Relevant bibliographies by topics / Mouse xenograft model

Academic literature on the topic 'Mouse xenograft model'

Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "Mouse xenograft model"

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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 (June 24, 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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Komen, Job, Sanne M. van Neerven, Elsbeth G. B. M. Bossink, Nina E. de Groot, Lisanne E. Nijman, Albert van den Berg, Louis Vermeulen, and Andries D. van der Meer. "The Effect of Dynamic, In Vivo-like Oxaliplatin on HCT116 Spheroids in a Cancer-on-Chip Model Is Representative of the Response in Xenografts." Micromachines 13, no. 5 (May 6, 2022): 739. http://dx.doi.org/10.3390/mi13050739.

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The cancer xenograft model in which human cancer cells are implanted in a mouse is one of the most used preclinical models to test the efficacy of novel cancer drugs. However, the model is imperfect; animal models are ethically burdened, and the imperfect efficacy predictions contribute to high clinical attrition of novel drugs. If microfluidic cancer-on-chip models could recapitulate key elements of the xenograft model, then these models could substitute the xenograft model and subsequently surpass the xenograft model by reducing variation, increasing sensitivity and scale, and adding human factors. Here, we exposed HCT116 colorectal cancer spheroids to dynamic, in vivo-like, concentrations of oxaliplatin, including a 5 day drug-free period, on-chip. Growth inhibition on-chip was comparable to existing xenograft studies. Furthermore, immunohistochemistry showed a similar response in proliferation and apoptosis markers. While small volume changes in xenografts are hard to detect, in the chip-system, we could observe a temporary growth delay. Lastly, histopathology and a pharmacodynamic model showed that the cancer spheroid-on-chip was representative of the proliferating outer part of a HCT116 xenograft, thereby capturing the major driver of the drug response of the xenograft. Hence, the cancer-on-chip model recapitulated the response of HCT116 xenografts to oxaliplatin and provided additional drug efficacy information.
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Wang, Zhijie, Jianglong Kong, Ziteng Chen, Meiru Mao, Jiacheng Li, Hui Yuan, Ya-nan Chang, Kui Chen, and Juan Li. "Human Glioma Nude Mouse Xenograft Model in situ." Diseases & Research 1, no. 1 (November 4, 2021): 1–5. http://dx.doi.org/10.54457/dr.202101003.

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Backgrounds: Surgery and chemotherapy are difficult because of the specific location of the glioma. The establishment of a suitable in situ model of glioma is the premise of the treatment of glioma. 8 week-old female BALB/c nude mice were chose to establish the glioma model. Methods: For the orthotopic glioma mice model, 1 × 105 cells/5 μL U87-MG-Luc or U87-MG cells which were trypsinized and resuspended in sterile PBS were slowly injected into the right corpus striatum (1.8 mm lateral, 0.6 mm anterior to the bregma and 3.0 mm in depth) by a stereotactic fixation device using a mouse adaptor. Results: The othotopic U87 glioma mice model identified by imaging on IVIS Spectrum and magnetic resonance imaging after 2 weeks from surgery. H&E-stained tumor sections in brain of the mice model were also observed. Conclusions: After identification, the glioma mouse xenograft in situ model obtained could be used in the evaluation system of therapeutic drugs or methods.
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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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Pascoal, Susana, Benjamin Salzer, Eva Scheuringer, Andrea Wenninger-Weinzierl, Caterina Sturtzel, Wolfgang Holter, Sabine Taschner-Mandl, Manfred Lehner, and Martin Distel. "A Preclinical Embryonic Zebrafish Xenograft Model to Investigate CAR T Cells in Vivo." Cancers 12, no. 3 (February 29, 2020): 567. http://dx.doi.org/10.3390/cancers12030567.

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Chimeric antigen receptor (CAR) T cells have proven to be a powerful cellular therapy for B cell malignancies. Massive efforts are now being undertaken to reproduce the high efficacy of CAR T cells in the treatment of other malignancies. Here, predictive preclinical model systems are important, and the current gold standard for preclinical evaluation of CAR T cells are mouse xenografts. However, mouse xenograft assays are expensive and slow. Therefore, an additional vertebrate in vivo assay would be beneficial to bridge the gap from in vitro to mouse xenografts. Here, we present a novel assay based on embryonic zebrafish xenografts to investigate CAR T cell-mediated killing of human cancer cells. Using a CD19-specific CAR and Nalm-6 leukemia cells, we show that live observation of killing of Nalm-6 cells by CAR T cells is possible in zebrafish embryos. Furthermore, we applied Fiji macros enabling automated quantification of Nalm-6 cells and CAR T cells over time. In conclusion, we provide a proof-of-principle study that embryonic zebrafish xenografts can be used to investigate CAR T cell-mediated killing of tumor cells. This assay is cost-effective, fast, and offers live imaging possibilities to directly investigate CAR T cell migration, engagement, and killing of effector cells.
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Davies, Jason M., Aaron E. Robinson, Cynthia Cowdrey, Praveen V. Mummaneni, Gregory S. Ducker, Kevan M. Shokat, Andrew Bollen, Byron Hann, and Joanna J. Phillips. "Generation of a patient-derived chordoma xenograft and characterization of the phosphoproteome in a recurrent chordoma." Journal of Neurosurgery 120, no. 2 (February 2014): 331–36. http://dx.doi.org/10.3171/2013.10.jns13598.

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Object The management of patients with locally recurrent or metastatic chordoma is a challenge. Preclinical disease models would greatly accelerate the development of novel therapeutic options for chordoma. The authors sought to establish and characterize a primary xenograft model for chordoma that faithfully recapitulates the molecular features of human chordoma. Methods Chordoma tissue from a recurrent clival tumor was obtained at the time of surgery and implanted subcutaneously into NOD-SCID interleukin-2 receptor gamma (IL-2Rγ) null (NSG) mouse hosts. Successful xenografts were established and passaged in the NSG mice. The recurrent chordoma and the derived human chordoma xenograft were compared by histology, immunohistochemistry, and phospho-specific immunohistochemistry. Based on these results, mice harboring subcutaneous chordoma xenografts were treated with the mTOR inhibitor MLN0128, and tumors were subjected to phosphoproteome profiling using Luminex technology and immunohistochemistry. Results SF8894 is a novel chordoma xenograft established from a recurrent clival chordoma that faithfully recapitulates the histopathological, immunohistological, and phosphoproteomic features of the human tumor. The PI3K/Akt/mTOR pathway was activated, as evidenced by diffuse immunopositivity for phospho-epitopes, in the recurrent chordoma and in the established xenograft. Treatment of mice harboring chordoma xenografts with MLN0128 resulted in decreased activity of the PI3K/Akt/mTOR signaling pathway as indicated by decreased phospho-mTOR levels (p = 0.019, n = 3 tumors per group). Conclusions The authors report the establishment of SF8894, a recurrent clival chordoma xenograft that mimics many of the features of the original tumor and that should be a useful preclinical model for recurrent chordoma.
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Honey, Christopher R., Modestus O. K. Obochi, Hao Shen, Philippe Margaron, Stephen Yip, and Julia G. Levy. "Reduced xenograft rejection in rat striatum after pretransplant photodynamic therapy of murine neural xenografts." Journal of Neurosurgery 92, no. 1 (January 2000): 127–31. http://dx.doi.org/10.3171/jns.2000.92.1.0127.

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Object. The goal of this study was to develop a method of reducing neural xenograft rejection by pretreating the graft with photodynamic therapy (PDT).Methods. Xenograft cell suspensions were prepared from fetal mouse mesencephalon, after which they were incubated for 30 minutes with various concentrations of a photosensitizer, verteporfin for injection, and light exposure. The xenograft cell suspensions were injected into the dopamine-depleted striata of 40 hemiparkinsonian rats assigned to different treatment groups. Four weeks after transplantation, xenograft function (determined by methamphetamine-induced rotation) and survival (determined by immunohistochemical staining for murine neurons) were compared. Group 1 animals (xenografts pretreated with 25 ng/ml verteporfin) and Group 3 animals (no verteporfin pretreatment, but daily administration of cyclosporin A) had significantly better xenograft survival and function compared with control animals (no pretreatment with verteporfin). Group 2 animals (xenografts pretreated with 250 ng/ml verteporfin) had no significant improvement.Conclusions. This work demonstrates improved neural xenograft survival and function when using pretransplant PDT of the graft in a rodent model. The potential benefits of this new therapy are its convenience (one pretransplant treatment) and its compatibility with host immunosuppression.
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Hayakawa, Jun, Matthew Hsieh, Naoya Uchida, Kareem Washington, Oswald Phang, David Eric Anderson, and John Tisdale. "A Practical Erythroid Assay in Humanized Xenograft Mouse Model." Blood 112, no. 11 (November 16, 2008): 2446. http://dx.doi.org/10.1182/blood.v112.11.2446.2446.

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Abstract Xenografting immunodeficient mice has been employed as a surrogate human hematopoietic stem cell (HSC) assay, however, erythroid output has not been reliably reported, limiting the usefulness of this model for erythroid disorders. We have previously demonstrated that busulfan preconditioning is sufficient to produce stable, high level engraftment of human cells in NOD/SCID/IL2Rγ null mice. Importantly, this high level engraftment can be achieved with low mortality, substantially reducing the number of animals required for experiments requiring long-term follow-up. Supplementation with human holo-transferrin (Tf) allows the detection human erythrocytes in this chimeric mouse assay at low levels, providing a potential model for the study of disorders affecting human red blood cells (2007 ASH meeting #3594). In the current work, we extend our observations and establish practical in vivo erythroid assay system of human HSCs in the humanized mouse model by the addition of an in vitro culture. Bone marrow (BM) from humanized mice containing 24.8±8.7% human cells (n=6) was first exposed to recombinant human (rHu) SCF+IL3 for 3 days in order to specifically enrich for human cells in the mixed chimera. After 3 days, human cells comprised 68.1±8.5% of the culture. The enriched cells were then cultured with rHu EPO+SCF+TGF-β for 7 additional days and then in rHu EPO+SCF for 7 days. After culture, and 98.9±1.47% of cells were of human origin. After centrifugation, the pellets were visibly red. Cells were assayed with both human CD71+ and GPA+ by flow cytometry: 64.0±7.44% were CD71+ and 69.2±7.02% were GPA+, and human α, β, and γ globin were confirmed by hemoglobin electrophoresis and mass spectrometry. In order to determine the utility of this approach, we tested 3 possible applications of this methodology: gene marking erythroid progeny, modeling of human hemoglobinopathies, and modeling of hemoglobin switching. We first transplanted human cord blood (CB) CD34+ cells after lentiviral transduction with a vector encoding GFP following busulfan conditioning. Three months post-transplant, bone marrow was harvested and placed in the in vitro culture. After in vivo culture, 98.9% of cells were of human origin and 60.7% were CD71+ and 72.3% were GPA+. The majority of CD71+ or GPA+ cells were GFP+ (82.3% and 87.7%, respectively). We subsequently transplanted human PB CD34+ cells derived from individuals with sickle cell trait (SCT) as we have previously demonstrated that these cells, unlike those from individuals with sickle cell disease, can be safely mobilized and processed. Further, the percentage of HbS expressed can be reliably measured. Three months post transplant, HbS was easily detectable by hemoglobin electrophoresis. Finally, we sought to address whether this model accurately reflects human erythropoiesis by examining hemoglobin switching after transplanting either CB expressing HbF or PB HSCs expressing HbA and monitoring the output of HbF and HbA over time. Early post-transplant, bone marrow derived from CB recipients expressed predominantly HbF after culture whereas that derived from PB HSC recipients expressed predominantly HbA. HbF declined during follow up and was replaced by HbA over 6 months of follow up from CB recipients, whereas HbA expression remained stable from PB HSC recipients. The time course of hemoglobin switching is similar to human ontogeny. In summary, our practical approach to model human erythropoiesis in the xenograft mouse should prove useful in the both the study of human erythroid disorders as well as therapeutic interventions.
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Frees, S., I. Moskalev, P. Raven, N. D’Costa, Z. Tan, W. Struss, C. Chavez-Munoz, and A. So. "Orthotopic sunitinib resistant renal cell carcinoma xenograft mouse model." European Urology Supplements 16, no. 3 (March 2017): e1477. http://dx.doi.org/10.1016/s1569-9056(17)30898-9.

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Thaler, Sonja, Angelika M. Burger, Thomas Schulz, Boris Brill, Alexandra Bittner, Patrick A. Oberholzer, Reinhard Dummer, and Barbara S. Schnierle. "Establishment of a mouse xenograft model for mycosis fungoides." Experimental Dermatology 13, no. 7 (July 2004): 406–12. http://dx.doi.org/10.1111/j.0906-6705.2004.00201.x.

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Dissertations / Theses on the topic "Mouse xenograft model"

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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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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.
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.
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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Hübner, Doreen, Christiane Rieger, Ralf Bergmann, Martin Ullrich, Sebastian Meister, Marieta Toma, Ralf Wiedemuth, 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, Martin Ullrich, Sebastian Meister, Marieta Toma, Ralf Wiedemuth, 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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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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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
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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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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Cahill, Fiona. "The role of LKB1 (STK11) in non-small cell lung cancer." Thesis, University of Oxford, 2017. https://ora.ox.ac.uk/objects/uuid:a3162d1b-96d3-4420-82eb-e261c9732f33.

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LKB1 is the second most commonly altered tumour suppressor gene in lung adenocarcinoma, the most prevalent form of lung cancer. LKB1 is a "master kinase" that has been shown to phosphorylate up to 13 downstream targets. We hypothesised that LKB1 loss is associated with an increased dependency on alternative, targetable pathways. The overall aims of this project were to better understand the role of LKB1 loss in lung cancer and to identify novel approaches to selectively target LKB1 mutated cells. We generated isogenic cells with or without LKB1 and used these to study the effect of LKB1 on cell proliferation. Importantly, we used a range of models including 2D culture, 3D spheroids and, sub-cutaneous and orthotopic xenograft models. To understand the role of LKB1 loss in lung cancer, the effect of LKB1 on mRNA expression was analysed using whole genome RNA Sequencing. To identify novel approaches to selectively target LKB1 mutated cells, we used biological screening methods and also investigated the effect of several metabolic inhibitors. We found that loss of LKB1 expression had no effect on cell proliferation in 2D culture, but was associated with increased growth in 3D spheroids, sub-cutaneous and orthotopic xenografts, as well as greater metastasis in a lung orthotopic model. Gene ontology analysis of the transcriptome identified that genes associated with cAMP signalling and cytoskeletal organisation were differentially expressed between LKB1 deficient and proficient cells. We confirmed that cAMP signalling was increased in LKB1 deficient cells, though there was no difference in sensitivity between LKB1 deficient and proficient cells to cAMP signalling modulators. The bioactive small molecule screen showed that LKB1 deficient cells underwent apoptosis more slowly and therefore, were less sensitive to many compounds, compared with LKB1 proficient cells. Screening in 3D spheroids was a novel approach that we used to identify microtubule inhibitors as potentially selective compounds acting in LKB1 deficient cells. Our RNASeq data suggests that there was a metabolic shift from oxidative phosphorylation to aerobic glycolysis in LKB1 deficient cells, although this did not affect sensitivity to complex I inhibitors. Importantly, LKB1 deficient cells were more sensitive to glucose and glutamine deprivation which suggests that targeting these metabolic pathways may hold the greatest promise to selectively inhibit proliferation in LKB1 mutated cells.
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Books on the topic "Mouse xenograft model"

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

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Hoffman, Robert M. Patient-Derived Mouse Models of Cancer: Patient-Derived Orthotopic Xenografts. Springer International Publishing AG, 2018.

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Book chapters on the topic "Mouse xenograft model"

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Hassan, Md Sazzad, and Urs von Holzen. "Animal Model: Xenograft Mouse Models in Esophageal Adenocarcinoma." In Methods in Molecular Biology, 151–64. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7734-5_14.

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Zhu, Qing, and Amy J. Weiner. "A Hepatitis C Virus Xenograft Mouse Efficacy Model." In Methods in Molecular Biology, 323–31. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-59745-447-6_14.

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Zhu, Xuguang, and Sheue-Yann Cheng. "Analysis of Thyroid Tumorigenesis in Xenograft Mouse Model." In Methods in Molecular Biology, 207–23. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7902-8_17.

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Yu, Valen Z., Joseph C. Y. Ip, Josephine M. Y. Ko, Lihua Tao, Alfred K. Lam, and Maria L. Lung. "Orthotopic Xenograft Mouse Model in Esophageal Squamous Cell Carcinoma." In Methods in Molecular Biology, 149–60. New York, NY: Springer US, 2020. http://dx.doi.org/10.1007/978-1-0716-0377-2_12.

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Hermanson, David L., Laura Bendzick, and Dan S. Kaufman. "Mouse Xenograft Model for Intraperitoneal Administration of NK Cell Immunotherapy for Ovarian Cancer." In Natural Killer Cells, 277–84. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3684-7_23.

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Mallesch, Julia L., Dino Chiaraviglio, Barry J. Allen, and Douglas E. Moore. "An Intra-Pancreatic and Hepatic Nude Mouse Cancer Xenograft Model for Boron Neutron Capture Therapy." In Advances in Neutron Capture Therapy, 547–50. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-2978-1_110.

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Liu, Yongtao. "Changes in the Urinary Proteome in a Patient-Derived Xenograft (PDX) Nude Mouse Model of Colorectal Tumor." In Urine, 105–17. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-9109-5_11.

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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, 463–76. Berlin, Heidelberg: 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, 477–90. Berlin, Heidelberg: 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, 498–512. Berlin, Heidelberg: Springer Berlin Heidelberg, 2001. http://dx.doi.org/10.1007/978-3-662-04605-0_36.

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Conference papers on the topic "Mouse xenograft model"

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Yan, Ying, Tengfei Yu, Wei Du, Guosheng Tong, Yuefei Yang, Tingting Tan, Xuqin Yang, et al. "Abstract 1210: A patient derived xenograft tumor model platform for “mouse trials”." 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.am2014-1210.

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Tilan, Jason U., Sung-Hyeok Hong, Susana Galli, Rachel Acree, Katherine Connors, Meredith Horton, Akanksha Mahajan, et al. "Abstract 2478: Tumor hypoxia promotes Ewing sarcoma metastases in a mouse xenograft model." 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.am2016-2478.

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Pernice, Tiziana, Alan Bishop, Oscar Cataluña, Mandy Palomares, Raquel Lopez, Práxedes Núñez, Carmen Cuevas, Maria José Guillén, and Pablo M. Aviles. "Abstract 4654: Plasma, tissue and tumor pharmacokinetics of PM060184 in NSCL xenograft mouse model." 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.am2014-4654.

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George, Jasmine, Minakshi Nihal, Mary A. Ndiaye, and Nihal Ahmad. "Abstract 1143: Pro-proliferative function of SIRT3 in a human melanoma xenograft mouse model." 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.am2016-1143.

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Devarajan, Asokan, Feng Su, Dawoud Sulaiman, Dorothy Nguyen, Robin Farias-Eisner, and Srinivasa T. Reddy. "Abstract 1472: Paraoxonase 3 is a novel tumor suppressor protein in xenograft mouse model." 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.am2020-1472.

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Lewis, Valerae O., Eswaran Devarajan, and Dennis PM Hughes. "Abstract 1261: Targeting IL-11Rα inhibits osteosarcoma pulmonary metastasis in an orthotopic xenograft mouse model." 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.am2014-1261.

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Takada, Marilia, Lauren Smyth, and Vilma Yuzbasiyan-Gurkan. "Abstract 2166: Dasatinib displays antitumor efficacy in an orthotopic xenograft mouse model of histiocytic sarcoma." 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.am2018-2166.

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Peng, Xianghong, Megan A. Mackey, Adegboyega Oyelere, Jun Zhang, Georgia Chen, Shuming Nie, Mostafa A. El-Sayed, and Dong M. Shin. "Abstract 5383: The plasmonic photothermal therapy efficacy of Au NRsin vivousing a SCCHN xenograft mouse model." 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.am2014-5383.

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Garcia, Patrick L., Tracy Gamblin, Leona N. Council, John D. Christein, Martin J. Heslin, Joseph Richardson, and Karina J. Yoon. "Abstract 2725: Establishment of the primary human tumor xenograft (tumorgraft) mouse model of pancreatic ductal adenocarcinoma." 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.am2013-2725.

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Hassan, Md Sazzad, Niranjan Awasthi, Roderich E. Schwarz, Margaret A. Schwarz, and Urs von Holzen. "Abstract 2826: A novel intraperitoneal metastatic xenograft mouse model for survival outcome assessment of esophageal adenocarcinoma." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-2826.

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Reports on the topic "Mouse xenograft model"

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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. Fort Belvoir, VA: Defense Technical Information Center, October 1999. http://dx.doi.org/10.21236/ada391179.

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