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Academic literature on the topic 'Orthotopic mouse model'

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Published: 10 December 2022
Last updated: 29 January 2023

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Journal articles on the topic "Orthotopic mouse model"

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Cui, Zheng Yun, Jin Seok Ahn, Jee Yun Lee, Won Seog Kim, Ho Yeong Lim, Hyun Jung Jeon, Soo Won Suh, et al. "Mouse Orthotopic Lung Cancer Model Induced by PC14PE6." Cancer Research and Treatment 38, no. 4 (2006): 234. http://dx.doi.org/10.4143/crt.2006.38.4.234.

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Chung, Jae-Seung, Somi Kim, Young-Sun Hwang, Xianlan Zhang, and In-Ho Cha. "An orthotopic nude mouse model of tongue carcinoma." Journal of the Korean Association of Oral and Maxillofacial Surgeons 37, no. 6 (2011): 490. http://dx.doi.org/10.5125/jkaoms.2011.37.6.490.

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Jungraithmayr, Wolfgang M., Stephan Korom, Sven Hillinger, and Walter Weder. "A mouse model of orthotopic, single-lung transplantation." Journal of Thoracic and Cardiovascular Surgery 137, no. 2 (February 2009): 486–91. http://dx.doi.org/10.1016/j.jtcvs.2008.10.007.

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Kang, Min, Wei Chen, Sixia Chen, Li Jiang, Gege Shu, Yuanxiu Yin, Zhipeng Quan, et al. "Establishment of a visualized mouse orthotopic model of nasopharyngeal carcinoma." Journal of Clinical Oncology 40, no. 16_suppl (June 1, 2022): e18048-e18048. http://dx.doi.org/10.1200/jco.2022.40.16_suppl.e18048.

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e18048 Background: Nasopharyngeal carcinoma, one of the most common head and neck tumors, is particularly prevalent in Southeast Asia and is characterized by high rates of metastasis and recurrence. Although mouse orthotopic tumor models are commonly employed in studies investigating the mechanisms underlying tumor development and progression, as well as preclinical treatment, currently no such model exists for nasopharyngeal carcinoma. The aim of the current study is to, therefore, establish an orthotopic murine model for nasopharyngeal carcinoma. Methods: To this end, human nasopharyngeal carcinoma C666-1-luc cells, stably expressing the firefly luciferase gene, were injected subcutaneously into the right axilla of BALB/C nude mice. Four weeks later, the resulting subcutaneous tumors were cut into small blocks and grafted into the nasopharynx of immunodeficient BALB/C nude mice to induce tumor formation. Tumor growth was monitored by bioluminescence imaging and small animal magnetic resonance imaging. The histological and immunological antigen expression associated with orthotopic nasopharyngeal carcinoma were analyzed by tissue section analysis and immunohistochemistry (IHC). Results: The tumor formation rate was over 90%. Fluorescence signal detection, micro-magnetic resonance imaging and hematoxylin and eosin staining revealed the successful growth of tumors in the nasopharynx of nude mice. Moreover, IHC analysis detected positive CK, CK5/6, P40 and P63 expression in the mouse orthotopic tumors, which is consistent with the reported antigen expression in the nasopharyngeal tumors of patients. Conclusions: Hence, we successfully established a mouse orthotopic model of nasopharyngeal carcinoma that is highly reproducible, and simple in operation, with low mortality and high tumor formation rates. Moreover, this model facilitates real-time monitoring of tumor growth via in vivo imaging technology, thus, providing a platform for researching nasopharyngeal carcinoma that is more conducive to preclinical research.
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Zhang, Wen-Ying, Zhen-Dong Jin, Feng Liu, Hai-Hua Yuan, and Bin Jiang. "Antitumor Activity of Intratumoral Ethanol Injection in an Orthotopic Pancreatic Cancer Cell Mouse Xenograft Model." Gastroenterology Research and Practice 2018 (2018): 1–8. http://dx.doi.org/10.1155/2018/7149565.

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Purpose. Pancreatic cancer is a lethal disease and usually is diagnosed at advanced stages of disease. This study assessed the effects of intratumoral ethanol injection using an endoscopic ultrasound (EUS) probe on the control of pancreatic cancer in a mouse orthotopic xenograft model. Materials and Methods. The subcutaneous and orthotopic human pancreatic cancer cell mouse xenograft models were established. Different concentrations of ethanol (0–95%) were injected into subcutaneous xenograft tumors. In the orthotopic tumor model, ethanol was injected into the tumor lesions under the guidance of a high-frequency EUS probe. Tumor volume, relative tumor volume (RTV), and histopathology were evaluated. The serum amylase level was analyzed at baseline and 24 h after treatment in the orthotopic tumor model. Results. Injection of 40–95% ethanol induced tumor necrosis in the subcutaneous tumor model, while there was no statistical difference between the RTVs of the two groups (P=0.81). In the orthotopic tumor model, the RTV of the 80% ethanol treatment group was less than that of the saline injection group (P<0.01); and histologically, there was a large area of necrosis observed in the 80% ethanol group. The serum amylase level was slightly elevated at 24 h after injection and returned to the baseline level at 7 days. Conclusion. Injection of 80% ethanol into xenograft tumor lesions of orthotopic pancreatic cancer resulted in tumor necrosis, and the procedure was safe and effective. Future studies will further confirm its antitumor activity as well as assess its safety and feasibility.
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Son, Yeseon, Changwook Lee, In Tag Yu, Mijin Lee, and Hangun Kim. "Evaluation of Anti-cancer Efficacy of Potassium Usnate using NIR Imaging of Orthotopic Breast Cancer Mouse Model." Yakhak Hoeji 66, no. 5 (October 31, 2022): 278–82. http://dx.doi.org/10.17480/psk.2022.66.5.278.

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Mouse cancer models are useful tools for evaluating in vivo tumor growth and metastasis, providing valuable information for preclinical testing. In this process, optical imaging enables the mouse models to easily identify the progress of disease in a non-invasive way. Here, we established an experimental bioimaging animal model of near-infrared (NIR) fluorescence by using a fluorescence-labeled organism bioimaging instrument (FOBI) and evaluated the anti-cancer effect of potassium usnate (KU) in an orthotopic breast cancer model. The cell viability assay revealed that KU had cytotoxicity with half maximal inhibitory concentration of approximately 138.57, 167.69, and 144.17 μM in 4T1-Fluc-Neo/iRFP-Puro (4T1-iRFP), MDA-MB-231, and MCF-7 cells, respectively. The measurement of NIR fluorescence from the 4T1-iRFP cells in a microtube via FOBI exhibited a strong correlation between cell number and fluorescence intensity, and the minimal detection limit was 10⁵ cells. Accordingly, NIR imaging was performed on the orthotopic breast cancer mouse model by using FOBI, and regression of tumor progression through intraperitoneal KU administration was successfully monitored. Our results demonstrated the establishment of NIR imaging in the orthotopic breast cancer animal model for evaluating the anti-cancer effect of KU.
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Rajput, Ashwani, Ekta Agarwal, Premila Leiphrakpam, Michael G. Brattain, and Sanjib Chowdhury. "Establishment and Validation of an Orthotopic Metastatic Mouse Model of Colorectal Cancer." ISRN Hepatology 2013 (April 21, 2013): 1–9. http://dx.doi.org/10.1155/2013/206875.

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Metastases are largely responsible for cancer deaths in solid tumors due to the lack of effective therapies against disseminated disease, and there is an urgent need to fill this gap. This study demonstrates an orthotopic colorectal cancer (CRC) mouse model system to develop spontaneous metastasis in vivo and compare its reproducibility against human CRC. IGF1R-dependent GEO human CRC cells were used to study metastatic colonization using orthotopic transplantation procedures and demonstrated robust liver metastasis. Cell proliferation assays were performed both in the orthotopic primary colon and liver metastatic tumors, and human CRC patient’s specimen and similar patterns in H&E and Ki67 staining were observed between the orthotopically generated primary and liver metastatic tumors and human CRC specimens. Microarray analysis was performed to generate gene signatures, compared with deposited human CRC gene expression data sets, analyzed by Oncomine, and revealed similarity in gene signatures with increased aggressive markers expression associated with CRC in orthotopically generated liver metastasis. Thus, we have developed an orthotopic mouse model that reproduces human CRC metastasis. This model system can be effective in developing new therapeutic strategies against disseminated disease and could be implemented for identifying genes that regulate the development and/or maintenance of established metastasis.
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Patel, Priya, Tatsuya Kato, Hideki Ujiie, Hironobu Wada, Daiyoon Lee, Hsin-pei Hu, Kentaro Hirohashi, Jin Young Ahn, Jinzi Zheng, and Kazuhiro Yasufuku. "Multi-Modal Imaging in a Mouse Model of Orthotopic Lung Cancer." PLOS ONE 11, no. 9 (September 1, 2016): e0161991. http://dx.doi.org/10.1371/journal.pone.0161991.

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Ip, Joseph Chok Yan, Josephine Mun Yee Ko, Valen Zhuoyou Yu, Kwok Wah Chan, Alfred K. Lam, Simon Law, Daniel King Hung Tong, and Maria Li Lung. "A Versatile Orthotopic Nude Mouse Model for Study of Esophageal Squamous Cell Carcinoma." BioMed Research International 2015 (2015): 1–10. http://dx.doi.org/10.1155/2015/910715.

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Increasing evidence indicates tumor-stromal interactions play a crucial role in cancer. Anin vivoesophageal squamous cell carcinoma (ESCC) orthotopic animal model was developed with bioluminescence imaging established with a real-time monitoring platform for functional and signaling investigation of tumor-stromal interactions. The model was produced by injection of luciferase-labelled ESCC cells into the intraesophageal wall of nude mice. Histological examination indicates this orthotopic model is highly reproducible with 100% tumorigenesis among the four ESCC cell lines tested. This new model recapitulates many clinical and pathological properties of human ESCC, including esophageal luminal stricture by squamous cell carcinoma with nodular tumor growth, adventitia invasion, lymphovascular invasion, and perineural infiltration. It was tested using an AKT shRNA knockdown of ESCC cell lines and thein vivotumor suppressive effects of AKT knockdown were observed. In conclusion, this ESCC orthotopic mouse model allows investigation of gene functions of cancer cells in a more natural tumor microenvironment and has advantages over previous established models. It provides a versatile platform with potential application for metastasis and therapeutic regimen testing.
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Haldorsen, Ingfrid S., Mihaela Popa, Tina Fonnes, Njål Brekke, Reidun Kopperud, Nicole C. Visser, Cecilie B. Rygh, et al. "Multimodal Imaging of Orthotopic Mouse Model of Endometrial Carcinoma." PLOS ONE 10, no. 8 (August 7, 2015): e0135220. http://dx.doi.org/10.1371/journal.pone.0135220.

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Dissertations / Theses on the topic "Orthotopic mouse model"

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Trimaglio, Giulia. "An orthotopic syngeneic mouse model to study the role of DCIR in colorectal cancer." Thesis, Toulouse 3, 2020. http://www.theses.fr/2020TOU30053.

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Le cancer colorectal (CCR) est le troisième cancer le plus fréquent et le deuxième cancer le plus mortel dans le monde. En conséquence, de nouveaux biomarqueurs diagnostiques ainsi qu’une amélioration des traitements actuels sont nécessaires. Les tumeurs se développent dans des microenvironnements complexes où les cellules cancéreuses interagissent et modulent la réponse immunitaire locale pour persister et se multiplier. Les lectines de type C, exprimées notamment par les cellules de l’immunité, régulent la réponse anti-cancéreuse, et donc le développement tumoral. Parmi elles, l'immunorécepteur des cellules dendritiques (DCIR), a été montré comme jouant un rôle immunitaire majeur au cours des maladies infectieuses et auto-immunes. À l’inverse, son rôle dans l'immunité tumorale reste méconnu. L'analyse des données transcriptomiques de deux cohortes de patients atteints de CCR a révélé un lien entre une expression élevée de DCIR et une meilleure survie des patients. Dans ce contexte, l'objectif principal de ma thèse était de déterminer l'impact de DCIR sur le développement du CCR et la réponse immunitaire associée. Dans ce but, j’ai établi un modèle murin préclinique, orthotopique et syngénique du CCR consistant en l'injection intracaecale de cellules tumorales MC38 exprimant la luciférase (MC38-fLuc+) dans des souris C57BL/6. Le suivi de la croissance tumorale par bioluminescence a montré que, malgré l’acquisition initiale de tumeurs solides par toutes les souris, seulement 30% des souris ont développé un CCR progressif et mortel, tandis que les autres animaux ont spontanément rejeté leurs tumeurs. Aucun rejet des tumeurs CCR MC38 n'a été observé en l'absence d'immunité adaptative, ni lors de l'injection de cellules MC38 dans d'autres sites anatomiques. L'immunophénotypage par transcriptomique et cytométrie de flux a révélé que les souris développant des tumeurs progressives présentaient une réponse immunitaire pro-tumorale, définie par une signature caractéristique des lymphocytes T régulateurs, détectable peu après l'implantation tumorale, et par une infiltration de cellules myéloïdes suppressives connues pour favoriser la croissance tumorale. En revanche, les souris rejetant les tumeurs présentaient une signature pro-inflammatoire précoce et un microenvironnement anti-tumoral enrichi en lymphocytes T CD8+. Ainsi, nos résultats démontrent un rôle du microenvironnement spécifique du côlon dans la régulation de l'équilibre entre les réponses immunitaires anti- ou pro-tumorales et souligne l'importance d'utiliser des modèles murins orthotopiques pour les études in vivo. Dans la seconde partie de ma thèse, j’ai utilisé ce modèle murin de CCR pour comparer le développement tumoral dans des souris C57BL/6 de type sauvage ou des souris déficientes pour l’expression de mDcir1 (mDcir1-KO), un homologue murin du DCIR humain. Bien que l'absence de mDCIR1 n'ait aucune incidence sur le pourcentage de souris développant ou rejetant les tumeurs du CCR, nous avons observé que les animaux mDcir1-KO développaient des tumeurs plus importantes que les sauvages En accord avec ce résultat, nous avons constaté une infiltration plus faible de lymphocytes CD8+ cytotoxiques et une activation moindre des lymphocytes T CD4+ et CD8+ (c'est-à-dire T-BET+, CD44haut, CTLA-4+) dans les tumeurs des souris mDcir1-KO par rapport aux souris sauvages. Ainsi, nos données indiquent un rôle protecteur et anti-tumoral de DCIR pendant le développement du CCR, probablement dû à une dérégulation de l'équilibre existant entre la tumeur et la réponse immunitaire. Dans l'ensemble, cette étude ouvre la voie à la mise au point éventuelle de biomolécules pharmacologiques ciblant DCIR pour déclencher une réponse immunitaire anti-tumorale efficace dans le contexte du CCR et au-delà
Colorectal cancer (CRC) is the third most common and second deadliest cancer worldwide accounting for 900.000 deaths in 2018. Consequently, there is a strong need for new biomarkers as well as an improvement of the current treatments. Tumors develop in complex microenvironments where cancer cells constantly crosstalk with, and modulate, the local immune response to persist and replicate. C-type lectins receptors, expressed in particular by immune cells, actively regulate the immune response to cancer cells and, therefore, tumor development. Dendritic cell immunoreceptor (DCIR), a C-type lectin expressed by myeloid cells, has been shown to play a major role in immunity to infectious and autoimmune diseases. Yet, the role played by DCIR in tumor immunity remains unknown. Analysis of publicly available transcriptomic data from two cohorts of CRC patients revealed an association between high DCIR gene expression and improved survival of patients. In this context, the principal objective of my PhD thesis was to determine the role played by DCIR in the immune response during CRC development. First, I developed an orthotopic syngeneic pre-clinical CRC mouse model consisting in the intra-caecal injection of engineered MC38 tumor cells expressing firefly luciferase (MC38-fLuc+) in C57BL/6 mice. Monitoring of the tumor growth by bioluminescence revealed that, despite an initial growth of solid tumors in all the mice, only 30% of mice developed a progressive lethal CRC, while the remaining animals spontaneously rejected their solid tumor and survived more than 100 days. No rejection of tumors was observed in the absence of adaptive immunity, nor when MC38-fLuc+ cells were injected in other anatomical locations (i.e., liver and skin). Immunophenotyping by transcriptomic and flow cytometry showed that mice with progressive CRC tumors exhibited a pro-tumor immune response, characterized by a regulatory T cell pattern, discernible shortly post-tumor implantation, as well as myeloid suppressor cells that are well-known to favor tumor growth. By contrast, tumor-rejecting mice presented an early pro-inflammatory response and an anti-tumor microenvironment enriched with CD8+ T cells. Taken together, our results demonstrate a preponderant role of the colon-specific microenvironment in regulating the balance between anti- or pro-tumor immune responses and underline the importance of using orthotopic mouse models for in vivo studies. In a second part of my thesis, we used this CRC mouse model to compare the tumor development in wild-type (WT) C57BL/6 mice or mice deficient for mDcir1 (mDcir1-KO), a murine homologue of human DCIR. While the lack of mDCIR1 has no impact on the percentage of mice developing or rejecting CRC tumors, we observed that mDcir1-KO animals developed bigger tumors than their WT counterparts. In line with this result, we found a lower infiltration of cytotoxic CD8+ and decreased activation of both CD4+ and CD8+ T cells (i.e., T-BET+, CD44high, CTLA-4+) in CRC tumors from mDcir1-KO mice compared to WT mice. Altogether, our data point to a protective and anti-tumor role of DCIR during CRC development, probably due to a dysregulation of the balance existing between the tumor and the immune response. Overall, this study paves the way for the potential future development of pharmacological biomolecules targeting DCIR to trigger an efficient anti-tumor immune response in the context of CRC and beyond
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Singh, Purba. "IN VIVO CHARACTERIZATION OF SYNGENEIC, ORTHOTOPIC MOUSE MODEL OF COX-2 POSITIVE RENAL CELL CANCER." OpenSIUC, 2013. https://opensiuc.lib.siu.edu/theses/1326.

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Renal cell carcinoma (RCC) is the third most common genito-urinary cancer. Beyond surgery, few other treatment options for RCC exist and about one-third of the patients who have had nephrectomy develop metastasis subsequently. The treatment of the metastatic disease remains a clinical challenge. Hence, novel therapeutic options are necessary for the patients with metastatic RCC. Immunotherapy is the most common mode of treatment in RCC presently; however, it contributes to a large number of toxic side effects to the patients. The immunotherapeutic regimens currently used to treat metastatic renal cancer are recombinant human interleukin -2 (IL-2) and recombinant human interferon alpha alone or in combination. However, the uses of these high dose cytokines are limited by their toxicity and poor patient response rates. Preclinical studies in animal tumor models of RCC are required to address the newer and effective therapeutic approaches for late stage metastatic RCC. A suitable animal model for studying RCC is lacking. Hence, development of a novel animal model would largely contribute in testing newer therapeutics and combating the metastatic disease. Cyclooxygenases are group of enzymes that catalyze the conversion of arachidonic acid to prostaglandins (PGE2). It comprises of two isoforms Cox-1 and Cox-2. Previous studies have implicated the potential role of Cox-2 in carcinogenesis and the expression of Cox-2 have been reported in colorectal, lung, breast, gastric and esophageal carcinomas. Cox-2 is also highly expressed in RCC and a potential biomarker in RCC. Based on emerging clinical evidences on the role of Cox-2 in several malignancies, we hypothesize that overexpression of Cox-2 in RCC promotes tumor growth and metastasis. Selective Cox-2 inhibitors act by inhibiting PGE2 synthesis and have been shown to retard tumor formation, metastasis, and angiogenesis. They induce apoptosis and inhibit the PGE2 induced immunosupression. Thus, a specific Cox-2 inhibitor like indomethacin or NS398 would be able to inhibit the tumorigenic properties of Cox-2, thereby attenuating tumor growth and dissemination to other organs. In this context, we injected the Cox-2 engineered Renca cell lines (COX2 -ve and COX2 +ve) in the subcapsular space of kidney of a Balbc/Cr mice. This resulted in the tumor growth, which was monitored by bioluminescence imaging (BLI) for a period of three weeks post-inoculation. Metastases were evident in distant organs such as lung, liver, spleen and lymph nodes. This was expressed as luciferase activity per milligram of protein of the particular tissue normalized with the background luciferase activity per milligram of the tissue from control (non-injected mice). Thus, the animal model was established and validated in our preliminary studies. To address the potential role of PGE2 in the tumor microenvironment, tumors were harvested and then processed for assessment by histology and immunohistochemistry. Initial characterization studies included immunohistochemical assessment of tumor vasculature as elucidated by staining with specific markers for lymphatic vessels (LYVE-1), blood endothelium (CD31) and tumor infiltrating macrophages (Cd11b). Macrophage recruitment close to the LYVE-1+ structures were also determined by the double positive events obtained by staining with both CD11b and LYVE-1. A large number of peripheral (18%±2.79), intratumoral (12%±3) and marginal (7%±2.01) LYVE-1+ve structures were found in PGE2 producing tumor than in the control tumor. Although, the frequency of blood vessels in both the tumor types were unaltered, however, an increased vascular area was obtained in the COX2 +ve tumor than in COX2 -ve tumor. There was a significant increase in the frequency of infiltrating macrophages in the peripheral (25%± 3.86), intratumoral (10%± 3.93) and tumor-kidney margin of COX-2 positive tumors (10%± 2.34) than in the COX-2 negative tumors (12% ± 2.36, 0% and 0%) respectively. Frequency of the blood vessels in both the tumors were unaltered, however, a significant increase in the mean fluorescent intensity (MFI) in the peripheral region (4.3±0.1) of COX2 +ve tumor was observed when compared to COX2 -ve tumors (2.3±0.05). These preliminary studies indicate the potential role of PGE2 in promoting tumor vasculature, increased macrophage recruitment within the tumors and tumor-kidney margins. In our initial studies, a significant enrichment of LYVE-1+ve macrophages were observed in the kidney-tumor sections of the COX2 +ve mice, which might indicate that, PGE2 may promote differentiation of the macrophages into a lymphatic phenotype. Thus, this animal model would further help in thorough characterization of other immune infiltrating cells like CD8+ T cells and NK cells and thereby lead us to identify the cause of immune dysregulation in renal cell carcinoma due to RCC derived soluble factors like PGE2 and TGF-beta. Furthermore, treatment with Cox-2 inhibitors like NS-398 should retard tumor growth, metastases, immune cell dysregulation, and tumor vasculature.
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Sanchez, Herrero Alvaro. "Tissue engineering of an orthotopic humanised bone-organ as a platform for preclinical multiple myeloma research." Thesis, Queensland University of Technology, 2020. https://eprints.qut.edu.au/203046/1/Alvaro_Sanchez%20Herrero_Thesis.pdf.

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This Thesis presents the first steps of the development of a humanized and patient-specific mouse model of multiple myeloma (MM). Novel therapeutic approaches are getting increasingly complex and relevant pre-clinical drug testing is becoming a great challenge. The mouse model presented here features a humanized bone marrow compartment with a humanized bone shell that is able to engraft MM cells and patient-derived hematopoietic stem cells, mimicking myeloma bone disease serving as a unique platform for MM drug testing and discovery.
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Wagner, Ferdinand. "Convergence of bioengineering, orthopaedics and tumour biology to develop and validate humanized rodent models for primary bone tumour research." Thesis, Queensland University of Technology, 2018. https://eprints.qut.edu.au/116423/1/Ferdinand_Wagner_Thesis.pdf.

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Preclinical osteosarcoma (OS) models often fail to predict effects of cancer drugs. Two humanized bone models are described which comprise human bone matrix, vascular and hematopoietic components. The first model utilizes ectopic implantation of human bone and rhBMP-7 into mice. Injection of OS cells produces high similarities to the human disease. A second scaffold-based model allows modular orthotopic application. Human osteoblasts seeded into mPCL-CaP scaffolds and human endothelial cells within a biomimetic hydrogel are positioned around the mouse femur. Human CD34+ transplantation allows humanization of the hematopoietic system. Analysis demonstrated that the models allow predictive marker studies of bone malignancies.
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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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Nortmeyer, Maike Christine [Verfasser], and Thomas [Akademischer Betreuer] Höfer. "MYCN dependency of MYCN amplified neuroblastoma cell lines analyzed in relation to their interaction with BET proteins and in a novel orthotopic mouse model / Maike Christine Nortmeyer ; Betreuer: Thomas Höfer." Heidelberg : Universitätsbibliothek Heidelberg, 2019. http://d-nb.info/1192373022/34.

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Nortmeyer, Maike [Verfasser], and Thomas [Akademischer Betreuer] Höfer. "MYCN dependency of MYCN amplified neuroblastoma cell lines analyzed in relation to their interaction with BET proteins and in a novel orthotopic mouse model / Maike Christine Nortmeyer ; Betreuer: Thomas Höfer." Heidelberg : Universitätsbibliothek Heidelberg, 2019. http://d-nb.info/1192373022/34.

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Lichtenegger, Eva [Verfasser], Per Sonne [Akademischer Betreuer] Holm, Gabriele [Gutachter] Multhoff, and Per Sonne [Gutachter] Holm. "Establishment of an orthotopic bladder cancer mouse model for the assessment of a novel YB-1 based viro-immunotherapy in vivo / Eva Lichtenegger ; Gutachter: Gabriele Multhoff, Per Sonne Holm ; Betreuer: Per Sonne Holm." München : Universitätsbibliothek der TU München, 2018. http://d-nb.info/1164591088/34.

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Ho, William Wee Teck. "Orthotopic liver metastasis mouse models of mismatch repair-proficient colorectal cancer recapitulate clinical inefficacy of immune checkpoint blockade." Thesis, Massachusetts Institute of Technology, 2020. https://hdl.handle.net/1721.1/132614.

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Thesis: Ph. D., Massachusetts Institute of Technology, Department of Chemical Engineering, May, 2020
Cataloged from the official PDF of thesis.
Includes bibliographical references (pages 70-75).
Liver metastasis is a major cause of mortality in patients with colorectal cancer (CRC). Immune checkpoint blockade (ICB) therapy has significantly improved overall survival in several cancer types including melanoma and non-small cell lung cancer. However, patients with mismatch repair-proficient (pMMR) metastatic CRC do not respond to ICB therapy. MC38 and CT26 are two of the most commonly used mouse syngeneic CRC cell lines in preclinical studies of colorectal cancer. In most of these preclinical studies, MC38 and CT26 are implanted under the skin in the hind flank of the mice where they grow into subcutaneous tumors. Several studies have shown that these subcutaneous MC38 or CT26 tumors respond very well to ICB treatment. However, MC38 and CT26 have been reported previously to be pMMR CRC cell lines, indicating that these subcutaneous tumor mouse models do not recapitulate the clinical reality well. In this thesis, we show that when pMMR CRC cell lines are implanted orthotopically in the liver as liver metastasis, the resultant liver metastases are unresponsive to ICB, which recapitulates the clinical reality that patients with pMMR metastatic CRC do not respond to ICB treatment. We further show that when treated with ICB, these orthotopic pMMR CRC liver metastasis mouse models have poor infiltration and activation of key immune cells and significantly decreased activity of key pathways that are critical for the efficacy of ICB. We also evaluated several strategies aimed at overcoming the inefficacy of ICB in these pMMR CRC liver metastasis mouse models. We found that radiation therapy was able to overcome inefficacy of ICB in the pMMR CRC liver metastasis mouse model with moderately low tumor mutational load. We also found that antibody-peptide epitope conjugates (APECs) were able to increase the efficacy of ICB in the pMMR CRC liver metastasis mouse model with very low tumor mutational load. Our results demonstrate that by implanting pMMR CRC cell lines in a relevant tissue site such as in the liver to model CRC liver metastasis, we can more accurately recapitulate the clinical efficacy of therapies such as ICB.
by William Wee Teck Ho.
Ph. D.
Ph.D. Massachusetts Institute of Technology, Department of Chemical Engineering
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Books on the topic "Orthotopic mouse model"

1

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 "Orthotopic mouse model"

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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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Greenaway, James B., and Jim J. Petrik. "Orthotopic, Syngeneic Mouse Model to Study the Effects of Epithelial–Stromal Interaction." In Methods in Molecular Biology, 409–23. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-547-7_31.

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Byrne, Frances L., Joshua A. McCarroll, and Maria Kavallaris. "Analyses of Tumor Burden In Vivo and Metastasis Ex Vivo Using Luciferase-Expressing Cancer Cells in an Orthotopic Mouse Model of Neuroblastoma." In Methods in Molecular Biology, 61–77. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3148-4_5.

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Jäger, Wolfgang, Igor Moskalev, Peter Raven, Akihiro Goriki, Samir Bidnur, and Peter C. Black. "Orthotopic Mouse Models of Urothelial Cancer." In Urothelial Carcinoma, 177–97. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7234-0_15.

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Qiu, Wanglong, and Gloria H. Su. "Development of Orthotopic Pancreatic Tumor Mouse Models." In Methods in Molecular Biology, 215–23. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-62703-287-2_11.

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Hoffman, Robert M. "Orthotopic Metastatic Mouse Models of Prostate Cancer." In Metastasis of Prostate Cancer, 143–69. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-5847-9_8.

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Zhang, George, and Yi-Chieh Nancy Du. "Orthotopic Pancreatic Tumor Mouse Models of Liver Metastasis." In Methods in Molecular Biology, 309–20. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-8879-2_27.

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Hoffman, Robert M. "Why Patient-Derived Mouse Models Need to Be Orthotopic." In Molecular and Translational Medicine, 277–84. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-57424-0_20.

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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, 307–17. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2297-0_15.

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Hoffman, Robert M., Atsushi Suetsugu, Tasuku Kiyuna, Shuya Yano, and Michael Bouvet. "Fluorescence Imaging of Tumors in Human Patient-Derived Orthotopic Xenograft (PDOX) Mouse Models." In Molecular and Translational Medicine, 207–16. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-57424-0_15.

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Conference papers on the topic "Orthotopic mouse model"

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Monclús, Silvia Garcia, Juan Huertas Martínez, Laura Lagares Tena, Santiago Rello Varona, Olga Almacellas Rabaiget, David Herrero Martin, Roser López Alemany, and Oscar Martinez Tirado. "Abstract 1929: A novel orthotopic mouse model in sarcomas." 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.am2017-1929.

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Lin, Yuchun, xinguo Jiang, Mohammad A. Khan, and Mark R. Nicolls. "Relaxin Attenuates Airway Fibrosis In Mouse Orthotopic Tracheal Transplantation Model." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a5122.

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Rainbolt, Elizabeth, Madelyn Cecil-Taylor, Andrew Wong, Robin Ball, Patrick Wood, Edgar R. Wood, Paula Miliani de Marval, and Susan Yeyeodu. "Abstract 2760: A mouse orthotopic model of pancreatic cancer and response to treatment." 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.am2020-2760.

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Gros, Stephanie J., Thorsten Dohrmann, Jussuf T. Kaifi, Michael Bouvet, Robert M. Hoffman, and Jakob R. Izbicki. "Abstract 1458: Orthotopic imageable peritoneal carcinomatosis GFP nude mouse model of human esophageal cancer." 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.am10-1458.

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Liu, Ling, Zhi Xiu Lin, and Po Sing Leung. "Abstract B23: Brucein D suppresses pancreatic tumor growth in a mouse orthotopic nude model." In Abstracts: AACR Special Conference on Pancreatic Cancer: Progress and Challenges; June 18-21, 2012; Lake Tahoe, NV. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.panca2012-b23.

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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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Ides, Johan, An Wouters, Jonas Messagie, Christel Vangestel, Bea Pauwels, Jurgen Joossens, Pieter Van der Veken, Koen Augustyns, Marc Peeters, and Filip Lardon. "Abstract 5250: Optimization of an orthotopic mouse model forin vivofluorescent uPA imaging in breast cancer." 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.am2012-5250.

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Robl, Bernhard, Sander Martijn Botter, Aleksandar Boro, Dario Neri, and Bruno Fuchs. "Abstract 589: Targeting of metastatic osteosarcoma with F8-TNF-alpha in an orthotopic 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.am2016-589.

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Okamoto, Takuya, Katsuyuki Yaginuma, Satoshi Nagayama, and Ryoji Yao. "Abstract 1949: Mouse model of metastatic colorectal cancer by orthotopic transplantation of patient derived organoids." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-1949.

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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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