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Bolander, Åsa. "Prognostic factors in malignant melanoma /". Uppsala : Acta Universitatis Upsaliensis : Universitetsbiblioteket [distributör], 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-9511.
Pełny tekst źródłaShort, Candice, i Ryan Short. "Uveal Melanoma". Digital Commons @ East Tennessee State University, 2019. https://dc.etsu.edu/etsu-works/7353.
Pełny tekst źródłaShort, Candice, i Ryan Short. "Uveal Melanoma". Digital Commons @ East Tennessee State University, 2020. https://dc.etsu.edu/etsu-works/7357.
Pełny tekst źródłaAliprandini, Eduardo. "Efeito da melanina e do oxigenio singlete na morte celular e fluxo de cálcio em células Melan-A e B16-F10". reponame:Repositório Institucional da UFPR, 2010. http://hdl.handle.net/1884/22552.
Pełny tekst źródłaDissertação (mestrado) - Universidade Federal do Paraná, Setor de Ciências Biológicas, Programa de Pós-Graduação em Bioquímica. Defesa: Curitiba, 12/02/2010
Bibliografia: 65-74
Área de concentração: Bioquímica
Resumo
Resumo: O melanoma e um tipo de cancer bastante relevante ja que as opcoes de tratamento eficazes sao limitadas. A presenca da melanina protege os individuos de pele escura contra os efeitos da radiacao solar, a principal causa de formacao do melanoma pela geracao de especies reativas de oxigenio (ROS). Porem, a melanina tambem pode ter um papel duplo, que e a de gerar especies reativas durante sua sintese que podem prejudicar a celula. Portanto, o objetivo deste trabalho foi a avaliacao das caracteristicas de morte celular causadas por uma ROS, o oxigenio singlete (1O2), nas celulas de melanoma murino B16-F10 com e sem estimulo para producao de melanina e nas celulas de melanocito murino Melan-a. O estimulo para a sintese de melanina foi obtido incubando-se as celulas por 48 horas com meio RPMI 1640 enriquecido com 400 ƒÊmol/L de L-tirosina e 10 mmol/L de cloreto de amonio. A concentracao de melanina aumentou em mais de nove vezes nas celulas B16-F10 e as celulas Melan-a tiveram aumento de menos de duas vezes. Foi utilizado o endoperoxido DHPNO2 10 mmol/L por 2 horas para a geracao de 1O2. Essa condicao causou queda na viabilidade avaliada pelo metodo do MTT para 78,0% nas celulas B16-F10, 70,2% nas B16-F10 estimuladas (B16-F10 Y) e 79,3% nas Melan-a. O ensaio foi feito apos 24 horas do inicio do tratamento com DHPNO2 e a viabilidade caiu para 49,7% nas B16-F10, 53,3% nas B16- F10 Y e 72,5% nas Melan-a. A avaliacao da morte celular utilizando laranja de acridina e brometo de etidio mostrou que apos o tratamento por 2 horas, somente as celulas B16- F10 tiveram aumento significativo na quantidade de celulas em apoptose, e as B16-F10 Y tiveram leve queda na quantidade de celulas viaveis, com tendencia ao aumento de celulas em apoptose. As celulas Melan-a nao tiveram diferenca entre os tratamentos. A liberacao do citocromo c foi determinada por HPLC e mostrou-se que apos 2 horas, as celulas B16-F10 tratadas com 1O2 tiveram mais citocromo c liberado para o citoplasma comparado com o controle. Nos demais grupos, nao houve alteracao com o tratamento. Porem, as celulas controle com mais melanina tiveram maior liberacao de citocromo comparado com o controle das celulas nao estimuladas, mostrando que as celulas estavam sofrendo algum dano inerente da sintese de melanina. A analise da fragmentacao do DNA apos 2 e 24 horas mostrou que nao houve aparecimento de quebras caracteristicas de apoptose pelo tratamento com 1O2 em nenhum dos grupos testados. As celulas B16-F10 Y controle apresentaram DNA fragmentado inespecificamente, representado como um arraste no gel de agarose, que nao foi alterado pelo tratamento. A razao entre ADP e ATP foi quantificada para avaliar o estado energetico da celula, que pode refletir algumas caracteristicas de morte. Nenhuma das celulas teve diferenca estatistica apos o tratamento de 2 horas com 1O2, mas foi observado que as razoes ADP/ATP das celulas controle B16-F10 com e sem estimulo apresentaram valores acima do valor considerado para celulas viaveis/proliferativas. Os resultados da celula Melan-a foram bem proximos dos valores ditos normais. O fluxo de calcio tambem foi avaliado e o 1O2 foi capaz de liberar calcio das reservas intracelulares para o citoplasma nas celulas B16-F10, sendo que nas celulas estimuladas, o aumento do calcio citoplasmatico foi menor, indicando a possivel recaptacao do calcio pela melanina. As celulas Melan-a nao sofreram grandes alteracoes na quantidade de calcio liberado para o citoplasma. Nao houve diferenca na liberacao de AIF em nenhuma das celulas. Em conjunto, os resultados mostram que a sintese da melanina estimulada pela suplementacao do meio foi deleteria as celulas, pois causou fragmentacao no DNA, liberacao de citocromo c e aumentou a razao ADP/ATP para valores considerados de celula em apoptose. Por outro lado, a presenca da melanina parece ter protegido as celulas da acao do 1O2, pois alguns resultados indicam uma tendencia de melhora dos parametros avaliados.
Abstract: Melanoma is a relevant type of cancer since the options for efficient treatment are limited. The presence of melanin protects the dark-skinned people against the effects of solar radiation, the main cause for melanoma development by the generation of reactive species of oxygen (ROS). However, melanin may also have a role on the generation of reactive species during its synthesis, which may harm the cell. So, the objective of this work was the evaluation of the characteristics of cell death caused by a ROS, the singlet oxygen (1O2) on murine melanoma cells B16-F10 with or without stimulation for synthesis of melanin and on murine melanocytes cells Melan-a. The stimulus for the synthesis of melanin was obtained treating the cells for 48 hours with medium RPMI 1640 supplemented with 400 ìmol/L of L-Tyrosine and 10 mmol/L of ammonium chloride. The concentration of melanin increased more than nine times in the B16-F10 cells and the Melan-a cells increase was almost twice the amount of the control. It was used the endoperoxide DHPNO2 10 mmol/L for 2 hours for the generation of 1O2. This condition caused the decrease in the viability determined by the method of MTT to 78% in B16-F10, 70,2% in B16-F10 that were stimulated (B16-F10 Y) and 79,3% in Melana cells. The test was performed after 24 hours from the beginning of the treatment with DHPNO2 and the viability decreased to 49,7% in B16-F10, 53,3% in B16-F10 Y and 72,5 % in Melan-a. The evaluation of cell death using acridine orange and ethidium bromide showed that after the two-hour treatment, only the B16-F10 cells had a significant increase of the number of apoptotic cells, and the B16-F10 Y cells had a slight decrease of the amount of viable cells, with the tendency of the increase of apoptotic cells. Melan-a cells did not show difference among the treatments. The release of cytochrome c was determined by HPLC and it showed that after two hours, B16-F10 cells had more cytochrome c released to the cytoplasm compared to the control. There was not any alteration for other groups of cells with the treatment. However, the control cells that had more melanin showed increased cytochrome c release compared to the control of the not-stimulated cells, demonstrating that the previous cells were suffering some kind of damage from the melanin synthesis. The analysis of DNA fragmentation revealed the absence of typical apoptosis fragmentation in any of the groups. B16-F10 Y control cells displayed unspecific DNA damage observed as a smear in the agarose gel, which was not altered by 1O2 treatment. The same result was observed after the treatment for 2 and 24 hours. The ratio between ADP and ATP was quantified to evaluate the energetic state of the cell, which may reflect some characteristics of cell death. None of the cells showed results statistically significant after the two-hour treatment 1O2, but it was shown that the values of ADP/ATP ratio of the B16-F10 control cells with and without stimulation were above of the threshold accepted for viable/proliferative cells. The results of Melan-a cells were very close to the values considered normal. The calcium flux was also evaluated and it was evidenced that 1O2 was capable of releasing calcium from the intracellular stores to the cytoplasm in B16- F10 cells, and the release of calcium was lower in B16-F10 Y, indicating the possibility of the binding of the metal to melanin. The Melan-a cells did not showed much increase in the quantities of calcium released to the cytoplasm. There was no difference in the release of AIF in any group. Over all, the results support that the synthesis of melanin that was stimulated by the supplementation of the medium was deleterious to the cells, since it caused DNA fragmentation, release of cytochrome c and increase of the ratio ADP/ATP to values of cells in apoptosis. On the other hand, the presence of melanin seemed to protect the cells against the action of 1O2, because some results indicate a tendency of improvement in the parameters evaluated.
Kohli, Jaskaren Singh. "Senescence and immortalisation in melanoma progression and multiple primary melanoma". Thesis, St George's, University of London, 2016. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.706529.
Pełny tekst źródłaWilson, Kenneth Scott. "Cutaneous malignant melanoma". Thesis, University of Edinburgh, 1994. http://hdl.handle.net/1842/27062.
Pełny tekst źródłaWiguna, Arlina Permatasari. "Immunoregulation in melanoma". Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2015. http://dx.doi.org/10.18452/17107.
Pełny tekst źródłaIL-10 and TGF-beta are immunosuppressive cytokines expressed in tumors including melanoma and, therefore, deemed major cause for failing anti-tumor immune responses. To re-evaluate their role, their expression was compared by quantitative RT-PCR in melanoma and skin of healthy individuals, their induction in dendritic cells and T cells co-cultured with tumor cells, and their effects on the immune cells were tested. Both cytokines as well as their receptors were expressed in melanoma at significantly lower levels than in healthy skin. Consequently, the expressions of IL-10-responsive SOCS-3 and TGF-beta-responsive Smad-7 were low in tumors but high in healthy skin. T cells co-cultured with tumor cells developed an anergic state but without increased IL-10 or TGF-beta expression. In vitro tumor-associated iDCs produced high IL-10 levels and were less efficient in inducing T cell proliferation. Nonetheless, they could be induced to mature, and blocking IL-10 did not alter the capacity of the resulting mDCs to induce T cell proliferation. mDCs co-cultured with tumor cells produced increased IL-10 but similar or decreased TGF-beta level and were more efficient in inducing T cell proliferation. The lack of correlation of IL-10 and TGF-beta with immune deficits in situ and in vitro suggests a necessity of re-evaluating their roles in cancer.
Winklmeier, Andreas. "Rolle der Transkription und Aktivität von MIA ("Melanoma Inhibitory Activity") im malignen Melanom". kostenfrei, 2009. http://www.opus-bayern.de/uni-regensburg/volltexte/2009/1301/.
Pełny tekst źródłaHering, Kathrin, Anke Bresch, Donald Lobsien, Wolf Müller, Rolf-Dieter Kortmann i Clemens Seidel. "Primary intradural extramedullary spinal melanoma in the lower thoracic spine". Universitätsbibliothek Leipzig, 2016. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-205904.
Pełny tekst źródłaGilbert, Amy. "Humoral immune response to melanoma : discovery and evaluation of anti-melanoma antibodies". Thesis, King's College London (University of London), 2013. https://kclpure.kcl.ac.uk/portal/en/theses/humoral-immune-response-to-melanoma-discovery-and-evaluation-of-antimelanoma-antibodies(34c0be73-e94a-4d3f-92b9-8888178c4cd2).html.
Pełny tekst źródłaHaridas, Parvathi. "In vitro characterisation of melanoma progression in a melanoma skin equivalent model". Thesis, Queensland University of Technology, 2018. https://eprints.qut.edu.au/118574/1/Parvathi_Haridas_Thesis.pdf.
Pełny tekst źródłaTatzel, Jutta. "Bedeutung von MIA (Melanoma inhibitory activity) bei der Entstehung und Progression des malignen Melanoms". [S.l.] : [s.n.], 2005. http://deposit.ddb.de/cgi-bin/dokserv?idn=975164775.
Pełny tekst źródłaWesterdahl, Johan. "Malignant melanoma risk factors /". Lund : Dept. of Surgery, Lund University, 1995. http://catalog.hathitrust.org/api/volumes/oclc/39204671.html.
Pełny tekst źródłaReiniger, Ingrid. ""Melanoma Inhibitory Activity" (MIA)". Diss., lmu, 2005. http://nbn-resolving.de/urn:nbn:de:bvb:19-34405.
Pełny tekst źródłaRobles, Espinoza Carla Daniela. "Drivers of melanoma susceptibility". Thesis, University of Cambridge, 2015. https://www.repository.cam.ac.uk/handle/1810/247224.
Pełny tekst źródłaAkhras, Victoria. "Lymphatic functions in melanoma". Thesis, St George's, University of London, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.546785.
Pełny tekst źródłaPearl, Robert Ashley. "Molecular targets in melanoma". Thesis, University College London (University of London), 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.497695.
Pełny tekst źródłaPane, Anthony Robert. "Ocular melanoma in Queensland /". [St. Lucia, Qld.], 2001. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe16144.pdf.
Pełny tekst źródłaCaputo, Emilia. "Analisi molecolare del melanoma". Doctoral thesis, Università di Catania, 2012. http://hdl.handle.net/10761/1214.
Pełny tekst źródłaMartens, Kelly A. "Utilization of extreme drug resistance testing in malignant melanoma new is not always better". Gold Coast, QLD : Bond University, 2005. http://epublications.bond.edu.au/theses/martens.
Pełny tekst źródła"A thesis submitted to Bond University in fulfillment of the requirements for the degree of Doctor of Health Sciences"-- t.p. Bibliography: pages 379-442. Also available via the World Wide Web.
Seguin, Fabiana 1984. "Estudo do papel biológico da enzima ácido graxo sintase (FASN) em células endoteliais derivadas dos vasos sanguíneos". [s.n.], 2011. http://repositorio.unicamp.br/jspui/handle/REPOSIP/290689.
Pełny tekst źródłaTese (doutorado) - Universidade Estadual de Campinas, Faculdade de Odontologia de Piracicaba
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Resumo: A enzima ácido graxo sintase (FASN), cuja expressão e atividade estão elevadas em várias neoplasias malignas humanas, é responsável pela síntese endógena de ácidos graxos saturados de cadeia longa e, consequentemente, pela a produção de fosfolipídios das membranas celulares. A inibição de FASN com orlistat (Xenical), uma droga anti-obesidade, é descrita como tendo propriedades anti-neoplásicas nos cânceres de próstata, mama, bem como no melanoma. Este composto parece desempenhar também um papel anti-angiogênico, uma vez que foi descrito como inibidor da proliferação de células endoteliais e da neovascularização em ensaio ex vivo. Em trabalho recente, realizado por nosso grupo de pesquisa, foi demonstrado que o tratamento de camundongos portadores de melanomas intraperitoneais com orlistat reduziu em cerca de 50% o número de metástases para linfonodos mediastínicos. Em outro estudo, também realizado por nosso grupo, foi observado que a inibição da atividade de FASN pode ter um papel sobre a angiogênese induzida por melanomas experimentais, pois a densidade de vasos sanguíneos ao redor destes tumores foi significantemente reduzida pelo tratamento com orlistat. Considerando as evidências sugerindo um papel biológico relevante de FASN na disseminação metastática de melanomas, o presente trabalho de pesquisa teve como objetivo principal investigar as consequências da inibição da atividade de FASN em cultura de células endoteliais de vasos sanguíneos, através da análise do ciclo celular e das taxas de apoptose. A expressão dos diversos fatores da família VEGF foi avaliada por RT-PCR quantitativo em células de melanoma e carcinoma espinocelular bucal. Os resultados obtidos mostram que orlistat e cerulenina inibem a viabilidade, induzem a apoptose e reduzem in vitro a formação de vasos sanguíneos pelas células endoteliais RAEC. No entanto, o mesmo tratamento não reduz a viabilidade e nem reduzem a formação de vasos sanguíneos in vitro pelas células endoteliais HUVEC. A inibição de FASN nas células neoplásicas SK-MEL-25 e SCC-9 aumenta a expressão de RNAs mensageiros para VEGFA e que o meio condicionado por estas células com orlistat reduz a formação in vitro de vasos sanguíneos e a proliferação das células HUVEC. Nossos resultados sugerem que FASN parece ser importante para a sobrevivência das células RAEC e que a inibição de FASN modula a expressão das isoformas de VEGFA
Abstract: Fatty acid synthase (FASN) is the anabolic enzyme with high expression and activity in several human malignancies, which is responsible for the endogenous synthesis of saturated fatty acids and consequently of the phospholipids present in cell membranes. Inhibition of FASN with orlistat (Xenical), an anti-obesity drug, is described as having anti-neoplastic properties in breast and prostate cancers as well as in melanoma. An anti-angiogenic role, has been attributed to this drug, since it inhibits the proliferation of endothelial cells and the neovascularization in ex vivo both assays. In recent studies performed by our group, it was demonstrated that the treatment of mice bearing intraperitoneal melanoma with orlistat reduced by 50% the number of metastases to mediastinal lymph nodes. In another study, also conducted by our group, we observed that the inhibition of FASN reduces the angiogenesis induced by experimental melanomas, since the density of blood vessels around tumors was significantly decreased by the treatment with orlistat. In the present work investigated the consequences of the treatment with FASN inhibitors the proliferation and apoptosis cultured endothelial cells. The expression of the VEGF family of growth factors were assessed by quantitative RT-PCR in both melanoma and squamous cell carcinoma cells. The results show that orlistat and cerulenin inhibit the viability and induce apoptosis and reduce the formation of blood vessels by RAEC cells in vitro. However, the same treatment does not reduce the viability and not reduce the formation of blood vessels by HUVEC cells in vitro. The inhibition of FASN in neoplastic cells SK-MEL-25 and SCC-9 increases the expression of mRNAs for VEGF and the conditioned medium by these cells with orlistat reduces the formation of blood vessels in vitro and proliferation of HUVEC cells. Together, the experiments show that FASN seems to be important for the survival of RAEC cells and FASN inhibition modulates the expression of VEGF isoforms
Doutorado
Patologia
Doutor em Estomatopatologia
Kmetiuk, Louise Nicolle Bach. "Desenvolvimento e avaliação comparativa do melanoma oral em camundongos, frente sua ocorrência espontânea em cães". Universidade Estadual de Ponta Grossa, 2016. http://tede2.uepg.br/jspui/handle/prefix/2761.
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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior
ntrodução: O Melanoma é a principal neoplasia em cavidade oral de cães domésticos. Ocorre principalmente em gengiva, e caracteriza-se pela progressão acelerada, altos índices de recidiva, metástase e resistência a terapias propostas. Tais aspectos impulsionaram o presente estudo, considerando a ausência de um modelo experimental para essa neoplasia, que possibilite a realização de ensaios pré-clínicos. Objetivos: Induzir a formação de melanoma oral murino em camundongos C57Bl/6J, e estudar suas características macroscópicas e histopatológicas. Método: trata-se de um estudo experimental. Trinta camundongos C57Bl/6J (Mus musculus) foram submetidos a indução tumoral através da injeção de células da linhagem de melanoma murino B16F10 em gengiva inferior direita porção vestibular, em duas concentrações celulares, originando dois grupos distintos: Grupo 1 (n=15) que receberam 0,1 ml contendo 1x104 células de melanoma murino B16F10; Grupo 2 (n=15) que receberam 0,1 ml contendo 5x104 células de melanoma murino B16F10. Para ambos os grupos foram realizadas eutanásias programadas aos sétimo, décimo quarto e vigésimoprimeiro dias de pós-operatório, com ressecção ex-vivo da hemicabeça direita. Após a exclusão dos indivíduos que foram a óbito antes do período determinado para eutanásia, obteve-se um número de indivíduos na amostra (n) de 21. Foi realizada análise macroscópica das formações tumorais. Para o estudo histológico comparativo, analisaram-se amostras de melanoma oral canino melânico no que tange aos aspectos morfométricos e morfológicos. Resultados: Houve diferença no desenvolvimento tumoral para cada concentração celular utilizada na indução. Notouse correlação positiva entre volume tumoral e número de células. Conclusão: A indução de melanoma oral em camundongos para fins de modelo de estudo pré-clínico para cães se mostrou uma alternativa útil, viável e reproduzível.
Introduction: Melanoma is the most common neoplasm in oral cavity of dogs. Melanoma has a predilection for the gum, and it is characterized by accelerated progression and high rates of relapse, metastasis and resistance to proposed therapies. Those factors inspires the present study, considering the lack of an experimental model for melanoma. Method: This is an experimental study. Thirty C57Bl / 6J mice (Mus musculus) were submitted to tumor induction by injecting murine melanoma B16F10 cells into the right lower gum using two different cell concentrations. Mice were divided in two groups: Group 1 (n = 15) received 1x104 murine melanoma B16F10 cells injection; Group 2 (n = 15) received 5x104 murine melanoma B16F10 cells injections. For both groups, euthanasia was scheduled at the 7th., 14th. and 21th. postoperative day, with post-mortem hemi-resection of the jaw. Individuals who died before the euthanasia period were excluded, leaving 21 mice. Macroscopic analysis of tumor formations was performed. For comparative histological study, oral canine melanoma samples were analyzed for morphological aspects. Data sete analyzed with BioStat 5.3 and submitted to non-parametric statistical tests. Results: Different tumor characteristics (tumor volume, presence of irregular margins, ulceration and dark coloration) were observed for each cell concentration used in the induction, as well perfect correlation between tumor volume and tumor growth. Conclusion: The induction of oral melanoma in mice for purposes of preclinical study model for dogs is an useful, viable and reproducible alternative.
Beddingfield, Frederick Coston. "Melanoma a decision analysis to estimate the effectiveness and cost-effectiveness of screening and an analysis of the relevant epidemiology of the disease /". Santa Monica, CA : RAND, 2002. http://catalog.hathitrust.org/api/volumes/oclc/51441066.html.
Pełny tekst źródłaLamberti, Arianna. "PRIMARY MELANOMA OF THE SKIN AND CUTANEOUS MELANOMA METASTASES: COMPARATIVE STUDY OF TUMOR MICROENVIRONMENT". Doctoral thesis, Università di Siena, 2019. http://hdl.handle.net/11365/1073036.
Pełny tekst źródłaRagnarsson, Olding Boel. "Malignant melanoma of the vulva /". Stockholm, 1999. http://diss.kib.ki.se/1999/91-628-3567-X/.
Pełny tekst źródłaBolander, Åsa. "Prognostic Factors in Malignant Melanoma". Doctoral thesis, Uppsala universitet, Enheten för onkologi, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-9511.
Pełny tekst źródłaFoss, Alexander James Easterbrook. "The pathobiology of uveal melanoma". Thesis, University of Oxford, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.337565.
Pełny tekst źródłaLi, Weiling. "Genetic changes in melanoma progression". Thesis, University of Edinburgh, 2011. http://hdl.handle.net/1842/5595.
Pełny tekst źródłaLang, Julie M. S. "Genetics of cutaneous malignant melanoma". Thesis, University of Glasgow, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.413378.
Pełny tekst źródłaHealy, Eugene. "Genetic changes in cutaneous melanoma". Thesis, University of Newcastle Upon Tyne, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.389573.
Pełny tekst źródłaHarries, Mark. "Enhancing anti-melanoma immune responses". Thesis, University College London (University of London), 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.325539.
Pełny tekst źródłaBlessing, Karen. "Prognostic factors in malignant melanoma". Thesis, University of Aberdeen, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.305319.
Pełny tekst źródłaKernohan, Neil M. "Cutaneous malignant melanoma - immunophenotypic considerations". Thesis, University of Aberdeen, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.305449.
Pełny tekst źródłaAnbunathan, Hima. "Genomic landscape of uveal melanoma". Thesis, Imperial College London, 2017. http://hdl.handle.net/10044/1/58247.
Pełny tekst źródłaMacKenzie, Ross Alastair Dudley. "Overcoming senescence in melanoma development". Thesis, University of Cambridge, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.611085.
Pełny tekst źródłaKayaga, Justina. "Allogenic tumour vaccines for melanoma". Thesis, St George's, University of London, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.394404.
Pełny tekst źródłaWhite, Nicholas. "Purinergic signalling in malignant melanoma". Thesis, University College London (University of London), 2005. http://discovery.ucl.ac.uk/1446032/.
Pełny tekst źródłaRobinson, June K., Katie Baker i Joel J. Hillhouse. "New Approaches to Melanoma Prevention". Digital Commons @ East Tennessee State University, 2017. https://dc.etsu.edu/etsu-works/73.
Pełny tekst źródłaMedic, Sandra. "PAX3 and cutaneous malignant melanoma". Thesis, Edith Cowan University, Research Online, Perth, Western Australia, 2006. https://ro.ecu.edu.au/theses/341.
Pełny tekst źródłaNg, Kin Cheung Philip. "The expression of XAF1 in melanoma and the role of ILK in melanoma invasive behavior". Thesis, University of British Columbia, 2007. http://hdl.handle.net/2429/31801.
Pełny tekst źródłaMedicine, Faculty of
Medicine, Department of
Experimental Medicine, Division of
Graduate
Karlsson, Pia. "Cutaneous melanoma in children and adolescents and aspects of naevus phenotype in melanoma risk assessment". Doctoral thesis, Linköping : Univ, 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-7703.
Pełny tekst źródłaErrico, Maria Cristina. "Melanoma stem-like cells and melanoma cell lines: main molecular pathways and possible microRNA involvement". Thesis, Universita' degli Studi di Catania, 2011. http://hdl.handle.net/10761/94.
Pełny tekst źródłaCho, Kenneth Kunhee. "Acral Melanoma: Epidemiology and Treatment Outcomes". Thesis, The University of Sydney, 2021. https://hdl.handle.net/2123/25557.
Pełny tekst źródłaVeronez, Luciana Chain. "Atividade da fosfoetanolamina sintética em melanoma murino experimental". Universidade de São Paulo, 2012. http://www.teses.usp.br/teses/disponiveis/17/17147/tde-15122012-123717/.
Pełny tekst źródłaThe low responsiveness of melanoma to traditional treatments together with its increasing incidence makes the development of new therapeutic strategies against this type of cancer extremely important. In this study, we used a murine melanoma model to evaluate the effects of synthetic phosphoethanolamine (PEA) on the development of this tumor. In vitro, PEA had an inhibitory effect on the proliferation of B16F10 cells, inducing apoptosis after 24 to 72h stimulation. In vivo, oral treatment of melanoma-bearing animals with different doses of PEA (10, 20 e 40mg/Kg) during 10 or 20 consecutive days resulted in reduced tumor volumes (at least 70% compared to the control) and in expressive macroscopic differences. PEA also induced a dose-dependent increase of apoptosis and decrease in tumor cell proliferation. The treatment also resulted in hematological changes, such as increased numbers of platelets, erythrocytes and leukocytes. Among leukocytes, we observed a higher proportion of lymphocytes and monocytes after 10 and 20 days of treatment, respectively. In addition, PEA induced higher levels of the pro-inflammatory cytokine IL-6 and of the anti-inflammatory cytokines IL-10 and TGF-, and it also induced a lower production of the pro-inflammatory cytokine IFN-. No differences were observed in the levels of IL-1, TNF-, IL-12p70 and IL-17 upon treatment. Our results demonstrate an inhibitory role of PEA in the development of melanoma, contributing to a better understanding of its antitumoral activity.
Liu, Yuxi. "Anti-melanoma effects and mechanisms of action of a Chinese medicine formula Huai-Hua-Jin-Yin-Jiu". HKBU Institutional Repository, 2020. https://repository.hkbu.edu.hk/etd_oa/802.
Pełny tekst źródłaPrado, Sara Santos Bernardes Real. "Estresse oxidativo e biomarcadores do metabolismo do ferro em pacientes com melanoma cutâneo e melanoma recidivado". Universidade Estadual de Londrina. Centro de Ciências Biológicas. Programa de Pós-Graduação em Patologia Experimental, 2014. http://www.bibliotecadigital.uel.br/document/?code=vtls000192063.
Pełny tekst źródłaSurgical removal of cutaneous melanoma can cure most of the patients, however, the risk of recurrence remains for years. One of the most accepted correlation in cutaneous melanoma prognosis is Breslow thickness, where high tumor thickness values at diagnosis is strongly related to melanoma spread and high morbidity. Oxidative stress in patients with cancer is reported in literature, but their role in prognosis is still controversial. The ferritin heavy (FHC) and light chains (FLC) are proteins involved in iron metabolism, related to a poor prognosis in cancer. The inflammatory mediator transforming growth factor beta-1 (TGF-β1) is closely linked with initiation, progression and tumor metastasis, and free radicals are capable of regulating their activation. The relationship between oxidative stress and related molecules such as those involved in the iron metabolism and inflammatory response is still not well characterized in melanoma. The objective of this study was to characterize these parameters in patients in different stages of this disease. Breslow thickness and the presence or absence of recurrence was used as parameters for group division. A total of 83 patients were recruited at the Cancer Hospital of Londrina between April 2011 and November 2012. The control group comprised 65 healthy volunteers. Venous blood was collected and used in systemic analyzes. Moreover, 70 blocks of paraffin-embedded melanoma from patients treated between 2004 to 2012 were randomly selectedand analyzed at the Department of Pathology, Cancer Hospital of Londrina, in order to study oxidative stress and related molecules in tumor tissue by immunohistochemistry. The higher the Breslow thickness and aggressiveness of the disease (recurrence) the more evident were the systemic inflammatory and oxidative modifications, mainly evidenced by increased levels of malondialdehyde (MDA) and C-reactive protein (CRP). Furthermore, skin tumors with higher Breslow thickness showed increased labeling of the protein oxidation product 3-nitrotyrosine in melanoma cells and peritumoral tissue compared to smaller tumors. Recurrence and high risk recurrence patients showed increased FHC levels, while all patients with melanoma had increased FHC:FLC ratio when compared to healthy subjects. The increased levels of FHC were followed by the increased systemic oxidative stress, measured by red blood cells lipid peroxidation. Melanoma cells showed FHC expression, but the levels did not differ between tumor stages. The p53, a protein involved in cell proliferation, had increased labeling in metastatic tissue compared with thin Breslow thickness cutaneous tumor. Recurrence patients had low TGF-β1 systemic levels, accompanied by high levels of MDA, red blood cells lipid peroxidation and 3-nitrotyrosine in tumoral tissue. The results show that oxidative stress and related molecules have characteristic profiles in different melanoma stages, adding a new perspective on the redox state and their possible involvement in disease progression.
Mendes, Rosemairy Luciene. "Morfologia e regimes de crescimento das linhagens celulares derivadas de melanoma murino B16F10, primário e metastático, em camundongos BALB/c". Universidade Federal de Viçosa, 2011. http://www.locus.ufv.br/handle/123456789/7113.
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Embora não esteja entre as neoplasias mais prevalentes é responsável pela quarta causa de morte entre os pacientes com câncer. A compreensão dos mecanismos envolvidos na gênese e progressão do melanoma é crucial para o seu tratamento. Modelos experimentais que representem as fases da progressão do melanoma ainda são raros, mas a cultura de células é uma ferramenta importante para tais investigações. Os objetivos deste trabalho foram: estabelecer um modelo de estudo do melanoma murino B16F10 por meio do estabelecimento de sublinhagens celulares que correspondem ao tumor primário e às metástases, após passagem dessas células in vivo em camundongos BALB/c; caracterizar morfologicamente por meio de microscopia óptica e eletrônica de transmissão (MET) e varredura (MEV) a linhagem B16F10 e as sublinhagens derivadas; e investigar as leis de escala que regem o crescimento das linhagens de células de melanoma. Nesse contexto, células de melanoma B16F10 foram injetadas subcutaneamente (sc.) em camundongo BALB/c e a linhagem derivada dos tumores primários foi denominada de B16F10B. A linhagem B16F10 e a sublinhagem B16F10B foram inoculadas endovenosamente (ev.) em camundongos BALB/c e as sublinhagens obtidas das metástases foram denominadas B16F10M e B16F10BM, respectivamente. A linhagem B16F10 e as sublinhagens B16F10B, -BM e -M foram analisadas em MO, MET e MEV, revelando uma grande heterogeneidade na morfologia dessas células e nos agregados por elas formados. As células B16F10 e B16F10B também revelaram à MET presença de partículas virais. Para a caracterização das leis de escala que regem os regimes de crescimento das células B16F10, -B, -BM e -M, as linhagens celulares foram cultivadas sobre lamínulas de vidro em placas de 24 poços e retiradas em intervalos de 24 horas, durante 7 dias. O número de células por agregado e o número total de agregados foram usados para determinar a função de distribuição de tamanho de agregados que sugerem uma transição nas funções de distribuição de um decaimento exponencial para um que segue lei de potência para as células B16F10B. As demais linhagens analisadas sempre exibiram um comportamento de lei de potência. A distribuição em leis de potência indica a ausência de um tamanho característico para os tamanhos dos agregados, podendo refletir na falta de mecanismos de controle da replicação celular aliada à estabilidade dos agregados. A transição no regime de crescimento exibido pelas células B16F10B sugere que o crescimento celular contínuo na cultura pode exercer forças seletivas que destroem os mecanismos de regulação, tais como a dependência de ancoragem e o crescimento de densidade-dependente. A caracterização morfológica, bem como do regime de crescimento das sublinhagens derivadas das células B16F10 mostrou que há diferenças e similaridades entre as mesmas, porém, para uma melhor caracterização dessas células, outras análises devem ser realizadas, tais como: resistência a drogas, integridade genômica e padrão de expressão de moléculas de adesão.
Melanoma is a malignant neoplasm derived from melanocytes, specialized pigmented cells that are found predominantly in the skin. Although it does not figure among the most prevalent cancer types, melanoma is responsible for the fourth leading cause of cancer patients death. Understanding of the mechanisms involved in the genesis and progression of melanoma is crucial for the cancer treatment. Experimental models that representing phases of melanoma progression are still rare, but the cell culture is an important tool for such investigations. The aims of the work were to determine a study model of murine melanoma B16F10 by the establishment of cell sublineages corresponding to the primary tumor and to the metastases, after passage of these cells in BALB/c mice; to characterize morphologically by optical microscopy (OM) and transmission electron (TEM) and scanning electron (SEM) the B16F10 lineage and sublineages derived from B16F10; to investigate the scaling laws that rule the growth of melanoma cell lines. In this context, B16F10 melanoma cells were injected subcutaneously (sc) in BALB/c mice and the subline derived from subcutaneous tumors was named B16F10B. The B16F10 lineage and the B16F10B sublineage were inoculated intravenous (iv) in BALB/c mice, and the sublineages of metastases obtained were named B16F10M and B16F10BM, respectively. The B16F10B lineage and the B16F10, -BM and -M sublineages were analyzed by OM, TEM and SEM, what revealed an extent heterogeneity in the morphology of these cells and clusters formed by them. B16F10 and B16F10B cells also disclosed to MET viral particles presence. To characterize the scaling laws that rule the growth regimes of the B16F10, -B, -BM and -M cells, the cells lineages were cultured on glass coverslips in 24-well plates and removed at intervals of 24 hours for 7 days. The number of cells per cluster and the total number of clusters were used to determine the cluster size functions. The results suggest distribution functions with a transition to an exponential decay that follows a power law for B16F10B cells. The other lineages analyzed always exhibits a power law behavior. The power law distribution indicates the absence of a characteristic size for the clusters sizes which, from the biological point of view, might reflect the lack of control mechanisms of cell replication allied to the stability of clusters. The transition in the growth regime exhibited by B16F10B cells suggests that the continued cell growth in culture may exert selective forces which destroy regulation mechanisms such as cell anchorage dependence and density-dependent growth.
Rooij, Michaela Johanna Maria de. "Volunteer melanoma screening pros and cons /". [Maastricht : Maastricht : Universiteit Maastricht] ; University Library, Maastricht University [Host], 1997. http://arno.unimaas.nl/show.cgi?fid=5922.
Pełny tekst źródłaBergman, Louise. "Uveal melanoma : epidemiological and clinical aspects /". Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-413-9/.
Pełny tekst źródłaBerg, Peter. "Malignant melanoma in children and adolescents /". Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-567-0/.
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