Relevant bibliographies by topics / Syngeneic model

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  2. Dissertations / Theses
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  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Syngeneic model'

Author: Grafiati
Published: 25 January 2025

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Journal articles on the topic "Syngeneic model"

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Filho, Ivo P. Torres, Beryl Hartley-Asp, and Per Borgström. "Quantitative Angiogenesis in a Syngeneic Tumor Spheroid Model." Microvascular Research 49, no. 2 (March 1995): 212–26. http://dx.doi.org/10.1006/mvre.1995.1017.

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Chen, Yi-Fen, Kuo-Wei Chang, I.-Ting Yang, Hsi-Feng Tu, and Shu-Chun Lin. "Establishment of syngeneic murine model for oral cancer therapy." Oral Oncology 95 (August 2019): 194–201. http://dx.doi.org/10.1016/j.oraloncology.2019.06.026.

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Farhoodi, Henry P., Aude I. Segaliny, Zachary W. Wagoner, Jason L. Cheng, Linan Liu, and Weian Zhao. "Optimization of a syngeneic murine model of bone metastasis." Journal of Bone Oncology 23 (August 2020): 100298. http://dx.doi.org/10.1016/j.jbo.2020.100298.

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Mezhir, James J., Kerrington D. Smith, Eric T. Kimchi, James O. Park, Carlos A. Lopez, Helena J. Mauceri, Micheal A. Beckett, Samual Hellman, Ralph R. Weichselbaum, and Mitchell C. Posner. "Establishment of a Syngeneic Model of Hepatic Colorectal Oligometastases." Journal of Surgical Research 136, no. 2 (December 2006): 288–93. http://dx.doi.org/10.1016/j.jss.2006.05.008.

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Mehr, Ramit, Alan S. Perelson, Ayala Sharp, Lee Segel, and Amiela Globerson. "MHC-Linked Syngeneic Developmental Preference in Thymic Lobes Colonized with Bone Marrow Cells: A Mathematical model." Developmental Immunology 5, no. 4 (1998): 303–18. http://dx.doi.org/10.1155/1998/65943.

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Reconstitution of the T-cell compartment after bone marrow transplantation depends on successful colonization of the thymus by bone-marrow-derived progenitor cells. Recent studies compared the development of syngeneic and allogeneic bone-marrow-derived cells in cocultures with lymphoid-depleted fetal thymus explants, leading to the discovery of MHC-linked syngeneic developmental preference (SDP) in the thymus. To determine the nature of cell interactions among the bone marrow and thymic elements that might underlie SDP, we analyzed this phenomenon by mathematical modeling. The results indicate that syngeneic mature T cells, responsible for inducing this preference, probably interfere both with the seeding of allogeneic bone-marrow-derived thymocyte progenitors in the thymic stroma and with their subsequent proliferation. In addition, the possibility of augmented death among the developing allogeneic thymocytes cannot be ruled out.
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Seishima, Noriko, William Becker, Purevdorj Olkhanud, Hoyoung Maeng, Miguel Lopez-Lago, Charles Wiseman, William Williams, and Jay Berzofsky. "Peptide-pulsed MHC class II allogeneic dendritic cell vaccine has superior efficacy providing allogeneic help in a murine cancer model." Journal of Immunology 212, no. 1_Supplement (May 1, 2024): 1097_4946. http://dx.doi.org/10.4049/jimmunol.212.supp.1097.4946.

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Abstract Allogeneic dendritic cell (DC) cancer vaccines present a promising alternative to autologous counterparts, offering an “off-the-shelf” solution for multiple patients and providing additional allogeneic help. We assessed the efficacy of a semi-allogeneic DC vaccine in comparison to a syngeneic one for tumor suppression. C57BL/6 mice were inoculated subcutaneously with human papillomavirus E6 and E7-expressing TC-1 cells. Syngeneic bone marrow DCs (BMDCs) were generated from C57BL/6 and semi-allogeneic BMDCs with a point mutation on either MHC class I or II were generated from B6.C-H2-Kbm1/By and B6(C)-H2-Ab1bm12/KhEg, respectively. The TC-1-bearing mice were injected with syngeneic or semi-allogeneic BMDCs pulsed with H-2Db-restricted E743-77 peptide. Compared with saline control, the MHC-I mutant BMDC vaccine reduced tumor growth no better than the syngeneic one. However, the MHC-II mutant BMDC vaccine was significantly better at delaying tumor growth. CD4+ or CD8+ T cell depletion showed that the syngeneic BMDC vaccine worked independently of CD4+ T cells, but the enhanced activity of the MHC-II mutant BMDC vaccine was dependent on CD4+ T cells at an early stage. Surprisingly, later depletion of CD4+ T cells improved vaccine efficacy, and this was confirmed to be due to Treg depletion. Thus, MHC class II allogeneic BMDCs proved more effective by inducing early allogeneic CD4+ T cell help, and this effect can by further enhanced by Treg depletion at a later stage.
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Ildstad, S. T., J. A. Bluestone, and D. H. Sachs. "Alloresistance to engraftment of allogeneic donor bone marrow is mediated by an Lyt-2+ T cell in mixed allogeneic reconstitution (C57BL/10Sn + B10.D2/nSn----C57BL/10Sn)." Journal of Experimental Medicine 163, no. 5 (May 1, 1986): 1343–48. http://dx.doi.org/10.1084/jem.163.5.1343.

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In the mixed allogeneic reconstitution (B10 + B10.D2----B10) model, alloresistance to engraftment of allogeneic donor results if the syngeneic component of the mixed bone marrow inoculum is not depleted of Lyt-2+ cells before transplantation. Resultant experimental animals repopulate as fully syngeneic, reject B10.D2 skin allografts, and are reactive to B10.D2 lymphoid cells in vitro, as assessed by mixed lymphocyte culture proliferative and cellular cytotoxicity assays. In contrast, depletion of Lyt-2-reactive cells from the syngeneic component of the mixed bone marrow inoculum results in mixed lymphopoietic chimerism and specific in vivo transplantation tolerance to B10.D2 allogeneic donor skin grafts and in vitro unreactivity to B10.D2 lymphoid elements. Full reactivity to third party is evident both in vitro and in vivo in these animals. This model may be helpful in further study of the syngeneic host-type cell phenotypes responsible for alloresistance to bone marrow engraftment.
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Seishima, Noriko, Purevdorj B. Olkhanud, William Becker, Hoyoung Maeng, Miguel Lopez-Lago, Charles Wiseman, William V. Williams, and Jay A. Berzofsky. "Peptide-pulsed MHC class II mutant dendritic cell vaccine has superior efficacy in a murine tumor model." Journal of Immunology 210, no. 1_Supplement (May 1, 2023): 159.10. http://dx.doi.org/10.4049/jimmunol.210.supp.159.10.

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Abstract Autologous dendritic cell (DC) vaccines with tumor antigens have been used clinically with limited therapeutic effects. Semi-allogeneic DC-based immunotherapy is still controversial, but it can be an alternative source and more attractive than autologous DC vaccines because the “off-the-shelf” DCs can be used for multiple patients without lengthy individual manufacturing time and may provide additional “allogeneic help”. This study aims to compare efficacy of syngeneic DC vaccines and semi-allogeneic DC vaccines and determine whether a therapeutic semi-allogeneic DC vaccine is more efficacious in tumor suppression. Female C57BL/6 mice were inoculated subcutaneously with human papillomavirus E6 and E7-expressing TC-1 cells. Syngeneic bone marrow dendritic cells (BMDCs) were generated from C57BL/6 and semi-allogeneic BMDCs were generated from two mouse strains, B6.C-H2-K bm1/ByJ and B6(C)-H2-Ab1 bm12/KhEgJ which had limited point mutations in the MHC class I H2-K ballele or H2-lA bMHC class II allele, respectively. Each BMDC was pulsed with H-2D b-restricted E7 43–77peptide and matured before injection. The mice received 4 intradermal injections of syngeneic or one of the semi-allogeneic E7-pulsed BMDC vaccines starting 8–9 days after the TC-1 implantation. Compared with saline control, the MHC class I mutant BMDC vaccine had efficacy similar to the syngeneic BMDC vaccine in suppressing TC-1 tumor growth. However, the MHC class II mutant BMDC vaccine had efficacy significantly superior to that of the other BMDC vaccines. Thus, MHC class II semi-allogeneic BMDCs may be more effective than syngeneic DC-based cancer vaccines, presumably because the class II alloantigens induce additional T cell help for anti-tumor immunity.
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Chade, Daher C., Priscila M. Andrade, Ricardo C. Borra, Katia R. Leite, Enrico Andrade, Fabiola E. Villanova, and Miguel Srougi. "Histopathological characterization of a syngeneic orthotopic murine bladder cancer model." International braz j urol 34, no. 2 (March 2008): 220–29. http://dx.doi.org/10.1590/s1677-55382008000200013.

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Quinn, Bridget A., Fang Xiao, Laura Bickel, Lainie Martin, Xiang Hua, Andres Klein-Szanto, and Denise C. Connolly. "Development of a syngeneic mouse model of epithelial ovarian cancer." Journal of Ovarian Research 3, no. 1 (2010): 24. http://dx.doi.org/10.1186/1757-2215-3-24.

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Dissertations / Theses on the topic "Syngeneic model"

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Lamkin, Donald Michael. "Inflammatory processes and depressive-like behavior in a syngeneic model of ovarian cancer." Diss., University of Iowa, 2010. https://ir.uiowa.edu/etd/693.

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Considerable data demonstrate a high prevalence of depression symptoms in patients with cancer, with some studies showing the prevalence for major depressive disorder (MDD) to be as high as 50%. Because depression researchers have found that a significant relationship exists between depression symptoms and indices of systemic inflammation and because several cancer types exploit the mechanisms of the body's inflammatory response to aid in their own progression, it was hypothesized that tumor in the body could be a cause of depression symptoms in cancer patients. Examination of this question was conducted using an immunocompetent mouse model of ovarian cancer and several measures of depressive-like and sickness behavior. Initial investigation of the model (Chapter 2) involved a series of pilot experiments that addressed methodology and demonstrated that ID8 murine ovarian carcinoma was capable of inducing elevated levels of systemic IL-6 and depressive-like behavior, specifically anhedonia as measured by a decrease in sucrose solution. In Chapter 3, a larger experiment (Experiment 1) was conducted that examined the effect of ovarian tumor on sucrose intake, food intake, body weight, locomotion, and rotarod performance. Results in the study indicated that sucrose-measured anhedonia in the model was not confounded by anorexia because tumor-bearing mice and control mice exhibited no significant difference in appetite. In Chapter 4, a second experimental factor, social housing, was added alongside tumor condition, and a second measure of depressive-like behavior, tail suspension test (TST) immobility, was added to measures from the previous experiment. The results of this second large experiment (Experiment 2) demonstrated that ovarian tumor had no significant effect on TST immobility, even though it did cause mice to exhibit less motor activity in the home cage. Housing condition did affect TST immobility. Mice that were individually-housed exhibited significantly more TST immobility than group-housed mice. Also, individually-housed mice exhibited less sucrose intake than group-housed mice. This gave rise to a significant interaction in sucrose preference among the four experimental groups where individually-housed tumor-bearing mice showed less sucrose preference than the other groups. In Chapter 5, systemic proinflammatory and antiinflammatory cytokines from both Experiment 1 and Experiment 2 were examined. Results indicated that both proinflammatory and antiinflammatory cytokines were significantly higher in tumor-bearing mice than in control mice, and these effects were largest for interleukin-6 (IL-6) and IL-10. Among tumor-bearing mice, significant correlations between IL-1β, IL-6, tumor necrosis factor alpha (TNF-α), transforming growth factor beta (TGF- β) and locomotion were noted, but there was no significant correlation between cytokines and anhedonia. No significant effect of housing condition on cytokines was found. In Chapter 6, principal findings of the project are summarized and discussed with a focus on anhedonia and psychomotor slowing in MDD. Current evidence suggests that dopaminergic and glutamatergic systems in the brain may underlie anhedonic and psychomotor features in inflammation-induced depression. Thus, future investigation of the mediators between ovarian tumor and these depressive-like behaviors in the model may benefit from targeting these specific neural mechanisms.
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Borgström, Annelie. "Analysis of tumour infiltrating leukocytes in colon cancer carcinoma in a syngeneic rat model." Thesis, Linköpings universitet, Institutionen för fysik, kemi och biologi, 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-56910.

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Tumour immunity is a balance between immune mediators that promote tumor progression versus mediators that promote tumor rejection. Infiltrating lymphocytes in human colorectal cancer tissues are independent prognostic factors for a better survival and a high number of cytotoxic CD8+ T-cells have been associated with a better prognosis in terms of a longer and disease free survival for the patient. In our syngeneic rat model we induce colon carcinoma subperitoneally by injecting a colon cancer cell line BN7005, a cell line expressing the epitope (Lewis Y) for the BR96 antibody. Tumours are dissected out and treated with different fixatives and then either frozen, snap-frozen or embedded in paraffin followed by sectioning. Immunohistochemistry using monoclonal antibodies against the tumour infiltrating leukocytes was performed on the tissue. The results were seen as an infiltration of different leukocytes in the tumours.
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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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Ichinose, You. "Reduction of tumorigenicity by an interferon-gamma-gene-transduced tumor on another syngeneic tumor in a murine model." Kyoto University, 1998. http://hdl.handle.net/2433/182248.

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Mendes, Odete Rodrigues. "Role of MMP2, MMP3 and MMP9 in the development of breast cancer brain and lung metastasis in a syngeneic rat model." Texas A&M University, 2005. http://hdl.handle.net/1969.1/2645.

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In order to study the expression of MMP2, MMP 3 and MMP9 in breast cancer brain and lung metastasis, we used a syngeneic rat model of distant metastasis of ENU1564, a carcinogen-induced mammary adenocarcinoma cell line. At six weeks post inoculation we observed development of micro-metastasis in the brain and lung. Immunohistochemistry and Western blotting analyses showed that MMP 2, -3 and -9 protein expression is consistently significantly higher in neoplastic brain tissue compared to normal brain tissue. Lung metastases express abundant MMP2, -3 and -9 in neoplastic cell cytoplasm. In situ zymography revealed gelatinase activity within the brain metastasis. Gel zymography showed an increase in MMP2 and MMP3 activity in brain metastasis. Furthermore, we were able to significantly decrease the development of breast cancer brain and lung metastasis in animals by treatment with PD 166793, a selective synthetic MMP inhibitor. In addition, PD 166793 decreased the in vitro invasive cell behavior of ENU1546. TIMP2 overexpression also decreased the development of breast cancer lung metastasis in our model. Our results suggest that MMP2, -3 and -9 may be involved in the process of metastasis of breast cancer to the brain and lung. Because astrocytes have been associated with breast cancer brain metastasis we evaluated the role of astrocytes and ERK2 pathway in MMP2 up-regulation in BC brain metastasis. A significant decrease in brain metastases development, and orthotopic tumor size and weight were observed in animals inoculated with ENU1564-TIMP2 cells. These were associated with decreased MMP2 activity, as demonstrated by gel zymography. Rat astrocyte-conditioned media increased expression of MMP2 in ENU15645 cells and increased in vitro cell invasion of ENU1564 and ENU1564-TIMP2 cells. Blockage of ERK1/2 phosphorylation by treatment with PD98059 decreased the expression of MMP2 in cancer cells grown in rat astrocyte-conditioned media. We determine that MMP2 plays a role in in vivo development of breast cancer brain metastases. Additionally, we conclude that astrocytes are associated with expression of MMP2 in cancer cells via ERK1/2 signaling pathway.
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Wenske, Britta [Verfasser], Uwe-Karsten [Akademischer Betreuer] Hanisch, Tobias [Gutachter] Pukrop, and Heidi [Gutachter] Hahn. "Establishing and application of a syngeneic cerebral metastasis mouse model / Britta Wenske. Betreuer: Uwe-Karsten Hanisch. Gutachter: Tobias Pukrop ; Heidi Hahn." Göttingen : Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2015. http://d-nb.info/1102535486/34.

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Harrison, Brown Meredith. "Whole body characterisation of bone marrow-derived cell kinetics: development of a syngeneic bone marrow chimera model for positron emission tomography with 18F-PBR111." Thesis, University of Sydney, 2020. https://hdl.handle.net/2123/23639.

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Monitoring of cell transplantation in vivo is crucial to understanding how the progeny of stem cells contribute to or ameliorate disease. Although animal models enable researchers to understand the behaviour of specific cell types in great detail, they typically require invasive procedures or large numbers of animals in order to track sdisease progression or treatment efficacy over time. Positron emission tomography (PET) has emerged as a promising non-invasive method of tracking transplanted cells in preclinical research, as it enables researchers to track cells longitudinally over the lifespan of the host animal. Although existing reporter gene PET methodologies are under development, they are subject to a number of restrictions which limit their usefulness in preclinical research. These limitations include the need to transduce cells with reporter genes, which is inefficient and may lead to unwanted phenotypic changes in the cells of interest. Another major limitation for many applications is the inability of many reporter ligands to cross an intact blood-brain barrier. Described in this thesis is a novel methodology utilising the transplantation of wild-type bone marrow cells into mice lacking the Translocator Protein (18kDa; TSPO). The TSPO knockout mouse serves as a null-background model for transplantation of unmodified bone marrow cells which express endogenous TSPO. These TSPO-expressing cells are then targeted for PET imaging by a TSPO-specific radio-ligand, 18F-PBR111. PBR111 binds selectively to TSPO and can penetrate the intact blood-brain barrier, making it a promising approach for overcoming some of the limitations of reporter gene imaging. In brief, TSPO-knockout mice (and wild-type controls) were conditioned with a sub-lethal dose of gamma radiation and transplanted with nucleated bone marrow cells from C57BL/6 mice engineered to express green fluorescent protein (GFP). At various stages of engraftment ranging from 1 to 12 months post-transplant, mice were anaesthetised with 1-4% isoflurane, cannulated via the tail vein, and injected with 0.2nM of 18F-PBR111. Data was collected with an Inveon pre-clinical PET/CT camera for 50 minutes post-injection. Images were re-constructed into 20 time frames and were again re-constructed using a 3-dimensional ordered subset expectation maximization algorithm (3D-OSEM). From this, time activity curves (TACs) were extracted from regions of interest drawn on co-registered PET/CT images, corresponding to whole organs. TACs were then used to calculate standardised uptake values for each region of interest. Sections taken from collected tissues were later incubated with 125I-CLINDE in order to visualise receptor density in tissues independently of pharmacokinetic parameters associated with IV tracer injection. Sections were also stained with a monoclonal TSPO antibody in order to identify the TSPO-expressing cells at high spatial resolution. Engraftment rates in blood were assessed at 1, 3 and 6 months post transplantation using quantitative real-time PCR in order to determine whether haematopoietic reconstitution in TSPO knockout mice resembles its wild-type counterparts, which is important for establishing whether the results observed in vivo are physiologically ‘normal’ and therefore applicable to models of disease. Although engraftment rates were equivalent in wild-type and TSPO-/- background recipient mice 1 and 3 months post-transplantation, at 6 months engraftment rates in the TSPO-/- mice were significantly higher. Nonetheless, both genotypes displayed persistent engraftment of donor cells at a minimum of 6 months post-transplant, and observed up to 12 months post-transplant in the TSPO-/- recipients. This engraftment was detectable using both in vitro and in vivo methods (PET) in spleen tissue throughout the duration of the study, and in some tissues susceptible to inflammation such as lung and salivary gland at 6 months post-transplant. A pilot of longitudinal imaging also suggested this persistent migration of donor-derived cells could be detected up to at least half of the animal’s lifespan. Although some major successes in longitudinal monitoring of TSPO-expressing donor-derived cells was observed in this study, there were some notable exceptions, such as the bone marrow itself, susceptible to major spillover associated with free fluorine accumulating within bone, and regions marked by low level engraftment of cells, including brain, and lung parenchyma. For each tissue of interest, an in-depth discussion of the implications of the findings are presented, followed by an outline of the methodological challenges associated with whole-body imaging of rodents in this context. Overall, the model presented in this study has the potential for adaptation to a variety of models incorporating cell-based diseases or treatments, with the ability to track the accumulation of inflammatory cells in a variety of organs.
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Bolin, Celeste, Caleb Sutherland, Ken Tawara, Jim Moselhy, and Cheryl Jorcyk. "Novel mouse mammary cell lines for in vivo bioluminescence imaging (BLI) of bone metastasis." BioMed Central, 2012. http://hdl.handle.net/10150/610032.

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BACKGROUND:Tumor cell lines that can be tracked in vivo during tumorigenesis and metastasis provide vital tools for studying the specific cellular mechanisms that mediate these processes as well as investigating therapeutic targets to inhibit them. The goal of this study was to engineer imageable mouse mammary tumor cell lines with discrete propensities to metastasize to bone in vivo. Two novel luciferase expressing cell lines were developed and characterized for use in the study of breast cancer metastasis to bone in a syngeneic mouse model.RESULTS:The 4 T1.2 luc3 and 66c14 luc2 cell lines were shown to have high levels of bioluminescence intensity in vitro and in vivo after orthotopic injection into mouse mammary fat pads. The 4 T1.2 luc3 cell line was found to closely model the sites of metastases seen in human patients including lung, liver, and bone. Specifically, 4 T1.2 luc3 cells demonstrated a high incidence of metastasis to spine, with an ex-vivo BLI intensity three orders of magnitude above the commercially available 4 T1 luc2 cells. 66c14 luc2 cells also demonstrated metastasis to spine, which was lower than that of 4 T1.2 luc3 cells but higher than 4 T1 luc2 cells, in addition to previously unreported metastases in the liver. High osteolytic activity of the 4 T1.2 luc3 cells in vivo in the bone microenvironment was also detected.CONCLUSIONS:The engineered 4 T1.2 luc3 and 66c14 luc2 cell lines described in this study are valuable tools for studying the cellular events moderating the metastasis of breast tumor cells to bone.
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Uonaga, Taeko. "FGF-21 enhances islet engraftment in mouse syngeneic islet transplantation modeｌ." Kyoto University, 2011. http://hdl.handle.net/2433/135378.

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Books on the topic "Syngeneic model"

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Stelljes, Matthias. Chimärismus syngener und allogener Lymphozyten nach nicht-myeloablativer Chemotherapie im murinen Modell. 1999.

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Book chapters on the topic "Syngeneic model"

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Kaminska, Paulina, Salwador Cyranowski, Paulina Pilanc, and Anna R. Malik. "Syngeneic Mouse Model of Glioblastoma: Intracranial Implantation of GL261 Cells." In Methods in Molecular Biology, 135–46. New York, NY: Springer US, 2023. http://dx.doi.org/10.1007/978-1-0716-3585-8_11.

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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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Rodríguez-Baena, Francisco Javier, Silvia Redondo-García, María del Carmen Plaza-Calonge, Rubén Fernández-Rodríguez, and Juan Carlos Rodríguez-Manzaneque. "Evaluation of Tumor Vasculature Using a Syngeneic Tumor Model in Wild-Type and Genetically Modified Mice." In Methods in Molecular Biology, 179–92. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7595-2_17.

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Eccles, S. A., H. P. Purvies, and D. P. McIntosh. "Prospects for the Use of Immunotoxins Against Solid Tumour Metastases: Studies in a Syngeneic Rat Model System." In Lectins and Glycoconjugates in Oncology, 103–12. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-73662-9_10.

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Corbett, Thomas H., Lisa Polin, Bill J. Roberts, Alfred J. Lawson, Wilbur R. Leopold, Kathryn White, Juiwanna Kushner, et al. "Transplantable Syngeneic Rodent Tumors." In Tumor Models in Cancer Research, 41–71. Totowa, NJ: Humana Press, 2002. https://doi.org/10.1007/978-1-59259-100-8_3.

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Nguyen-Hoai, Tam, Antonio Pezzutto, and Jörg Westermann. "Gene Gun Her2/neu DNA Vaccination: Evaluation of Vaccine Efficacy in a Syngeneic Her2/neu Mouse Tumor Model." In Methods in Molecular Biology, 17–37. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2727-2_2.

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Nguyen-Hoai, Tam, Oliver Hohn, Antonio Pezzutto, and Jörg Westermann. "Gene Gun Her2/neu DNA Vaccination: Evaluation of Vaccine Efficacy in a Syngeneic Her2/neu Mouse Tumor Model." In Methods in Molecular Biology, 129–54. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2441-8_7.

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Bulin, Anne-Laure, Jean-François Adam, and Hélène Elleaume. "Stereotaxic Implantation of F98 Cells in Fischer Rats: A Syngeneic Model to Investigate Photodynamic Therapy Response in Glioma." In Methods in Molecular Biology, 203–10. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2099-1_15.

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Giavazzi, Raffaella, and Alessandra Decio. "Syngeneic Murine Metastasis Models: B16 Melanoma." In Methods in Molecular Biology, 131–40. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-8244-4_10.

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Polin, Lisa, Thomas H. Corbett, Bill J. Roberts, Alfred J. Lawson, Wilbur R. Leopold, Kathryn White, Juiwanna Kushner, et al. "Transplantable Syngeneic Rodent Tumors: Solid Tumors in Mice." In Tumor Models in Cancer Research, 43–78. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-968-0_3.

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Conference papers on the topic "Syngeneic model"

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Piranlioglu, Raziye, Maria Ouzounova, Eunmi Lee, Alicia Hudson, Sumeyye Korkaya, Ali Arbab, and Hasan Korkaya. "Abstract 908: Immune regulation of tumor dormancy in syngeneic 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.am2016-908.

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Zhang, Lan, Binchen Mao, and Qian Shi. "Abstract 1665: MuScreenTM: A well-characterized syngeneic model platform for rapidin vivoscreening." 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.am2017-1665.

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Matsumoto, Takuro, Atsushi Suetsugu, Yuhei Shibata, Nobuhiko Nakamura, Hitomi Aoki, Takahiro Kunisada, Masahito Shimizu, Hisashi Tsurumi, and Robert M. Hoffman. "Abstract 4201: Development of a syngeneic metastatic mouse model of malignant lymphoma." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-4201.

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Tang, Xin, Lily Tong, Annie Xiaoyu An, Likun Zhang, Jie Cai, Qian Shi, Jean Pierre Wery, and Davy Xuesong Ouyang. "Abstract A003: Developing an AML mouse syngeneic model for combinatory chemotherapy and immunotherapy." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics; October 26-30, 2017; Philadelphia, PA. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1535-7163.targ-17-a003.

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Nafia, Imane, Assia Chaibi, Doriane Bortolotto, Christophe Rey, Antoine Italiano, and Alban Bessede. "Abstract 6658: Deciphering anti-PDL1 effect in a syngeneic mouse model of sarcoma." 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.am2020-6658.

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Hum, Nicholas, Aimy Sebastian, Wei He, Monica L. Moya, William F. Hynes, Jonathan J. Adorno, Aubree Hinckley, Elizabeth K. Wheeler, Matthew A. Coleman, and Gabriela G. Loots. "Abstract 37: RNA-seq comparisons ofin vitroandin vivocancer model platforms: Monolayer, spheroids, immunodeficient, and syngeneic mouse model." 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.am2019-37.

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Hum, Nicholas, Aimy Sebastian, Wei He, Monica L. Moya, William F. Hynes, Jonathan J. Adorno, Aubree Hinckley, Elizabeth K. Wheeler, Matthew A. Coleman, and Gabriela G. Loots. "Abstract 37: RNA-seq comparisons ofin vitroandin vivocancer model platforms: Monolayer, spheroids, immunodeficient, and syngeneic mouse model." 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.sabcs18-37.

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Zhivkova, N., J. Schäfer, H. Alizor, I. Ernst, D. Gottfried-Brand, H. Janssen, D. Strand, PR Galle, and S. Strand. "Sirtuin 6 regulates innate immune responses in a syngeneic mouse model of hepatocellular carcinoma." In 35. Jahrestagung der Deutschen Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0038-1677244.

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Urs, Sumithra, Sheri Barnes, Stacey Roys, and Maryland R. Franklin. "Abstract 3718: ID8-Luc syngeneic ovarian cancer model for preclinical evaluation of immunomodulatory molecules." 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.am2019-3718.

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Rolland, Sylvie, Stephan Klinz, Sophie Chaumeron, Florence Meyer-Losic, and Marc Hillairet de Boisferon. "Abstract PO053: Efficacy of cabozantinib after immune checkpoint inhibition in a syngeneic tumor model." In Abstracts: AACR Virtual Special Conference: Tumor Immunology and Immunotherapy; October 19-20, 2020. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/2326-6074.tumimm20-po053.

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