subject:(Carmustine)

Oregon State University

1. Giese, Neill Alan. The effect of carmustine (BCNU) on hepatic UDP-glucuronyltransferase activity in the rat.

Degree: MS, Pharmacology and Toxicology, 1980, Oregon State University

URL: http://hdl.handle.net/1957/42315

Subjects/Keywords: Carmustine

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Giese, N. A. (1980). The effect of carmustine (BCNU) on hepatic UDP-glucuronyltransferase activity in the rat. (Masters Thesis). Oregon State University. Retrieved from http://hdl.handle.net/1957/42315

Chicago Manual of Style (16^th Edition):

Giese, Neill Alan. “The effect of carmustine (BCNU) on hepatic UDP-glucuronyltransferase activity in the rat.” 1980. Masters Thesis, Oregon State University. Accessed January 18, 2021. http://hdl.handle.net/1957/42315.

MLA Handbook (7^th Edition):

Giese, Neill Alan. “The effect of carmustine (BCNU) on hepatic UDP-glucuronyltransferase activity in the rat.” 1980. Web. 18 Jan 2021.

Vancouver:

Giese NA. The effect of carmustine (BCNU) on hepatic UDP-glucuronyltransferase activity in the rat. [Internet] [Masters thesis]. Oregon State University; 1980. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/1957/42315.

Council of Science Editors:

Giese NA. The effect of carmustine (BCNU) on hepatic UDP-glucuronyltransferase activity in the rat. [Masters Thesis]. Oregon State University; 1980. Available from: http://hdl.handle.net/1957/42315

2. Daminelli, Elaine Nunes. Uso de carmustina associada a nanoemulsões ricas em colesterol (LDE) para tratamento da aterosclerose induzida em coelhos.

Degree: PhD, Cardiologia, 2015, University of São Paulo

URL: http://www.teses.usp.br/teses/disponiveis/5/5131/tde-11052015-161325/ ;

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A aterosclerose é uma doença inflamatória crônica e proliferativa que tem início quando fatores de risco alteram o endotélio vascular. As partículas da nanoemulsão lipídica… (more)

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A aterosclerose é uma doença inflamatória crônica e proliferativa que tem início quando fatores de risco alteram o endotélio vascular. As partículas da nanoemulsão lipídica LDE concentram-se em sítios inflamatórios e de intensa proliferação celular, como acontece nas lesões ateroscleróticas. A carmustina, um fármaco antiproliferativo usado na quimioterapia do câncer, não foi ainda explorada no tratamento da aterosclerose. Em trabalhos anteriores, mostrou-se que a associação com a LDE reduz drasticamente a toxicidade da carmustina, o que já foi demonstrado em pacientes com câncer avançado. O propósito do estudo é avaliar se a carmustina associada à LDE pode promover o efeito antiproliferativo nas lesões ateroscleróticas induzidas em coelhos. No presente trabalho, dezoito coelhos machos da raça New Zealand, receberam dieta rica em colesterol a 1% durante 8 semanas. Depois de 4 semanas foram divididos em dois grupos: grupo controle, que recebeu injeção endovenosa contendo apenas solução salina e grupo tratado, que recebeu LDE-carmustina na dose de 4mg/Kg semanalmente durante 4 semanas. Foram avaliados perfil hematológico, lipídico, bioquímico, ponderal e o consumo de ração. Após a eutanásia, foram medidas as lesões ateroscleróticas macroscópicas. Em seguida, o arco aórtico foi analisado por morfometria e por imunohistoquímica. Observou-se que não houve diferença no perfil ponderal e no consumo de ração entre os grupos de estudo. Não houve toxicidade hematológica, hepática e renal no grupo tratado. No perfil lipídico, ao final do estudo, as concentrações de colesterol total, não HDL-C e triglicerídeos aumentaram em todos os grupos. Portanto, o tratamento com LDE-carmustina inibiu as lesões ateroscleróticas em aproximadamente 90%, comparado ao grupo controle. LDE-carmustina também reduziu a presença de macrófagos, de células de músculo liso e das células reguladoras de linfócitos T na íntima arterial, bem como a expressão protéica de MMP9, das citocinas inflamatórias e dos receptores de lipoproteínas. O tratamento da aterosclerose induzida em coelho com LDE-carmustina resultou em marcante redução das lesões na aorta, da proliferação e invasão da íntima por macrófagos e células musculares lisas, características da doença, além dos fatores inflamatórios. Tendo em vista que, associada à LDE, a carmustina tem baixa toxicidade, a nova preparação LDE-carmustina tem grande potencial para a terapêutica das doenças cardiovasculares de natureza aterosclerótica

Atherosclerosis is a chronic inflammatory and proliferative disease that starts when risk factors alter vascular endothelium. The particles of the lipid nanoemulsion LDE concentrate on inflammatory sites and with intense cell proliferation, as occurs in atherosclerotic lesions. The carmustine, an antiproliferative drug used in cancer chemotherapy has not yet been explored for the treatment of atherosclerosis. In previous work, we showed that the association with LDE drastically reduces toxicity of carmustine, which has been demonstrated in patients with advanced cancer.…

Advisors/Committee Members: Maranhao, Raul Cavalcante.

Subjects/Keywords: Aterosclerose; Atherosclerosis; Carmustina; Carmustine; Coelhos; Hipercolesterolemia; Hypercholesterolemia; Inflamação; Inflammation; Nanoparticles; Nanopartículas; Rabbits

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Daminelli, E. N. (2015). Uso de carmustina associada a nanoemulsões ricas em colesterol (LDE) para tratamento da aterosclerose induzida em coelhos. (Doctoral Dissertation). University of São Paulo. Retrieved from http://www.teses.usp.br/teses/disponiveis/5/5131/tde-11052015-161325/ ;

Chicago Manual of Style (16^th Edition):

Daminelli, Elaine Nunes. “Uso de carmustina associada a nanoemulsões ricas em colesterol (LDE) para tratamento da aterosclerose induzida em coelhos.” 2015. Doctoral Dissertation, University of São Paulo. Accessed January 18, 2021. http://www.teses.usp.br/teses/disponiveis/5/5131/tde-11052015-161325/ ;.

MLA Handbook (7^th Edition):

Daminelli, Elaine Nunes. “Uso de carmustina associada a nanoemulsões ricas em colesterol (LDE) para tratamento da aterosclerose induzida em coelhos.” 2015. Web. 18 Jan 2021.

Vancouver:

Daminelli EN. Uso de carmustina associada a nanoemulsões ricas em colesterol (LDE) para tratamento da aterosclerose induzida em coelhos. [Internet] [Doctoral dissertation]. University of São Paulo; 2015. [cited 2021 Jan 18]. Available from: http://www.teses.usp.br/teses/disponiveis/5/5131/tde-11052015-161325/ ;.

Council of Science Editors:

Daminelli EN. Uso de carmustina associada a nanoemulsões ricas em colesterol (LDE) para tratamento da aterosclerose induzida em coelhos. [Doctoral Dissertation]. University of São Paulo; 2015. Available from: http://www.teses.usp.br/teses/disponiveis/5/5131/tde-11052015-161325/ ;

Univerzitet u Beogradu

3. Stojković-Burić, Sonja M., 1985-. Model ćelija C6 glioma pacova kao oruđe za pronalaženje novih terapeutskih strategija: karakterizacija rezistentnog fenotipa in vitro i in vivo.

Degree: Biološki fakultet, 2017, Univerzitet u Beogradu

URL: https://fedorabg.bg.ac.rs/fedora/get/o:15650/bdef:Content/get

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Molekularna onkologija - Kancerogeneza / Molecular oncology - Cancerogenesis

Uspešnost terapije glioblastoma, najĉešćeg i najagresivnijeg malignog tumora centralnog nervnog sistema, je osujećena usled visokog stepena… (more)

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Molekularna onkologija - Kancerogeneza / Molecular oncology - Cancerogenesis

Uspešnost terapije glioblastoma, najĉešćeg i najagresivnijeg malignog tumora centralnog nervnog sistema, je osujećena usled visokog stepena invazivnosti, kao i pojave rezistencije na hemioterapiju. Cilj ove doktorske disertacije je bio da se uspostavi i okarakteriše rezistentni gliomski model koji bi imao primenu u ispitivanju novih terapeutskih strategija u leĉenju ove teške bolesti. Kao poĉetni materijal korišćena je pacovska C6 ćelijska linija glioma, fenotipski sliĉna humanim glioblastomima. Za uspostavljanje rezistencije korišćen je prvi odobreni antigliomski lek 1,3-bis(2-hloroetil)-1-nitrozoureom (BCNU, karmustin), alkilirajući agens koji se koristi u terapiji primarnih i rekurentnih glioblastoma. Kontinuirana primena BCNU je dovela do razvoja rezistencije C6 ćelija ne samo na ovaj hemioterapeutik, već i na druge DNK oštećujuće agense, cisplatin (CPt) i temozolomid (TMZ). Novouspostavljena rezistentna ćelijska linija je oznaĉena kao RC6. Ispitivanje mehanizama rezistencije je obuhvatilo analizu promena na nivou apoptotske mašinerije i oštećenja DNK lanaca, kao i analizu promena u antioksidativnom kapacitetu izmeĊu C6 i RC6 ćelija. Rezistentna RC6 linija pokazuje smanjenu osetljivost na indukciju ćelijske smrti koja je praćena smanjenjem ekspresije antiapoptotskog faktora Bcl-2, proapoptotskog faktora Bad i efektorske kaspaze 3 na nivou iRNK i proteina. TakoĊe je pokazano smanjenje ekspresije iRNK antiapoptoskog Bcl-Xl i proapoptotskog Bax-a. Razvoj rezistencije je doveo i do znaĉajnog povećanja produkcije reaktivnih kiseoniĉnih vrsta (ROS) i smanjenja odnosa koncentracije oksidovanog i redukovanog glutationa. Zapaţeno je povećanje ekspresije iRNK komponenti antioksidativnog sistema (MnSOD, iNOS, GPx i MRP1) i smanjenje ekspresije iRNK za HIF-1α kod RC6 ćelija u odnosu na C6 ćelije. RC6 ćelije pokazuju povećanu osetljivost na delovanje doksorubicina (DOX). UtvrĊeno je da RC6 ćelije akumuliraju više DOX-a od C6 ćelija ĉemu doprinosi znaĉajno smanjenje ekspresije iRNK za ABCB1 membranski transporter, kao i smanjenje unutarćelijskog pH. Pored toga, RC6 ćelije proliferišu znatno sporije u odnosu na C6 ćelije što je karakteristiĉno za rezistentne ćelije, ali i za ćelije sa većim invazivnim sposobnostima. Rezultati potvrĊuju da invazivnosti RC6 ćelija doprinosi povišena ekspresija iRNK za metaloproteinazu MMP9...

Advisors/Committee Members: Matić, Gordana, 1953-.

Subjects/Keywords: Glioblastoma; chemoresistance; carmustine (BCNU); temozolomide (TMZ); collateral sensitivity; invasiveness; antiglioma therapy; CoQ10

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Stojković-Burić, Sonja M., 1. (2017). Model ćelija C6 glioma pacova kao oruđe za pronalaženje novih terapeutskih strategija: karakterizacija rezistentnog fenotipa in vitro i in vivo. (Thesis). Univerzitet u Beogradu. Retrieved from https://fedorabg.bg.ac.rs/fedora/get/o:15650/bdef:Content/get

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Stojković-Burić, Sonja M., 1985-. “Model ćelija C6 glioma pacova kao oruđe za pronalaženje novih terapeutskih strategija: karakterizacija rezistentnog fenotipa in vitro i in vivo.” 2017. Thesis, Univerzitet u Beogradu. Accessed January 18, 2021. https://fedorabg.bg.ac.rs/fedora/get/o:15650/bdef:Content/get.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Stojković-Burić, Sonja M., 1985-. “Model ćelija C6 glioma pacova kao oruđe za pronalaženje novih terapeutskih strategija: karakterizacija rezistentnog fenotipa in vitro i in vivo.” 2017. Web. 18 Jan 2021.

Vancouver:

Stojković-Burić, Sonja M. 1. Model ćelija C6 glioma pacova kao oruđe za pronalaženje novih terapeutskih strategija: karakterizacija rezistentnog fenotipa in vitro i in vivo. [Internet] [Thesis]. Univerzitet u Beogradu; 2017. [cited 2021 Jan 18]. Available from: https://fedorabg.bg.ac.rs/fedora/get/o:15650/bdef:Content/get.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Stojković-Burić, Sonja M. 1. Model ćelija C6 glioma pacova kao oruđe za pronalaženje novih terapeutskih strategija: karakterizacija rezistentnog fenotipa in vitro i in vivo. [Thesis]. Univerzitet u Beogradu; 2017. Available from: https://fedorabg.bg.ac.rs/fedora/get/o:15650/bdef:Content/get

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Freie Universität Berlin

4. Gutowski, Pawel. The survival benefit for glioblastoma patients treated with carmustine wafer in relation to the methylation of O6-Methylguanine-DNA-Methyltransferase promoter.

Degree: 2016, Freie Universität Berlin

URL: http://dx.doi.org/10.17169/refubium-5535

► Glioblastoma multiforme is the most common and most aggressive primary brain tumor (WHO grade IV). Despite all the care taken to treat the tumor the… (more)

Subjects/Keywords: glioblastoma multiforme; GBM; MGMT; Gliadel; Carmustine Wafer; Pyrosequencing; 600 Technik, Medizin, angewandte Wissenschaften::610 Medizin und Gesundheit

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Gutowski, P. (2016). The survival benefit for glioblastoma patients treated with carmustine wafer in relation to the methylation of O6-Methylguanine-DNA-Methyltransferase promoter. (Thesis). Freie Universität Berlin. Retrieved from http://dx.doi.org/10.17169/refubium-5535

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Gutowski, Pawel. “The survival benefit for glioblastoma patients treated with carmustine wafer in relation to the methylation of O6-Methylguanine-DNA-Methyltransferase promoter.” 2016. Thesis, Freie Universität Berlin. Accessed January 18, 2021. http://dx.doi.org/10.17169/refubium-5535.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Gutowski, Pawel. “The survival benefit for glioblastoma patients treated with carmustine wafer in relation to the methylation of O6-Methylguanine-DNA-Methyltransferase promoter.” 2016. Web. 18 Jan 2021.

Vancouver:

Gutowski P. The survival benefit for glioblastoma patients treated with carmustine wafer in relation to the methylation of O6-Methylguanine-DNA-Methyltransferase promoter. [Internet] [Thesis]. Freie Universität Berlin; 2016. [cited 2021 Jan 18]. Available from: http://dx.doi.org/10.17169/refubium-5535.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Gutowski P. The survival benefit for glioblastoma patients treated with carmustine wafer in relation to the methylation of O6-Methylguanine-DNA-Methyltransferase promoter. [Thesis]. Freie Universität Berlin; 2016. Available from: http://dx.doi.org/10.17169/refubium-5535

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

5. Mihaliak, Alicia M. Clinically Relevant Doses of Chemotherapy Drugs Selectively and Reversibly Block Glioblastoma Neurosphere Proliferation in vitro: A Dissertation.

Degree: Interdisciplinary Graduate Program, Biochemistry and Molecular Pharmacology, 2010, U of Massachusetts : Med

URL: https://escholarship.umassmed.edu/gsbs_diss/492

► My thesis research began with a project in which we were trying to determine the function of embryonic stem cell (ESC)-specific miRNAs. Using luciferase… (more)

▼ My thesis research began with a project in which we were trying to determine the function of embryonic stem cell (ESC)-specific miRNAs. Using luciferase constructs containing miRNA binding sites, luciferase expression was inhibited by endogenous miRNAs in ESCs, and by exogenous miRNAs in HeLa cells. Inhibition of luciferase expression by miRNAs was inhibited in HeLa cells using 2’O-methyl-oligonucleotides. In ESCs, 2’O-methyl-oligonucleotides were only effective in partially inhibiting miR290 function. Partial inhibition of miR290 did not result in any obvious phenotypic changes in mESCs. Later studies using 2’O-methyl-oligonucleotides in ESCs were also unsuccessful. The function of ESC-specific miRNAs has since been studied by re-introducing miRNAs into Dicer -/- cells which cannot make miRNAs. These studies have shown that ESC-specific miRNAs are involved in de novo DNA methylation, self-renewal, and cell-cycle regulation. Newly diagnosed glioblastoma (GBM) patients rarely survive more than two years even after surgery, radiotherapy, and chemotherapy using temozolomide (TMZ) or 1,3-bis(2-chloroethy)-1-nitrosourea (BCNU). Eventual regrowth of the tumor indicates that some tumor cells are resistant to therapy. GBM neurosphere-initiating cells (NICs) are thought to be similar to tumor-initiating cells in vivo, and will form invasive tumors in mice, making neurosphere cultures a good model system for studying GBMs. To test whether GBM NICs were resistant to chemotherapy, we used a neurosphere formation assay to measure the number of proliferating NICs in the presence of TMZ or BCNU. The concentrations of chemotherapy drugs required to inhibit neurosphere formation were much less than those required to inhibit bulk cell proliferation or to induce cell death in our neurosphere cultures. For some cultures, there was a robust recovery of neurosphere formation after chemotherapy treatment which appeared to be DNA damage independent. Some of the cultures that showed significant recovery of neurosphere formation underwent reversible cell cycle arrest, possibly reducing chemotoxicity in these cultures. Collectively, these results indicate that GBM neurosphere cultures can regrow after being treated with clinically relevant doses of chemotherapy drugs. Chemotherapy-treated neurosphere cultures remained viable, and formed tumors when injected into mice. Our experiments show that these in vitro assays may be useful in predicting in vivo responses to chemotherapeutic agents. Advisors/Committee Members: Alonzo Ross, PhD.

Subjects/Keywords: Glioblastoma; Drug Therapy; Cell Proliferation; Carmustine; Dacarbazine; Cancer Biology; Cells; Embryonic Structures; Genetic Phenomena; Heterocyclic Compounds; Neoplasms; Organic Chemicals; Pharmaceutical Preparations; Therapeutics

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Mihaliak, A. M. (2010). Clinically Relevant Doses of Chemotherapy Drugs Selectively and Reversibly Block Glioblastoma Neurosphere Proliferation in vitro: A Dissertation. (Doctoral Dissertation). U of Massachusetts : Med. Retrieved from https://escholarship.umassmed.edu/gsbs_diss/492

Chicago Manual of Style (16^th Edition):

Mihaliak, Alicia M. “Clinically Relevant Doses of Chemotherapy Drugs Selectively and Reversibly Block Glioblastoma Neurosphere Proliferation in vitro: A Dissertation.” 2010. Doctoral Dissertation, U of Massachusetts : Med. Accessed January 18, 2021. https://escholarship.umassmed.edu/gsbs_diss/492.

MLA Handbook (7^th Edition):

Mihaliak, Alicia M. “Clinically Relevant Doses of Chemotherapy Drugs Selectively and Reversibly Block Glioblastoma Neurosphere Proliferation in vitro: A Dissertation.” 2010. Web. 18 Jan 2021.

Vancouver:

Mihaliak AM. Clinically Relevant Doses of Chemotherapy Drugs Selectively and Reversibly Block Glioblastoma Neurosphere Proliferation in vitro: A Dissertation. [Internet] [Doctoral dissertation]. U of Massachusetts : Med; 2010. [cited 2021 Jan 18]. Available from: https://escholarship.umassmed.edu/gsbs_diss/492.

Council of Science Editors:

Mihaliak AM. Clinically Relevant Doses of Chemotherapy Drugs Selectively and Reversibly Block Glioblastoma Neurosphere Proliferation in vitro: A Dissertation. [Doctoral Dissertation]. U of Massachusetts : Med; 2010. Available from: https://escholarship.umassmed.edu/gsbs_diss/492

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