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Dissertations / Theses on the topic 'Antineoplastic Methotrexate Cell line'

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1

Fotoohi, Alan Kambiz. "Pharmacological and molecular investigations on the mechanisms underlying resistance of human leukaemia cells to the antimetabolites methotrexate, 6-mercaptopurine and 6-thioguanine /." Stockholm, 2007. http://diss.kib.ki.se/2007/978-91-7357-087-9/.

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2

Yu, Weiping. "Mechanisms of RRR-[alpha]-tocopheryl succinate (VES) induction of growth inhibition and apoptosis in the human breast cancer cell line, MDA-MB-435 /." Digital version accessible at:, 2000. http://wwwlib.umi.com/cr/utexas/main.

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3

Lindskog, Magnus. "Tumor lipid status and the responses to therapy in neuroblastoma : with emphasis on treatment monitoring by proton magnetic resonance spectroscopy /." Stockholm, 2004. http://diss.kib.ki.se/2004/91-7140-160-1/.

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4

Shor, Audrey Cathryn. "Src kinase inhibitors for the treatment of sarcomas : cellular and molecular mechanisms of action." [Tampa, Fla] : University of South Florida, 2007. http://purl.fcla.edu/usf/dc/et/SFE0001906.

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5

Kinkade, Rebecca. "Rb-Raf-1 interaction as a therapeutic target for proliferative disorders." [Tampa, Fla] : University of South Florida, 2008. http://purl.fcla.edu/usf/dc/et/SFE0002426.

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6

Charcosset, Jean-Yves. "Etude sur le mécanisme d'action de dérivés de l'ellipticine sur des cellules en culture sensibles et résistantes à la 9-hydroxyellipticine." Paris 6, 1986. http://www.theses.fr/1986PA066109.

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7

Salord, Jérôme. "L'ecto-nad**(+) glycohydrolase : une cible cellulaire specifique pour le pilotage de molecules bio-actives au moyen de liposomes." Université Louis Pasteur (Strasbourg) (1971-2008), 1987. http://www.theses.fr/1987STR13083.

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Nous avons mis au point un systeme de ciblage de molecules bio-actives au moyen de liposomes, base sur la reconnaissance entre une ecto-enzyme et un ligand de petite taille greffe de maniere covalente sur des vesicules preformees. L'ecto-nad**(+) glycohydrolase (e. C. 3. 2. 2. 6) a ete choisie comme cible cellulaire pour des liposomes porteurs a leur surface du (3,4-(ch3)2)pdad**(+), inhibiteur competitif de l'enzyme. En vue du couplage covalent, le ligand a ete derivatise en position n**(6) de l'adenine par un bras hydrophile espaceur termine par une fonction thiol, destine a reagir avec des
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8

Craperi, Delphine. "Thérapie génique des gliomes : caractérisation des voies cytotoxiques déclenchées par le système thymidine kinase herpétique/ganciclovir." Université Joseph Fourier (Grenoble ; 1971-2015), 1998. http://www.theses.fr/1998GRE10073.

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La therapie genique par transfert du gene de la thymidine kinase du virus de l'herpes simplex de type 1 (hsv1-tk) suivi d'un traitement avec la prodrogue ganciclovir (gcv) a ete utilisee pour le traitement de divers cancers. L'efficacite de cette therapie est en partie due a l'existence d'un effet de toxicite de voisinage : le traitement au ganciclovir entraine non seulement la mort des cellules exprimant hsv1-tk mais aussi celle des cellules adjacentes non transfectees. Nous avons entrepris une etude in vitro des mecanismes moleculaires de la toxicite de ce systeme enzyme/prodrogue sur des li
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9

Agarwal, Nitin Kumar. "Proteome-wide Identification of New Molecular Targets Affected by Methotrexate in Acute Promyelocytic Leukaemia Cell Line." Doctoral thesis, 2007. http://hdl.handle.net/11858/00-1735-0000-000D-F227-3.

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10

"The anti-cancer activities of paeoniae radix extracts on human hepatocellular carcinoma cell-line HepG2 and multidrug resistant human hepatocellular carcinoma cell-line R-HepG2 and their action mechanisms." 2004. http://library.cuhk.edu.hk/record=b6073630.

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Li Lok Yee Mandy.<br>"June 2004."<br>Thesis (Ph.D.)--Chinese University of Hong Kong, 2004.<br>Includes bibliographical references (p. 155-165).<br>Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web.<br>Mode of access: World Wide Web.<br>Abstracts in English and Chinese.
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11

Agarwal, Nitin Kumar [Verfasser]. "Proteome-wide identification of new molecular targets affected by methotrexate in acute promyelocytic leukaemia cell line / vorgelegt von Nitin Kumar Agarwal." 2007. http://d-nb.info/987826999/34.

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12

Kuschak, Theodore I. "Selection of an ICRF-187-resistant CHO cell line and measurement of cytotoxicity, additive cytotoxicity, and cross-resistance of bisdioxopiperazines, anthracyclines, and other antineoplastic agents in wildtype and resistant cells." 1994. http://hdl.handle.net/1993/18148.

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13

Pors, Klaus, Z. Paniwnyk, Laurence H. Patterson, K. C. Ruparelia, J. A. Hartley, and L. R. Kelland. "Synthesis and biological evaluation of novel chloroethylaminoanthraquinones with potent cytotoxic activity against cisplatin-resistant tumor cells." 2004. http://hdl.handle.net/10454/3164.

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No<br>Novel 1- and 1,4-substituted chloroethylaminoanthraquinones with DNA binding and alkylating properties along with their respective hydroxyethylaminoanthraquinone intermediates were synthesized. Selected chloroethylaminoanthraquinones were shown to cross-link DNA and alkylate guanines (at low nM concentration) with a preference for reaction sites containing 5'-PyG. A compound (Alchemix) with the bis-chloroethyl functionality confined to one side chain alkylated but did not cross-link DNA. All the 1,4-disubstituted chloroethylaminoanthraquinones were potently cytotoxic (nM IC50s) against c
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14

Thomas, A., T. Perry, S. Berhane, et al. "The dual-acting chemotherapeutic agent Alchemix induces cell death independently of ATM and p53." 2015. http://hdl.handle.net/10454/9412.

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Yes<br>Topoisomerase inhibitors are in common use as chemotherapeutic agents although they can display reduced efficacy in chemotherapy-resistant tumours, which have inactivated DNA damage response (DDR) genes, such as ATM and TP53. Here, we characterise the cellular response to the dual-acting agent, Alchemix (ALX), which is a modified anthraquinone that functions as a topoisomerase inhibitor as well as an alkylating agent. We show that ALX induces a robust DDR at nano-molar concentrations and this is mediated primarily through ATR- and DNA-PK- but not ATM-dependent pathways, despite DNA doub
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15

Curtis, VF, H. Wang, P. Yang, et al. "A PK2/Bv8/PROK2 antagonist suppresses tumorigenic processes by inhibiting angiogenesis in glioma and blocking myeloid cell infiltration in pancreatic cancer." Thesis, 2013. http://hdl.handle.net/10161/4982.

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Infiltration of myeloid cells in the tumor microenvironment is often associated with enhanced angiogenesis and tumor progression, resulting in poor prognosis in many types of cancer. The polypeptide chemokine PK2 (Bv8, PROK2) has been shown to regulate myeloid cell mobilization from the bone marrow, leading to activation of the angiogenic process, as well as accumulation of macrophages and neutrophils in the tumor site. Neutralizing antibodies against PK2 were shown to display potent anti-tumor efficacy, illustrating the potential of PK2-antagonists as therapeutic agents for the treatment of c
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16

Sutherland, Mark H., Jason H. Gill, Paul M. Loadman, et al. "Antitumor activity of a duocarmycin analogue rationalized to be metabolically activated by cytochrome P450 1A1 in human transitional cell carcinoma of the bladder." 2012. http://hdl.handle.net/10454/6210.

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No<br>We identify cytochrome P450 1A1 (CYP1A1) as a target for tumor-selective drug development in bladder cancer and describe the characterization of ICT2700, designed to be metabolized from a prodrug to a potent cytotoxin selectively by CYP1A1. Elevated CYP1A1 expression was shown in human bladder cancer relative to normal human tissues. RT112 bladder cancer cells, endogenously expressing CYP1A1, were selectively chemosensitive to ICT2700, whereas EJ138 bladder cells that do not express CYP1A1 were significantly less responsive. Introduction of CYP1A1 into EJ138 cells resulted in 75-fold inc
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17

Shakibaei, M., A. Mobasheri, C. Lueders, F. Busch, P. Shayan, and A. Goel. "Curcumin enhances the effect of chemotherapy against colorectal cancer cells by inhibition of NF-kappaB and Src protein kinase signaling pathways." 2013. http://hdl.handle.net/10454/6183.

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OBJECTIVE: Development of treatment resistance and adverse toxicity associated with classical chemotherapeutic agents highlights the need for safer and effective therapeutic approaches. Herein, we examined the effectiveness of a combination treatment regimen of 5-fluorouracil (5-FU) and curcumin in colorectal cancer (CRC) cells. METHODS: Wild type HCT116 cells and HCT116+ch3 cells (complemented with chromosome 3) were treated with curcumin and 5-FU in a time- and dose-dependent manner and evaluated by cell proliferation assays, DAPI staining, transmission electron microscopy, cell cycle analys
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18

Teesdale-Spittle, P. H., Klaus Pors, R. Brown, Laurence H. Patterson, and J. A. Plumb. "Development of nonsymmetrical 1,4-disubstituted anthraquinones that are potently active against cisplatin-resistant ovarian cancer cells." 2005. http://hdl.handle.net/10454/3191.

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No<br>A novel series of 1,4-disubstituted aminoanthraquinones were prepared by ipso-displacement of 1,4-difluoro-5,8-dihydroxyanthraquinones by hydroxylated piperidinyl- or pyrrolidinylalkyl-amino side chains. One aminoanthraquinone (13) was further derivatized to a chloropropyl-amino analogue by treatment with triphenylphosphine-carbon tetrachloride. The compounds were evaluated in the A2780 ovarian cancer cell line and its cisplatin-resistant variants (A2780/ cp70 and A2780/MCP1). The novel anthraquinones were shown to possess up to 5-fold increased potency against the cisplatin-resistant ce
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19

Burns, C. J., E. Fantino, A. K. Powell, et al. "The microtubule depolymerizing agent CYT997 causes extensive ablation of tumor vasculature in vivo." 2011. http://hdl.handle.net/10454/5902.

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The orally active microtubule-disrupting agent (S)-1-ethyl-3-(2-methoxy-4-(5-methyl-4-((1-(pyridin-3-yl)butyl)amino)pyrimidin-2- yl)phenyl)urea (CYT997), reported previously by us (Bioorg Med Chem Lett 19:4639-4642, 2009; Mol Cancer Ther 8:3036-3045, 2009), is potently cytotoxic to a variety of cancer cell lines in vitro and shows antitumor activity in vivo. In addition to its cytotoxic activity, CYT997 possesses antivascular effects on tumor vasculature. To further characterize the vascular disrupting activity of CYT997 in terms of dose and temporal effects, we studied the activity of the com
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20

Williams, K. J., M. R. Albertella, B. Fitzpatrick, et al. "In vivo activation of the hypoxia-targeted cytotoxin AQ4N in human tumor xenografts." 2009. http://hdl.handle.net/10454/6236.

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AQ4N (banoxantrone) is a prodrug that, under hypoxic conditions, is enzymatically converted to a cytotoxic DNA-binding agent, AQ4. Incorporation of AQ4N into conventional chemoradiation protocols therefore targets both oxygenated and hypoxic regions of tumors, and potentially will increase the effectiveness of therapy. This current pharmacodynamic and efficacy study was designed to quantify tumor exposure to AQ4 following treatment with AQ4N, and to relate exposure to outcome of treatment. A single dose of 60 mg/kg AQ4N enhanced the response of RT112 (bladder) and Calu-6 (lung) xenografts to t
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