Literatura científica selecionada sobre o tema "Preclinical tumor models"
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Artigos de revistas sobre o assunto "Preclinical tumor models"
Varticovski, L., M. G. Hollingshead, M. R. Anver, A. I. Robles, J. E. Green, K. W. Hunter, G. Merlino et al. "Preclinical testing using tumors from genetically engineered mouse mammary models". Journal of Clinical Oncology 24, n.º 18_suppl (20 de junho de 2006): 10067. http://dx.doi.org/10.1200/jco.2006.24.18_suppl.10067.
Texto completo da fonteKlenner, Marbod, Pia Freidel, Mariella G. Filbin e Alexander Beck. "DIPG-39. New preclinical models for Diffuse Midline Glioma". Neuro-Oncology 24, Supplement_1 (1 de junho de 2022): i27. http://dx.doi.org/10.1093/neuonc/noac079.096.
Texto completo da fonteCosta, Alice, Livia Gozzellino, Margherita Nannini, Annalisa Astolfi, Maria Abbondanza Pantaleo e Gianandrea Pasquinelli. "Preclinical Models of Visceral Sarcomas". Biomolecules 13, n.º 11 (6 de novembro de 2023): 1624. http://dx.doi.org/10.3390/biom13111624.
Texto completo da fonteLlaguno-Munive, Monserrat, Wilberto Villalba-Abascal, Alejandro Avilés-Salas e Patricia Garcia-Lopez. "Near-Infrared Fluorescence Imaging in Preclinical Models of Glioblastoma". Journal of Imaging 9, n.º 10 (6 de outubro de 2023): 212. http://dx.doi.org/10.3390/jimaging9100212.
Texto completo da fonteSewduth, Raj N., e Konstantina Georgelou. "Relevance of Carcinogen-Induced Preclinical Cancer Models". Journal of Xenobiotics 14, n.º 1 (5 de janeiro de 2024): 96–109. http://dx.doi.org/10.3390/jox14010006.
Texto completo da fonteRoosen, Mieke, Chris Meulenbroeks, Phylicia Stathi, Joris Maas, Julie Morscio, Jens Bunt e Marcel Kool. "BIOL-11. PRECLINICAL MODELLING OF PEDIATRIC BRAIN TUMORS USING ORGANOID TECHNOLOGY". Neuro-Oncology 25, Supplement_1 (1 de junho de 2023): i8. http://dx.doi.org/10.1093/neuonc/noad073.030.
Texto completo da fonteStripay, Jennifer L., Thomas E. Merchant, Martine F. Roussel e Christopher L. Tinkle. "Preclinical Models of Craniospinal Irradiation for Medulloblastoma". Cancers 12, n.º 1 (5 de janeiro de 2020): 133. http://dx.doi.org/10.3390/cancers12010133.
Texto completo da fonteSitta, Juliana, Pier Paolo Claudio e Candace M. Howard. "Virus-Based Immuno-Oncology Models". Biomedicines 10, n.º 6 (18 de junho de 2022): 1441. http://dx.doi.org/10.3390/biomedicines10061441.
Texto completo da fonteOrtiz, Michael Vincent, Armaan Siddiquee, Daoqi You, Prabhjot Singh Mundi, Lianna Marks, Kristina Guillan, Daniel Diolaiti et al. "Preclinical evaluation of XPO1 inhibition in Wilms tumors." Journal of Clinical Oncology 38, n.º 15_suppl (20 de maio de 2020): 3580. http://dx.doi.org/10.1200/jco.2020.38.15_suppl.3580.
Texto completo da fonteBella, Ángela, Claudia Augusta Di Trani, Myriam Fernández-Sendin, Leire Arrizabalaga, Assunta Cirella, Álvaro Teijeira, José Medina-Echeverz, Ignacio Melero, Pedro Berraondo e Fernando Aranda. "Mouse Models of Peritoneal Carcinomatosis to Develop Clinical Applications". Cancers 13, n.º 5 (25 de fevereiro de 2021): 963. http://dx.doi.org/10.3390/cancers13050963.
Texto completo da fonteTeses / dissertações sobre o assunto "Preclinical tumor models"
MINOLI, LUCIA. "TUMOR MICROENVIRONMENT IN EXPERIMENTAL PRECLINICAL MOUSE MODELS OF HUMAN CANCER: MORPHOLOGICAL APPROACH". Doctoral thesis, Università degli Studi di Milano, 2020. http://hdl.handle.net/2434/704551.
Texto completo da fonteChen, Liu Qi. "Development and Application of AcidoCEST MRI for Evaluating Tumor Acidosis in Pre-Clinical Cancer Models". Diss., The University of Arizona, 2014. http://hdl.handle.net/10150/323450.
Texto completo da fonteDenton, Nicholas Lee Denton. "Modulation of tumor associated macrophages enhances oncolytic herpes virotherapy in preclinical models of Ewing sarcoma". The Ohio State University, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=osu1523892800897524.
Texto completo da fonteTOSCA, ELENA MARIA. "Dynamic energy budget based models of tumor-in-host growth inhibition and cachexia onset in preclinical settings". Doctoral thesis, Università degli studi di Pavia, 2019. http://hdl.handle.net/11571/1242427.
Texto completo da fonteThe anticancer drug development process is characterized by the highest attrition rates in the clinical setting, primarily due to adverse efficacy and safety results. Preclinical animal models slightly representative of the human condition and an inadequate predictive paradigm of preclinical to clinical translation may be likely causes of this. Pharmacometric models, able to extract, synthesize and integrate preclinical information, could support the transfer of the preclinical results to the clinical setting. Within the paradigm of the Model-Informed Drug Discovery and Development, my thesis deals with the development, implementation and analysis of new mathematical modeling approaches to exploit data routinely generated in the preclinical phases of anticancer drug development process. In all the described research activities it can be recognized the importance of PK/PD modeling in better characterizing, understanding and predicting PK/PD behaviour of oncology agents. The focus of this work is a mathematical modeling of interactions between tumor and host organism during anticancer drug treatments in preclinical experiments. To this aim, a tumor-in-host modeling approach is proposed on the basis of a set of tumor-host interaction rules taken from the Dynamic Energy Budget (DEB) theory. This framework, suitably adapted to several experimental contexts, is able to integrate the different aspects characterizing the in vivo tumor growth studies: the drug cytotoxic or cytostatic activity on the tumor, the eventually onset of cachexia due to the treatment, the effect of the tumor on the host and, viceversa, the influence of the host condition on tumor dynamics. In particular, a tumor-in-host DEB-based model describing the cachexia onset and tumor growth inhibition (TGI) after the administration of cell-killing agents has been developed, mathematically analysed and, subsequently, applied on a etoposide experiment in Wistar rats. The cytostatic anticancer effect of angiogenesis inhibitors in xenograft mice has been, also, modeled within the tumor-in-host DEB-based framework. This DEB-TGI anti-angiogenic model has proved to be extremely useful to describe and understand the complexities of an hypoxia-triggered resistance to bevacizumab. Finally, starting from the previous developed TGI models, a tumor-in-host approach to analyse combination experiments and assess possible drug-drug interaction between anti-angiogenic and chemotherapeutic agents is proposed.
Lahr, Christoph Alexander. "Tissue-engineering humanised bone sarcoma models in rodents-a preclinical study platform for orthopaedic research". Thesis, Queensland University of Technology, 2021. https://eprints.qut.edu.au/207759/1/Christoph%20Alexander_Lahr_Thesis.pdf.
Texto completo da fonteLaranga, Roberta <1985>. "Development of Preclinical Models of Mammary Carcinogenesis: Functional Role of Her2 and its Isoforms in Tumor Progression and in Drug Resistance". Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2017. http://amsdottorato.unibo.it/7832/1/Laranga_Roberta_Tesi.pdf.
Texto completo da fonteFuchs, Jeannette [Verfasser], e Thorsten [Akademischer Betreuer] Stiewe. "Establishment and characterization of preclinical mouse models for evaluation of oncogenic and tumor-suppressive properties of p53 family members / Jeannette Fuchs ; Betreuer: Thorsten Stiewe". Marburg : Philipps-Universität Marburg, 2017. http://d-nb.info/1131253272/34.
Texto completo da fonteFerreira, Luís Pedro Correia Pinto. "Development of multicelular 3D cancer testing platforms for evaluation of new anti-cancer therapies". Master's thesis, Universidade de Aveiro, 2017. http://hdl.handle.net/10773/22713.
Texto completo da fonteO cancro do pulmão (CP) é um dos cancros mais diagnosticados a nível mundial e também um dos mais mortíferos. Atualmente, as terapias administradas a nível clínico para o tratamento do CP são ainda extremamente ineficazes e limitadas no que diz respeito ao aumento da taxa de sobrevivência dos pacientes oncológicos. Esta realidade demonstra a necessidade de investigar ativamente novas terapias para o tratamento desta neoplasia. No entanto a validação pré-clínica de terapias inovadoras para o CP tem-se revelado extremamente difícil devido à inexistência de plataformas que sejam adequadas para testes a nível laboratorial, uma vez que as culturas celulares in vitro bidimensionais (2D), recomendadas pelas agências regulatórias são incapazes de mimetizar as caraterísticas principais dos tumores humanos. Estas limitações têm originado uma fraca correlação entre a performance das terapias nos estudos in vitro e a obtida em ensaios clínicos controlados. Neste contexto, os modelos de tumores tridimensionais (3D) in vitro têm vindo a ser reconhecidos como uma solução para este problema, pois podem recapitular várias componentes do microambiente tumoral. Das várias plataformas 3D in vitro de CP investigadas atualmente muito poucas avaliaram o papel da inclusão de células estaminais mesenquimais (MSCs). Para colmatar esta lacuna, o trabalho de investigação desenvolvido no âmbito desta dissertação descreve a produção e otimização de novos modelos hétero-celulares 3D in vitro. Estas plataformas são compostas por células tumorais do CP (A549) e do seu estroma, nomeadamente fibroblastos da pele e células estaminais mesenquimais derivadas da medula óssea (BM-MSCs). Estes três tipos de células foram co-cultivadas em micropartículas poliméricas de policaprolactona revestidas por ácido hialurónico, com o objetivo de incluir este componente da matriz extracelular que se encontra presente no microambiente do CP. Esta abordagem permitiu formar a nível laboratorial microtecidos multicelulares 3D híbridos que melhor mimetizam a heterogeneidade celular das neoplasias pulmonares. Os resultados obtidos demonstraram que os microtumores formados através da técnica de sobreposição-líquida são reprodutíveis em termos de morfologia e tamanho, apresentaram núcleos necróticos, organização celular 3D e produziram proteínas do microambiente tumoral. Além destas caraterísticas, os dados obtidos através de microscopia de fluorescência revelaram que as BM-MSCs migram para o interior dos microtumores ao longo do tempo. A avaliação da citotoxicidade da Doxorubicina, um fármaco anti-tumoral rotineiramente utilizado a nível clínico, demonstrou que a inclusão de micropartículas aumenta a resistência das células tumorais em modelos homotípicos. Nos modelos tri-cultura heterotípicos a citotoxicidade foi comparável à obtida em microtumores sem micropartículas. Estes resultados evidenciam assim o papel importante dos fibroblastos e das BM-MSCs na resposta dos microtumores. Numa visão global, os modelos 3D formados recapitulam com mais exatidão o microambiente do cancro do pulmão e poderão servir no futuro como plataformas de teste para descobrir ou aperfeiçoar novas terapias, ou combinações de terapêuticas, para este tipo de neoplasia.
Lung cancer (LC) is one the most commonly diagnosed cancers worldwide, being also one of the deadliest. Currently, clinically administered therapies for treatment of LC are still extremely ineffective and limited in increasing oncologic patients survival rates. This reality evidences the necessity of actively investigating novel therapies for the treatment of LC. However, preclinical validation of novel therapies as revealed itself as an extremely arduous process, due to the lack of suitable laboratory testing platforms since the recommend in vitro bi-dimensional (2D) cell cultures are unable to fully mimic the main hallmarks of human tumors. In this context, in vitro tridimensional (3D) tumor models are being increasingly recognized as a solution due to their ability to correctly recapitulate several characteristics of the tumor microenvironment (TME). Amongst currently developed 3D in vitro platforms for the study of LC, few have included or studied the role of mesenchymal stem cells (MSCs). To provide further insights into this hypothesis, the research work developed in this thesis describes the production and optimization of novel heterotypic in vitro 3D models, comprised by non-small-cell lung cancer cells (A549) and stromal cells, namely skin fibroblasts (HFs), and bone-marrow derived mesenchymal stem cells (BM-MSCs). These three diverse cell populations were co-cultured in hyaluronic acid coated polymeric polycaprolactone microparticles (LbL-MPs) as to include this key extracellular matrix component of LC TME. This approach allowed the formation of 3D multicellular heterotypic microtissues (3D-MCTS) that better recapitulate the cellular heterogeneity of LC TME in the laboratory. The obtained findings demonstrate that these models formed via the liquid-overlay technique were reproducible in terms of morphology and size, presented necrotic core formation, 3D cellular organization, and deposited matrix proteins in a similar manner as in the TME. Besides this, fluorescence microscopy data revealed that BM-MSCs migrated overtime into the microtumors core . Performed doxorubicin in vitro cytotoxicity assays revealed that the inclusion of LbL-MPs lead to an increased resistance of homotypic A549 monoculture models against this anti-cancer drug commonly used in clinical treatments. Alongside, the cytotoxicity obtained in triculture heterotypic models was comparable to that of microtumors without LbL-MPs inclusion, showcasing the role of HFs and BM-MSCs in microtumors response to therapy. Globally, the herein bioengineered 3D models were able to recapitulate with an increased precision the TME of LC, making them suitable test platforms for development or improvement of standalone or combinatorial therapies for this type of neoplasia.
Wolska-Krawczyk, Malgorzata [Verfasser], e Arno [Akademischer Betreuer] Bücker. "Evaluation of liver tumor perfusion by intraarterial transcatheder magnetic resonance angiography during transarterial chemoembolization in patients with hepatocellular carcinoma : Preclinical instrument validation in vascular models and clinical study / Malgorzata Wolska-Krawczyk. Betreuer: Arno Bücker". Saarbrücken : Saarländische Universitäts- und Landesbibliothek, 2014. http://d-nb.info/1056906979/34.
Texto completo da fonteDobosz, Michael [Verfasser], Vasilis [Akademischer Betreuer] Ntziachristos e Hans-Jürgen [Akademischer Betreuer] Wester. "The application of in vivo and ex vivo multispectral epi-fluorescence imaging for the preclinical discovery and development of monoclonal antibodies in tumor xenograft models / Michael Dobosz. Betreuer: Vasilis Ntziachristos. Gutachter: Hans-Jürgen Wester ; Vasilis Ntziachristos". München : Universitätsbibliothek der TU München, 2014. http://d-nb.info/1080903682/34.
Texto completo da fonteLivros sobre o assunto "Preclinical tumor models"
Fiebig, H. H. Revelance Of Tumor Models For Anticancer Drug Development (CONTRIBUTIONS TO ONCOLOGY). Editado por H. H. Fiebig. Karger, 1999.
Encontre o texto completo da fonteHolland, Eric C. Mouse Models of Human Cancer. Wiley-Liss, 2004.
Encontre o texto completo da fontePowell, Craig M. PTEN and Autism With Macrocepaly. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199744312.003.0010.
Texto completo da fonteCapítulos de livros sobre o assunto "Preclinical tumor models"
Teicher, Beverly A. "Preclinical Tumor Response End Points". In Tumor Models in Cancer Research, 571–605. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-968-0_23.
Texto completo da fonteMorton, Christopher L., e Peter J. Houghton. "The Pediatric Preclinical Testing Program". In Tumor Models in Cancer Research, 195–213. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-968-0_8.
Texto completo da fonteGerner, Eugene W., Natalia A. Ignatenko e David G. Besselsen. "Preclinical Models for Chemoprevention of Colon Cancer". In Tumor Prevention and Genetics, 58–71. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003. http://dx.doi.org/10.1007/978-3-642-55647-0_6.
Texto completo da fonteBoss, Mary-Keara, Gregory M. Palmer e Mark W. Dewhirst. "Imaging the Hypoxic Tumor Microenvironment in Preclinical Models". In Hypoxia and Cancer, 157–78. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-9167-5_7.
Texto completo da fonteNathanson, S. David. "Preclinical Models of Regional Lymph Node Tumor Metastasis". In Cancer Metastasis And The Lymphovascular System: Basis For Rational Therapy, 129–56. Boston, MA: Springer US, 2007. http://dx.doi.org/10.1007/978-0-387-69219-7_10.
Texto completo da fonteHillman, Gilda G. "Experimental Animal Models for Investigating Renal Cell Carcinoma Pathogenesis and Preclinical Therapeutic Approaches". In Tumor Models in Cancer Research, 287–305. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-968-0_12.
Texto completo da fonteSadekar, Shraddha, Isabel Figueroa e Harish Shankaran. "Evaluation of Tumor Growth Inhibition in Preclinical Tumor Models: A Quantitative Approach". In Development of Antibody-Based Therapeutics, 171–86. Singapore: Springer Singapore, 2018. http://dx.doi.org/10.1007/978-981-13-0496-5_8.
Texto completo da fonteParchment, Ralph E. "Bone Marrow as a Critical Normal Tissue that Limits Drug Dose/Exposure in Preclinical Models and the Clinic". In Tumor Models in Cancer Research, 521–52. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-968-0_21.
Texto completo da fonteChambers, Ann F., Eva A. Turley, John Lewis e Leonard G. Luyt. "Preclinical Cell and Tumor Models for Evaluating Radiopharmaceuticals in Oncology". In Monoclonal Antibody and Peptide-Targeted Radiotherapy of Cancer, 397–417. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2010. http://dx.doi.org/10.1002/9780470613214.ch11.
Texto completo da fonteJacoberger-Foissac, Celia, Bertrand Allard, David Allard e John Stagg. "Assessing the Efficacy of Immune Checkpoint Inhibitors in Preclinical Tumor Models". In Methods in Molecular Biology, 151–69. New York, NY: Springer US, 2023. http://dx.doi.org/10.1007/978-1-0716-2914-7_11.
Texto completo da fonteTrabalhos de conferências sobre o assunto "Preclinical tumor models"
Bagley, Rebecca G., Yi Ren, Leslie Kurtzberg, William Weber, Dinesh Bangari e Beverly A. Teicher. "Abstract 1596: Human choriocarcinomas: Placental growth factor-dependent preclinical tumor models". In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-1596.
Texto completo da fonteFaia, Kerrie, Alberto Toso, Kristina Fetalvero, Marly Roche, Steven Bench, Erin O'Hearn, Qiongfang Cao et al. "Abstract 1717: MAP4K1 inhibition enhances immune cell activation and anti-tumor immunity in preclinical tumor models". In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-1717.
Texto completo da fonteWelm, Alana L. "Abstract IA07: Breast tumor grafts as preclinical models for anti-metastasis therapy". In Abstracts: AACR Special Conference on Advances in Breast Cancer Research: Genetics, Biology, and Clinical Applications - October 3-6, 2013; San Diego, CA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1557-3125.advbc-ia07.
Texto completo da fonteDoody, Jacqueline, Sneha Mathew, Lan Wu, Yanxia Li, Ying Wang, Kris Persaud, Douglas Burtrum et al. "Abstract 3539: Anti-CSF-1R antibodies reduce tumor-associated macrophages and inhibit tumor growth in preclinical models". In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-3539.
Texto completo da fonteLi, Yanxia, Sneha Mathew, Lan Wu, Ying Wang, Jessica Kearney, Kris Persaud, Douglas Burtrum et al. "Abstract C224: Anti-CSF-1R antibodies reduce tumor-associated macrophages and inhibit tumor growth in preclinical models." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 12-16, 2011; San Francisco, CA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1535-7163.targ-11-c224.
Texto completo da fonteLi, Yanxia, Sneha Mathew, Lan Wu, Ying Wang, Kris Persaud, Douglas Burtrum, Paul Balderes et al. "Abstract A235: Anti-CSF-1R antibodies reduce tumor-associated macrophages and inhibit tumor growth in preclinical models." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Oct 19-23, 2013; Boston, MA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1535-7163.targ-13-a235.
Texto completo da fonteStaniszewska, Anna, Joshua Armenia, Matthew King, Chrysiis Michaloglou, Maneesh Singh, Maryann San Martin, Zena Wilson et al. "Abstract 967: Anti-tumor and immune effects of olaparib +/- anti-PD-L1 in preclinical BRCA1mut tumor models". In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-967.
Texto completo da fonteHeuer, Timothy S., Richard Ventura, Joanna Waszczuk, Kasia Mordec, Julie Lai, Russell Johnson, Lilly Hu et al. "Abstract 1815: Efficacy of FASN-selective small molecule inhibitors in preclinical tumor models". In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-1815.
Texto completo da fonteSriram, Venkataraman, Michael E. Bigler, Holly Cherwinski, Erin Murphy, Terrill K. McClanahan e Joseph H. Phillips. "Abstract 5025: Dissecting the dynamics of anti-PD1 immunotherapy in preclinical tumor models". In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-5025.
Texto completo da fonteHeuer, Timothy S., Minchao Chen, Richard Ventura, Joanna Waszczuk, Satya Yendluri, Julie Lai, Samnang Tep et al. "Abstract B261: Characterization of FASN-selective small-molecule inhibitors in preclinical tumor models." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Oct 19-23, 2013; Boston, MA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1535-7163.targ-13-b261.
Texto completo da fonte