Relevant bibliographies by topics / Mouse xenograft models

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  1. Journal articles
  2. Dissertations / Theses
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  4. Book chapters
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Academic literature on the topic 'Mouse xenograft models'

Author: Grafiati
Published: 4 June 2021
Last updated: 4 February 2022

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Journal articles on the topic "Mouse xenograft models"

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Zhang, Yanmei, Sau Har Lee, Cheng Wang, Yunhe Gao, Jiyang Li, and Wei Xu. "Establishing metastatic patient-derived xenograft model for colorectal cancer." Japanese Journal of Clinical Oncology 50, no. 10 (2020): 1108–16. http://dx.doi.org/10.1093/jjco/hyaa089.

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Abstract Background Patient-derived xenograft model is a powerful and promising tool for drug discovery and cancer biology studies. The application of previous metastatic colorectal cancer models has been greatly limited by its low success rate and long time to develop metastasis. Therefore, in this study, we aim to describe an optimized protocol for faster establishment of colorectal cancer metastatic patient-derived xenograft mouse models. Methods Smaller micro tissues (˂150 μm in diameter) mixed with Matrigel were engrafted subcutaneously into NSG mice to generate the passage 1 (P1) patient-derived xenograft. The micro tumours from P1 patient-derived xenograft were then excised and orthotopically xenografted into another batch of NSG mice to generate a metastatic colorectal cancer patient-derived xenograft, P2. Haematoxylin and eosin and immunohistochemistry staining were performed to compare the characters between patient-derived xenograft tumours and primary tumours. Results About 16 out of 18 P1 xenograft models successfully grew a tumour for 50.8 ± 5.1 days (success rate 89.9%). Six out of eight P1 xenograft models originating from metastatic patients successfully grew tumours in the colon and metastasized to liver or lung in the NSG recipients for 60.9 ± 4.5 days (success rate 75%). Histological examination of both P1 and P2 xenografts closely resembled the histological architecture of the original patients’ tumours. Immunohistochemical analysis revealed similar biomarker expression levels, including CDH17, Ki-67, active β-catenin, Ki-67 and α smooth muscle actin when compared with the original patients’ tumours. The stromal components that support the growth of patient-derived xenograft tumours were of murine origin. Conclusions Metastatic patient-derived xenograft mouse model could be established with shorter time and higher success rate. Although the patient-derived xenograft tumours were supported by the stromal cells of murine origin, they retained the dominant characters of the original patient tumours.
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Sari, Gulce, Gertine W. van Oord, Martijn D. B. van de Garde, Jolanda J. C. Voermans, Andre Boonstra, and Thomas Vanwolleghem. "Sexual Dimorphism in Hepatocyte Xenograft Models." Cell Transplantation 30 (January 1, 2021): 096368972110061. http://dx.doi.org/10.1177/09636897211006132.

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Humanized liver mouse models are crucial tools in liver research, specifically in the fields of liver cell biology, viral hepatitis and drug metabolism. The livers of these humanized mouse models are repopulated by 3-dimensional islands of fully functional primary human hepatocytes (PHH), which are notoriously difficult to maintain in vitro. As low efficiency and high cost hamper widespread use, optimization is of great importance. In the present study, we analyzed experimental factors associated with Hepatitis E virus (HEV) infection and PHH engraftment in 2 xenograft systems on a Nod-SCID-IL2Ry-/- background: the alb-urokinase plasminogen activator mouse model (uPA-NOG, n=399); and the alb-HSV thymidine kinase model (TK-NOG, n = 198). In a first analysis, HEV fecal shedding in liver humanized uPA-NOG and TK-NOG mice with comparable human albumin levels was found to be similar irrespective of the mouse genetic background. In a second analysis, sex, mouse age at transplantation and hepatocyte donor were the most determinant factors for xenograft success in both models. The sexual imbalance for xenograft success was related to higher baseline ALT levels and lower thresholds for ganciclovir induced liver morbidity and mortality in males. These data call for sexual standardization of human hepatocyte xenograft models, but also provide a platform for further studies on mechanisms behind sexual dimorphism in liver diseases.
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Richmond, A., and Y. Su. "Mouse xenograft models vs GEM models for human cancer therapeutics." Disease Models and Mechanisms 1, no. 2-3 (2008): 78–82. http://dx.doi.org/10.1242/dmm.000976.

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Goyama, Susumu, Mark Wunderlich, and James C. Mulloy. "Xenograft models for normal and malignant stem cells." Blood 125, no. 17 (2015): 2630–40. http://dx.doi.org/10.1182/blood-2014-11-570218.

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Abstract The model systems available for studying human hematopoiesis, malignant hematopoiesis, and hematopoietic stem cell (HSC) function in vivo have improved dramatically over the last decade, primarily due to improvements in xenograft mouse strains. Several recent reviews have focused on the historic development of immunodeficient mice over the last 2 decades, as well as their use in understanding human HSC and leukemia stem cell (LSC) biology and function in the context of a humanized mouse. However, in the intervening time since these reviews, a number of new mouse models, technical approaches, and scientific advances have been made. In this review, we update the reader on the newest and best models and approaches available for studying human malignant and normal HSCs in immunodeficient mice, including newly developed mice for use in chemotherapy testing and improved techniques for humanizing mice without laborious purification of HSC. We also review some relevant scientific findings from xenograft studies and highlight the continued limitations that confront researchers working with human HSC and LSC in vivo.
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Guihard, Soizic, Pauline Peyrouze, and Meyling H. Cheok. "Pharmacogenomic considerations of xenograft mouse models of acute leukemia." Pharmacogenomics 13, no. 15 (2012): 1759–72. http://dx.doi.org/10.2217/pgs.12.158.

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Morton, J. Jason, Gregory Bird, Yosef Refaeli, and Antonio Jimeno. "Humanized Mouse Xenograft Models: Narrowing the Tumor–Microenvironment Gap." Cancer Research 76, no. 21 (2016): 6153–58. http://dx.doi.org/10.1158/0008-5472.can-16-1260.

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Aparicio, Samuel, Manuel Hidalgo, and Andrew L. Kung. "Examining the utility of patient-derived xenograft mouse models." Nature Reviews Cancer 15, no. 5 (2015): 311–16. http://dx.doi.org/10.1038/nrc3944.

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Boetto, Julien, Matthieu Peyre, and Michel Kalamarides. "Mouse Models in Meningioma Research: A Systematic Review." Cancers 13, no. 15 (2021): 3712. http://dx.doi.org/10.3390/cancers13153712.

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Meningiomas are the most frequent primitive central nervous system tumors found in adults. Mouse models of cancer have been instrumental in understanding disease mechanisms and establishing preclinical drug testing. Various mouse models of meningioma have been developed over time, evolving in light of new discoveries in our comprehension of meningioma biology and with improvements in genetic engineering techniques. We reviewed all mouse models of meningioma described in the literature, including xenograft models (orthotopic or heterotopic) with human cell lines or patient derived tumors, and genetically engineered mouse models (GEMMs). Xenograft models provided useful tools for preclinical testing of a huge range of innovative drugs and therapeutic options, which are summarized in this review. GEMMs offer the possibility of mimicking human meningiomas at the histological, anatomical, and genetic level and have been invaluable in enabling tumorigenesis mechanisms, including initiation and progression, to be dissected. Currently, researchers have a range of different mouse models that can be used depending on the scientific question to be answered.
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Gamble, John T., Daniel J. Elson, Juliet A. Greenwood, Robyn L. Tanguay, and Siva K. Kolluri. "The Zebrafish Xenograft Models for Investigating Cancer and Cancer Therapeutics." Biology 10, no. 4 (2021): 252. http://dx.doi.org/10.3390/biology10040252.

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In order to develop new cancer therapeutics, rapid, reliable, and relevant biological models are required to screen and validate drug candidates for both efficacy and safety. In recent years, the zebrafish (Danio rerio) has emerged as an excellent model organism suited for these goals. Larval fish or immunocompromised adult fish are used to engraft human cancer cells and serve as a platform for screening potential drug candidates. With zebrafish sharing ~80% of disease-related orthologous genes with humans, they provide a low cost, high-throughput alternative to mouse xenografts that is relevant to human biology. In this review, we provide background on the methods and utility of zebrafish xenograft models in cancer research.
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Bobbs, Alexander S., Jennifer M. Cole, and Karen D. Cowden Dahl. "Emerging and Evolving Ovarian Cancer Animal Models." Cancer Growth and Metastasis 8s1 (January 2015): CGM.S21221. http://dx.doi.org/10.4137/cgm.s21221.

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Ovarian cancer (OC) is the leading cause of death from a gynecological malignancy in the United States. By the time a woman is diagnosed with OC, the tumor has usually metastasized. Mouse models that are used to recapitulate different aspects of human OC have been evolving for nearly 40 years. Xenograft studies in immunocompromised and immunocompetent mice have enhanced our knowledge of metastasis and immune cell involvement in cancer. Patient-derived xenografts (PDXs) can accurately reflect metastasis, response to therapy, and diverse genetics found in patients. Additionally, multiple genetically engineered mouse models have increased our understanding of possible tissues of origin for OC and what role individual mutations play in establishing ovarian tumors. Many of these models are used to test novel therapeutics. As no single model perfectly copies the human disease, we can use a variety of OC animal models in hypothesis testing that will lead to novel treatment options. The goal of this review is to provide an overview of the utility of different mouse models in the study of OC and their suitability for cancer research.
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Dissertations / Theses on the topic "Mouse xenograft models"

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Lämmer, Friederike [Verfasser], and Kaspar [Akademischer Betreuer] Matiasek. "Impact of aldehyde Dehydrogenase isotypes on xenograft and syngeneic mouse models of human primary glioblastoma multiforme / Friederike Lämmer. Betreuer: Kaspar Matiasek." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2016. http://d-nb.info/1093122129/34.

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Ebinger, Sarah [Verfasser], and Dirk [Akademischer Betreuer] Eick. "Characterization of dormant and drug resistant stem cells using xenograft mouse models of patient-derived acute leukemia cells / Sarah Ebinger ; Betreuer: Dirk Eick." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2018. http://d-nb.info/1155097602/34.

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Hübner, Doreen, Christiane Rieger, Ralf Bergmann, et al. "An orthotopic xenograft model for high-risk non-muscle invasive bladder cancer in mice: influence of mouse strain, tumor cell count, dwell time and bladder pretreatment." Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2018. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-231536.

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Background Novel theranostic options for high-risk non-muscle invasive bladder cancer are urgently needed. This requires a thorough evaluation of experimental approaches in animal models best possibly reflecting human disease before entering clinical studies. Although several bladder cancer xenograft models were used in the literature, the establishment of an orthotopic bladder cancer model in mice remains challenging. Methods Luciferase-transduced UM-UC-3LUCK1 bladder cancer cells were instilled transurethrally via 24G permanent venous catheters into athymic NMRI and BALB/c nude mice as well as into SCID-beige mice. Besides the mouse strain, the pretreatment of the bladder wall (trypsin or poly-L-lysine), tumor cell count (0.5 × 106–5.0 × 106) and tumor cell dwell time in the murine bladder (30 min – 2 h) were varied. Tumors were morphologically and functionally visualized using bioluminescence imaging (BLI), magnetic resonance imaging (MRI), and positron emission tomography (PET). Results Immunodeficiency of the mouse strains was the most important factor influencing cancer cell engraftment, whereas modifying cell count and instillation time allowed fine-tuning of the BLI signal start and duration – both representing the possible treatment period for the evaluation of new therapeutics. Best orthotopic tumor growth was achieved by transurethral instillation of 1.0 × 106 UM-UC-3LUCK1 bladder cancer cells into SCID-beige mice for 2 h after bladder pretreatment with poly-L-lysine. A pilot PET experiment using 68Ga-cetuximab as transurethrally administered radiotracer revealed functional expression of epidermal growth factor receptor as representative molecular characteristic of engrafted cancer cells in the bladder. Conclusions With the optimized protocol in SCID-beige mice an applicable and reliable model of high-risk non-muscle invasive bladder cancer for the development of novel theranostic approaches was established.
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Hübner, Doreen, Christiane Rieger, Ralf Bergmann, et al. "An orthotopic xenograft model for high-risk non-muscle invasive bladder cancer in mice: influence of mouse strain, tumor cell count, dwell time and bladder pretreatment." BioMed Central, 2017. https://tud.qucosa.de/id/qucosa%3A30688.

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Background Novel theranostic options for high-risk non-muscle invasive bladder cancer are urgently needed. This requires a thorough evaluation of experimental approaches in animal models best possibly reflecting human disease before entering clinical studies. Although several bladder cancer xenograft models were used in the literature, the establishment of an orthotopic bladder cancer model in mice remains challenging. Methods Luciferase-transduced UM-UC-3LUCK1 bladder cancer cells were instilled transurethrally via 24G permanent venous catheters into athymic NMRI and BALB/c nude mice as well as into SCID-beige mice. Besides the mouse strain, the pretreatment of the bladder wall (trypsin or poly-L-lysine), tumor cell count (0.5 × 106–5.0 × 106) and tumor cell dwell time in the murine bladder (30 min – 2 h) were varied. Tumors were morphologically and functionally visualized using bioluminescence imaging (BLI), magnetic resonance imaging (MRI), and positron emission tomography (PET). Results Immunodeficiency of the mouse strains was the most important factor influencing cancer cell engraftment, whereas modifying cell count and instillation time allowed fine-tuning of the BLI signal start and duration – both representing the possible treatment period for the evaluation of new therapeutics. Best orthotopic tumor growth was achieved by transurethral instillation of 1.0 × 106 UM-UC-3LUCK1 bladder cancer cells into SCID-beige mice for 2 h after bladder pretreatment with poly-L-lysine. A pilot PET experiment using 68Ga-cetuximab as transurethrally administered radiotracer revealed functional expression of epidermal growth factor receptor as representative molecular characteristic of engrafted cancer cells in the bladder. Conclusions With the optimized protocol in SCID-beige mice an applicable and reliable model of high-risk non-muscle invasive bladder cancer for the development of novel theranostic approaches was established.
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Linder, Keith Emerson. "Development and application of the skin xenograft mouse model to study host resistance to Demodex canis." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/NQ56286.pdf.

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Sargeant, Aaron Matthew. "Preclinical Efficacy and Safety Evaluation of Novel Small-Molecule Targeted Agents for the Prevention and Treatment of Prostate Cancer." The Ohio State University, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=osu1243948876.

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Tanaka, Kuniaki. "Direct Delivery of piggyBac CD19 CAR T Cells Has Potent Anti-tumor Activity against ALL Cells in CNS in a Xenograft Mouse Model." Kyoto University, 2021. http://hdl.handle.net/2433/261609.

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Kok, Cornelius Wilhelmus. "Molecular characterization of human vaginal mucosa obtained from fresh harvest and implants in an experimental nude mouse model." Thesis, Stellenbosch : University of Stellenbosch, 2011. http://hdl.handle.net/10019.1/6879.

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Thesis (MMedSc )--University of Stellenbosch, 2011.<br>ENGLISH ABSTRACT: The present study investigated in particularly the specific nature of the supporting stromal layer located between the implanted human cyst and host murine tissue, which has yet to be reported. During an initial phase of this study, the particular light microscopic properties of the existing hematoxylin and eosin (H&E) stained experimental cyst was investigated, with regards to the presence or absence of specific morphological features, namely spongiosis, exocytosis, epithelial keratinization, epithelial thickness and hyperplasia, and the vascularity and fibrosis present in the stroma of these experimental sections. Subsequent analysis reported significant spongiosis, in addition to increased exocytosis of immune cells and epithelial keratinization in a number of cysts. Additionally, increased epithelial thickness and hyperplasia was reported in only 2 / 10 experimental tissues, whereas increased vascularity was observed in the stroma following analysis of H&E and Special staining, such as Verhoeff-von Gieson and Masson trichrome results. During the second phase of the study, immunohistochemical analysis with a particularly wide array of antibodies raised against specific human and mouse antigens had been applied. This involved automated immunohistochemical staining with mouse anti-human primary antibodies, in addition to manual staining with rabbit anti-mouse primary antibodies. Subsequent visualization was achieved by means of linking to biotinylated secondary antibodies, and Streptavidin-HRP incubation for standard visualization, followed by counterstaining with Hematoxylin. Maintained positive expression of cytokeratins 5, 13, and 14 was demonstrated in both control human vaginal mucosa and experimental cysts, whereas similar findings were not reported for cytokeratin 1, given the vast keratinization which was observed. Human collagen type IV and laminin of the basement membrane reported positive expression in 9 / 10 and 6 / 10 control human vaginal mucosa tissues respectively. In comparison, negative mouse collagen type IV and laminin was reported in most experimental cysts compared to positive staining in positive control mouse tissues. Immunohistochemical staining for human elastin, fibronectin, von Willebrand factor, and fibroblasts revealed maintained positive staining in all control human vaginal mucosa and experimental cysts. However, maintained expression of CD34 (endothelial marker), CD1a (langerhans cells), and human VEGFR-3 in experimental cysts was not demonstrated, compared to positive expression in control human vaginal mucosa. Subsequent analysis of murine antigens illustrated uniformly negative staining for mouse fibronectin, langerhans cells (CD207), and fibroblasts, in addition to negative staining in positive control mouse tissue sections. Furthermore, negative staining for mouse VEGFR-2 was reported in all experimental cysts; however strong positive staining of this marker in mouse kidney tissue had been reported. The findings of this study suggested that the exact nature of the stromal layer is of both human and murine origin. Furthermore, the tissue region located beneath the human vaginal epithelium is suggested to be of human nature, whereas the second distinct region located at the periphery of experimental cyst tissues, is suggested to be murine origin; however the findings of immunohistochemical analysis could not illustrate definitively the exact nature of the intermediate stromal layer, but could in fact demonstrate a mixture of human and murine tissue.<br>AFRIKAANSE OPSOMMING: Die huidige studie het die spesifieke molekulêre en histologiese eienskappe van die stromale laag geleë tussen menslike sist- en muis velweefsel bestudeer, wat tans nog nie bekend is nie. Gedurende die eerste fase van hierdie studie is die besondere lig-mikroskopiese eienskappe van die bestaande hematoksilien en eosien (H&E) eksperimentele siste bestudeer, met betrekking tot die aan- of afwesigheid van spesifieke morfologiese eienskappe, naamlik spongiose, eksositose van immuunselle, epiteel keratinisasie, epiteel dikte en hiperplasie, en laastens die stromale vaskulariteit en fibrose. Gevolglike analise het daarop gedui dat beduidende spongiose, eksositose en epiteel keratinisasie gevind word in die eksperimentele siste in vergelyking met kontrole vaginal weefsel. Hierteenoor is die verdikking van die epiteel en hiperplasie in slegs 2 / 10 eksperimentele siste gevind, terwyl vermeerderde vaskulariteit aangedui is na gevolglike H&E en spesiale (soos byvoorbeeld Verhoeff-von Gieson en Masson trichrome) kleuringsresultate. Die tweede fase van die studie het die immunokleuring met verskeie mens- en muis spesifieke antiliggame behels, waarby die uitdrukking van verskeie mens antigene vergelyk is met dié van muis. As sulks is ge-automatiseerde immunohistochemie toegepas met muis primêre antiliggame, tesame met fisiese kleuring met konyn primêre antiliggame toegepas. Gevolglike visualisasie is aangedui deur middel van binding met sekondêre antiliggaam en Streptavidin- HRP, gevolg deur teenkleuring met Hematoksilien. Algehele behoud van positiewe uitdrukking van sitokeratien 5, 13, en 14 is bevind, terwyl sitokeratien 1 uitdrukking nie daarwerklik vergelykbaar is met dié van kontrole mens vaginale weefsel nie. Die uitdrukking van mens kollageen IV en laminien van die basaal membraan is verder bestudeer, en het egter positiewe kleuring in 9 / 10 en 6 / 10 van kontrole mens vaginale mukosa aangedui. In vergelykking hiermee kon die huidige bevindings egter net positiewe kleuring in 4 / 10 en 3 / 10 eksperimentele siste vir kollageen IV en laminien onderskeidelik, illustreer. Immunohistochemiese analise van menslike elastien, fibronektien, von Willebrand (vW) faktor en fibroblaste het op deurgaans positiewe uitdrukking van hierdie merkers aangedui in beide eksperimentele en kontrole menslike weefsel. In teenstelling hiermee is volgehoue uitdrukking van CD34 (endoteel merker), CD1a (Langerhans sel merker) en mens VEGFR-3 in ekperimentele siste egter nie illustreerbaar nie, in vergelykking met deurgaans positiewe uitdrukking van hierdie antigene in kontrole mens vaginale mukosa. In opvolging is deurgaans negatiewe uitdrukking van muis fibronektien, langerhans sel (CD207) en fibroblaste bevestig, terwyl negatiewe kleuring ook deurgaans in positiwe kontrole muis weefsel, bekom deur die disseksie van ‘n naakte muis, gevind is. Verder is ook negatiewe kleuring vir VEGFR-2 in alle eksperimentele siste gevind, terwyl egter sterk positiewe kleuring in muis nierweefsel as positiewe weefsel gevind is. Die resultate van die huidige studie het daarop gedui dat die stromale laag onderliggend tot mens vaginale epiteel van menslike oorsprong is, terwyl die periferale stroma onderliggend tot muis velweefsel, ongetwyfeld van muis oorsprong is. Laastens kon die spesifieke oorsprong van die tussenliggende stroma nie aangedui word nie, maar dat dit moontlik uit beide menslike- en muisweefsel bestaan.
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Devaud, Christel. "Etude in vivo du potentiel anti-tumoral des lymphocytes Tγδ Vδ2 négatifs humains dans un modèle murin". Thesis, Bordeaux 2, 2009. http://www.theses.fr/2009BOR21684/document.

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Les lymphocytes T ?d seraient des effecteurs essentiels dans la réponse immunitaire aux stress induits notamment par les infections et la tumorigénèse. Plusieurs arguments dont leur localisation intra-épithéliale mais aussi leurs capacités effectrices multiples et rapides les caractérisent comme des acteurs primordiaux dans l’immunité anti-tumorale. Mon projet de thèse consistait à examiner le potentiel anti-tumoral des lymphocytes T ?d humains, Vd2 négatifs (neg), dans un contexte in vivo, grâce à l’utilisation d’un modèle murin. Des études antérieures menées au laboratoire démontraient une expansion de lymphocytes T Vd2neg dans la circulation sanguine de transplantés rénaux développant une infection à cytomégalovirus (CMV). Des clones T Vd2neg, isolés de ces patients, présentaient une forte réactivité in vitro contre des cellules infectées par le CMV mais aussi contre des cellules tumorales notamment d’origine colique (comme la lignée HT29). Un ligand commun induit par l’infection à CMV et la transformation tumorale, reconnu par les clones T Vd2neg serait à l’origine de cette double réactivité. La première partie de mon projet s’est concentrée sur l’étude du potentiel anti-tumoral de ces clones T Vd2neg in vivo, qui comprenait leur capacité à atteindre des cellules tumorales d’origines coliques (HT29) et à les lyser. Dans un modèle de xénogreffe dans des souris immunodéficientes, nous avons démontré que les clones TVd2neg, injectés dans le péritoine (i.p) pouvaient retarder la croissance de tumeurs solides HT29 sous-cutanées. D’après nos résultats, cette inhibition du développement tumoral proviendrait d’une action précoce et spécifique des cellules T Vd2neg et impliquerait le récepteur à chimiokine CCR3. Nos données suggèrent donc que des lymphocytes T Vd2neg, réactifs contre le CMV, pourraient migrer in vivo jusqu’au site d’injection des cellules tumorales et inhiber la croissance de la tumeur probablement grâce à leur acticité cytolytique. La deuxième partie de mon projet de thèse proposait d’approfondir l’étude du rôle des lymphocytes T Vd2neg contre les tumeurs coliques. Ainsi nous avons testé, in vivo, l’implication de lymphocytes T Vd1+ humains, une population représentative des épithéliums intestinaux, dans le cancer métastatique colorectal (CMC). Nous avons développé un modèle d’implantation orthotopique de cellules tumorales HT29 dans des souris immunodéficientes, qui mime le développement du CMC chez l’homme. Des tumeurs primaires intra-caecales et des métastases pulmonaires et hépatiques se développent chez les souris. De plus, nous avons pu suivre leur croissance grâce à l’introduction de la luciférase dans les HT29 et à une technique d’imagerie in vivo en bioluminescence. Nos résultats montrent qu’un traitement continu des souris par des injections de lignée T Vd1+ en i.p inhibe le développement des tumeurs primaires et retarde l’apparition des métastases à distance. Ces données soutiennent l’implication des lymphocytes T Vd2neg dans le contrôle des CMC. De façon intéressante, elles mettent en avant une implication anti-métastatique des cellules T Vd2neg. L’ensemble de nos travaux souligne le rôle des cellules T Vd2neg dans la réponse immunitaire contre les cancers colorectaux et étaye leur potentiel d’action lors de la progression des tumeurs vers des métastases, ouvrant ainsi des perspectives pour l’utilisation de ces cellules dans les thérapies des CMC<br>Gamma delta (?d) T lymphocytes contribute to host immune competence uniquely especially during stress immune responses to infections and tumors. Because ?d T cells colonize epithelial surfaces, where they can exert rapid and pleiotropic effector functions, they are critical protagonists in anti-cancer response. During my Phd project we explored the anti-tumor potential of Vd2 negatives (neg) ?d T lymphocytes, in vivo using a mouse xenograft tumor model. A few years ago, studies in our laboratory showed an increase of peripheral blood Vd2neg ?d T lymphocytes in allograft recipients infected by cytomegalovirus (CMV). Interestingly, Vd2neg ?d T clones isolated from these patients showed a cytotoxic activity against CMV infected fibroblast in vitro. Moreover, they were able to kill colon cancer cells (HT29) in vitro, in contrast to normal epithelial cells. Cancer cell- as well as CMV infected cell- killing involved T cell receptor (TCR) engagement, independently of major histocompatibility complex (CMH) recognition, probably with a common ligand. The first part of my Phd project was undertaken to evaluate the in vivo tumor reactivity of anti-CMV Vd2neg clones, including their ability to inhibit tumor growth as well as their migratory potential toward colon cancer cells. In immunodeficient mice, we showed that systemic intraperitoneal (i.p) injections with human Vd2neg clones inhibited the growth of HT29 hypodermal tumors xenografts. Furthermore, our results demonstrated that Vd2neg T cells had an early and specific anti-tumor effect, and that such activity could be hampered in vivo using an anti-CCR3 antibody. Our study suggest that Vd2neg T cells with an anti-viral potential are able to reach a tumor site in vivo, and inhibit tumoral growth exercising a cytolytic activity. The second part of my Phd project proposed to get further insights on the role of Vd2neg T cells in the immune surveillance against colon cancer. To this aim, we tested, the involvement of human Vd1+ T lymphocytes, a substantial fraction of T cells in intestinal epithelia, in limiting tumor spread in vivo, using a mouse model of colorectal carcinoma (CRC). We sat up a physiological mouse model of CRC by orthotopic microinjection of HT29 colon cell, which mimics the natural history of human CRC. Indeed, primary colic tumors and pulmonary and hepatic distant metastases grew in mice. Furthermore, bioluminescence imaging was used to follow the outcome of luciferase expressing cancer cells. We showed that systemic treatment with human Vd1+ T lymphocytes could inhibit the growth of intracaecal HT29 tumors and led a substantial reduction of distant metastases. Our results are the first arguing for a crucial role of ?d T cells against CRC, specially in preventing the dissemination of colon cancer cells. Taken together, our results underline the role of of ?d T cells in theimmune response against colorectal cancer. Our findings put forward Vd2neg T cells as attractive candidates for novel anti-tumor immunotherapy protocols
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Schmidt, Anna Christina Verfasser], and Udo [Akademischer Betreuer] [Schumacher. "E- and P-selectins are essential for repopulation of chronic myelogenous and chronic eosinophilic leukemias in a scid mouse xenograft model / Anna Christina Schmidt. Betreuer: Udo Schumacher." Hamburg : Staats- und Universitätsbibliothek Hamburg, 2015. http://d-nb.info/1068316608/34.

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Books on the topic "Mouse xenograft models"

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Hoffman, Robert M. Patient-Derived Mouse Models of Cancer: Patient-Derived Orthotopic Xenografts. Humana, 2017.

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Book chapters on the topic "Mouse xenograft models"

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Green, Colin, Hakim Djeha, Gail Rowlinson-Busza, Christina Kousparou, and Agamemnon A. Epenetos. "Xenograft Mouse Models for Tumour Targeting." In Antibody Engineering. Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-01147-4_35.

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Sharma, Surinder K., and R. Barbara Pedley. "Xenograft Mouse Models for Tumour Targeting." In Antibody Engineering. Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-01147-4_36.

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Rowlinson-Busza, Gail, Julie Cook, and Agamemnon A. Epenetos. "Xenograft Mouse Models for Tumour Targeting." In Antibody Engineering. Springer Berlin Heidelberg, 2001. http://dx.doi.org/10.1007/978-3-662-04605-0_36.

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Hassan, Md Sazzad, and Urs von Holzen. "Animal Model: Xenograft Mouse Models in Esophageal Adenocarcinoma." In Methods in Molecular Biology. Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7734-5_14.

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Noto, Fallon K., and Tseten Yeshi. "Humanized Mouse and Rat PDX Cancer Models." In Patient-Derived Xenograft Models of Human Cancer. Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-55825-7_4.

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McKenzie, I. F. C., Y. Q. Li, and M. S. Sandrin. "Transgenic Mouse Models and Knockout Mouse Models to Manipulate the Xenograft Response." In Organtransplantation in Rats and Mice. Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-642-72140-3_61.

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Rubio-Viqueira, Belen, and Manuel Hidalgo. "Mouse Xenograft Models for Drug Discovery in Pancreatic Cancer." In Drug Discovery in Pancreatic Cancer. Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-1160-5_2.

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Liu, Ming, W. Robert Bishop, Yaolin Wang, and Paul Kirschmeier. "Transgenic Versus Xenograft Mouse Models of Cancer: Utility and Issues." In Molecular Cancer Therapeutics. John Wiley & Sons, Inc., 2004. http://dx.doi.org/10.1002/047165616x.ch10.

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Peldschus, Kersten, and Harald Ittrich. "Magnetic Resonance Imaging of Metastases in Xenograft Mouse Models of Cancer." In Methods in Molecular Biology. Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-8244-4_16.

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Benavente, Claudia A., and Michael A. Dyer. "Genetically Engineered Mouse and Orthotopic Human Tumor Xenograft Models of Retinoblastoma." In Methods in Molecular Biology. Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2297-0_15.

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Conference papers on the topic "Mouse xenograft models"

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Lamminen, Tarja, Katja Kaipio, Piia Mikkonen, Pia Roering, and Olli Carpén. "Abstract B43: Xenograft mouse models for ovarian cancer." In Abstracts: AACR Special Conference on Advances in Ovarian Cancer Research: From Concept to Clinic; September 18-21, 2013; Miami, FL. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1078-0432.ovca13-b43.

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Tedesco, Donato, Kyle Bonneau, Mikhail Makhanov, et al. "Abstract 3172: Pooled RNAi screens in xenograft mouse models." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-3172.

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Sicinska, Ewa, Samuel Moss, Joseph Brito, et al. "Abstract 4197: Mouse xenograft models of human soft tissue sarcomas." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-4197.

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Li, Na, Xin K. Ye, Ming-Xiao He, et al. "Abstract 647: In situ detection of human and mouse species-specific molecules in patient derived xenograft mouse models." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-647.

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Guo, Shanchun, Changde Zhang, Jiawang Liu, Shilong Zheng, Lin Yang, and Guangdi Wang. "Abstract 2688: ZB716 is orally efficacious in blocking tumor growth in mouse xenograft models." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-2688.

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Qi, Lin, Baxter A. Patricia, Kogiso Mari, et al. "Abstract 1450: Autopsy derived orthotopic xenograft (ADOX) mouse models for terminal pediatric brain tumors." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-1450.

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Heirich, Kyra, Melanie M. Triboulet, Corinne M. Renier, Vishnu C. Ramani, Elodie Sollier, and Stefanie S. Jeffrey. "Abstract 1525: Vortex technology for label-free enrichment of CTC from mouse xenograft models." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-1525.

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Kogiso, Mari, Lin Qi, Frank K. Braun, et al. "Abstract 2455: Development of patient-derived orthotopic xenograft mouse models of pediatric low grade gliomas." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-2455.

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Gu, S.-M., X. Zhang, R.-M. Li, et al. "P2-09-14: Evaluation of Angiogenesis Using Synchrotron Radiation in Xenograft Mouse Models of Breast Cancer." In Abstracts: Thirty-Fourth Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 6‐10, 2011; San Antonio, TX. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/0008-5472.sabcs11-p2-09-14.

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Stantz, Keith M., Bo Liu, Minsong Cao, et al. "Evaluating dynamic contrast-enhanced and photoacoustic CT to assess intra-tumor heterogeneity in xenograft mouse models." In Medical Imaging, edited by Armando Manduca and Amir A. Amini. SPIE, 2006. http://dx.doi.org/10.1117/12.654056.

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Reports on the topic "Mouse xenograft models"

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Weisberg, Tracey F. The Role of Growth Hormone and Insulin-Like Growth Factor-1 in Human Breast Cancer Growth in a Mouse Xenograft Model. Defense Technical Information Center, 1999. http://dx.doi.org/10.21236/ada391179.

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