stacking intercalation with DNA. The covalent binding activity associated with 3478MEEN was also evident in an interstrand crosslink assay which involved a novel application of a urea-based denaturing agarose slab gel electrophoresis and 5′FAM linear dsDNA substrate. The Linear Amplification (LA) reaction was employed to characterise metallo-drug induced inhibition of DNA replication in addition to identifying the test compound’s sequence binding specificity. A novel application of Rhodamine 6G labelled nucleotides was used to quantify metallo-drug induced inhibition of DNA replication by a DNA polymerase. Furthermore, the application of a 5′FAM labelled primer in a LA reaction together with separation of the products by Capillary Electrophoresis with Laser Induced Fluorescence (CE-LIF) was performed. From these data, sites of adduct formation were identified that corresponded to the known sequence specificity of cisplatin, in addition the binding specificity of other metallo-drugs were determined. A kinetic study was employed to measure metallo-drug thiol bond reactivity with GSH. It was demonstrated that the thiol bond reactivity with the control platinum(II) compounds cisplatin, oxaliplatin and carboplatin were in agreement with published data, in addition novel reactivity data were obtained for compounds not previously studied. Finally, an in vitro competitive assay and analysis protocol was developed to quantitatively analyse the binding preference of the metallo-drug between DNA and GSH. A 2D scatter plot analysis of metallo-drug reactivity with GSH and DNA revealed that Cu56MESS and the DNA strand breaker, phleomycin, exhibit a similar DNA and GSH reaction profiles in the absence of a reducing agent which warrants further investigation. Overall, developed methodologies produced data that showed that the platinum(II) metallo-intercalator 3478MEEN adopted dual covalent binder and π-π base stacking DNA binding modes. The copper(II) metallo-drug Cu56MESS showed negligible DNA strand breaking activity in the absence of a reducing agent like H2O2, however, it did exhibit GSH reactivity suggesting that the need for a reducing agent may not be necessary for reactions with other biological substrates. Finally, the ruthenium(II) groove binder RuP2 with its additional pyrrole ligand compared to RuP1 could substantially increase the molecular weight of a linear dsDNA substrate.

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MARZO, TIZIANO. « FROM CONVENTIONAL TO NOVEL Pt-BASED ANTINEOPLASTIC AGENTS : MECHANISTIC ASPECTS AND BIOLOGICAL EFFECTS ». Doctoral thesis, 2016. http://hdl.handle.net/2158/1022440.

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In the last decades the research on inorganic drugs in medicine has registered remarkable progresses with particular emphasis to the field of anticancer drugs. Cisplatin, carboplatin and oxaliplatin are today widely used in the treatment of different type of malignance and often represent, even in combination with other drugs, a first choice therapy. Since the serendipitous discover of cisplatin and despite the efforts, still nowadays, these drug are the most important research products in this field, although resistance to the treatments and heavy side effects, are important limiting factors to their use in clinical protocols. Thus, there is urgent need of new and more effective Pt-based anticancer drugs able to circumvent these problems. The development of new metal-based anticancer molecules is not easy, mostly because it is difficult to predict their effects in vivo, starting from the analysis of the cellular effects in vitro. Furthermore it should taken into account the extreme complexity of biological systems; even limiting our consideration only to studies at the cellular level, already, there are an outstanding number of factors and variables to be consider. In this frame we have carried out studies on cell-free systems as well as cellular studies, characterising the reactivity and the cellular effects of cisplatin and a series of its analogues to shed light on analogies and differences between these drugs. Interestingly, it has been extensively characterised their interaction with model proteins. Despite today it is recognised that formation of Pt-protein adducts, is of central importance in relation to overall pharmacological and toxicological impact of cisplatin and its analogues, yet, the structural information concerning platination of protein, and the characterization of the resulting adducts, is limited. Thus the studies summarising in this thesis aimed to: i) gather information on mechanistic aspects correlated with the mode of action of Pt-based anticancer compounds that, to date, remains in part unclear; ii) compare, at different level, the behaviour of conventional platinum anticancer drugs with experimental complexes in order to find differences that may be significant in terms of pharmacological effect in vivo, iii) evaluate or re-evaluate comparatively the anticancer properties of selected cisplatin analogues. All these issues are addressed within this work, where the comparative characterization of protein binding for conventional platinum-based anticancer drugs is reported (chapter 3) as well as the reappraisal of old cisplatin analogues, overlooked so far as anticancer agents, studied in comparison with clinical used Pt compounds (chapter 4 and 5). Preliminary in vivo studies are also described (chapter 6).

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KOPEČNÁ, Jana. « Functional characterization of \kur{in vitro} activity of the \kur{Trypanosoma brucei} mitochondrial RNA binding MRP1/MRP2 complex \& ; Structural differentiations of DNA adducts formed by enantiomeric analogues of antitumor cisplatin ». Master's thesis, 2007. http://www.nusl.cz/ntk/nusl-44033.

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Livres sur le sujet "Cisplatin analogues"

Morley, Christopher. Analogues of cisplatin from diamino carbohydrates and related compounds. Norwich : University of East Anglia, 1986.

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Chapitres de livres sur le sujet "Cisplatin analogues"

Kerpel-Fronius, Sándor. « Cisplatin and its Analogues for Cancer Chemotherapy ». Dans Analogue-based Drug Discovery, 385–94. Weinheim, FRG : Wiley-VCH Verlag GmbH & Co. KGaA, 2006. http://dx.doi.org/10.1002/3527608001.ch19.

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Ackland, Stephen P., et Nicholas J. Vogelzang. « Cisplatin, Platinum Analogues, and Other Heavy Metal Complexes ». Dans Cancer Chemotherapy by Infusion, 145–60. Dordrecht : Springer Netherlands, 1987. http://dx.doi.org/10.1007/978-94-009-3193-0_11.

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Majima, Hisashi. « Clinical Studies with Cisplatin Analogues, 254-S, DWA2114R and NK121 ». Dans Platinum and Other Metal Coordination Compounds in Cancer Chemotherapy, 345–55. Boston, MA : Springer US, 1991. http://dx.doi.org/10.1007/978-1-4899-0738-7_32.

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Bertani, Roberta, Silvia Mazzega Sbovata, Valentina Gandin, Rino A. Michelin et Cristina Marzano. « Synthesis of Cisplatin Analogues : Cytotoxic Efficacy and Anti-tumour Activity of Bis-Amidine and Bis-Iminoether Pt(II) Complexes ». Dans Platinum and Other Heavy Metal Compounds in Cancer Chemotherapy, 49–56. Totowa, NJ : Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-459-3_7.

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Baranska, H., J. Kuduk-Jaworska et C. Cacciari. « Raman Study of Cisplatin and Carboplatin Analogs ». Dans Spectroscopy of Biological Molecules, 547–48. Dordrecht : Springer Netherlands, 1995. http://dx.doi.org/10.1007/978-94-011-0371-8_252.

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Li, Jie Jack. « Imatinib Mesylate (Gleevec) ». Dans Top Drugs. Oxford University Press, 2015. http://dx.doi.org/10.1093/oso/9780199362585.003.0010.

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Great strides had been made in the war against cancer with chemotherapy even before the emergence of protein kinase inhibitors. For instance, prior to vinblastine (1, Velban) became available in 1964 for the treatment of lymphoma, the diagnosis of Hodgkin’s disease (a cancer of the lymph nodes) was virtually a death sentence. Today there is a 90% chance of survival with the treatment by vinca alkaloids such as 1 and other chemotherapies. Similarly, when Sidney Farber discovered the effects of methotrexate (2, Trexall) on leukemia, it marked the beginning of the triumph over childhood leukemia. Following Barnett Rosenberg’s discovery of cisplatin (3, Platinol)’s effects on tumor cells in 1967, cisplatin and its analogs such as carboplatin (4, Paraplatin) and oxaliplatin (5, Eloxatin) contributed significantly in boosting the survival rate of patients with metastatic testicular cancer, ovarian tumors, and bladder cancer. Most significantly, breast cancer, a malady striking one in eight women, has been effectively managed via a plethora of treatments including surgery, radiation, and chemotherapies. The arsenal of chemotherapeutics for treating breast cancer includes SERMs such as tamoxifen (6) and raloxifene (7, Evista). Type I, II, and III aromatase inhibitors have now also been widely prescribed to combat breast cancers (more details may be found in chap. 4). Today, breast cancer is sometimes viewed as a chronic disease that can be managed, rather than a lethal disease. Despite the efficacy of the aforementioned chemotherapeutics, they kill cancer cells and normal cells with equal ferocity. (Some have compared chemotherapy to a “carpet bombing” strategy.) However, the reason these chemotherapies are effective is that cancer cells divide at much faster rate than normal cells; therefore, chemotherapies kill more malignant cells than healthy cells. Chemotherapies invariably come with significant side effects rooted. For example, hair follicle cells have a physiologically high mitosis rate; therefore, chemotherapies kill them faster than other healthy cells. In the same vein, other common side effects of chemotherapy include diarrhea (because ephithelial renewal is inhibited), bone marrow suppression (because granulopoiesis, thrombopoiesis, cytopoiesis, and erythropoiesis are inhibited), and lymph node damage (because of lymphocyte multiplication inhibition causes immune weakness).

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Actes de conférences sur le sujet "Cisplatin analogues"

He, Chenchen, J. Oomens, Juehan Gao, M. Rodgers, C. Chow, Y.-W. Nei, Bett Kimutai, Stephen Strobehn, Yanlong Zhu et Xun Bao. « STRUCTURE DETERMINATION OF CISPLATIN-AMINO ACID ANALOGUES BY INFRARED MULTIPLE PHOTON DISSOCIATION ACTION SPECTROSCOPY ». Dans 70th International Symposium on Molecular Spectroscopy. Urbana, Illinois : University of Illinois at Urbana-Champaign, 2015. http://dx.doi.org/10.15278/isms.2015.mi12.

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