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Journal articles on the topic 'Orthotopic mouse model'

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Author: Grafiati

Published: 10 December 2022

Last updated: 29 January 2023

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1

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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2

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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3

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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4

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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8

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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9

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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10

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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11

Cohen, Jacob T., Ziv Gil, Yoav Binenbaum, Shorook Na’ara, and Moran Amit. "An Orthotopic Mouse Model of Laryngeal Squamous Cell Carcinoma." Annals of Otology, Rhinology & Laryngology 124, no. 2 (September 9, 2014): 143–47. http://dx.doi.org/10.1177/0003489414549575.

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12

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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13

Okazaki, M., A. S. Krupnick, C. G. Kornfeld, J. M. Lai, J. H. Ritter, S. B. Richardson, H. J. Huang, et al. "A Mouse Model of Orthotopic Vascularized Aerated Lung Transplantation." American Journal of Transplantation 7, no. 6 (June 2007): 1672–79. http://dx.doi.org/10.1111/j.1600-6143.2007.01819.x.

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14

Alencar, Herlen, Ray King, Martin Funovics, Charles Stout, Ralph Weissleder, and Umar Mahmood. "A novel mouse model for segmental orthotopic colon cancer." International Journal of Cancer 117, no. 3 (2005): 335–39. http://dx.doi.org/10.1002/ijc.21185.

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15

Myers, Molly S., Elizabeth A. Kosmacek, Arpita Chatterjee, and Rebecca E. Oberley-Deegan. "CT vs. bioluminescence: A comparison of imaging techniques for orthotopic prostate tumors in mice." PLOS ONE 17, no. 11 (November 4, 2022): e0277239. http://dx.doi.org/10.1371/journal.pone.0277239.

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Prostate cancer is one of the most diagnosed cancers in men in the United States. In mouse models, orthotopic tumors are favored for their biological relevance and simulation of growth in a microenvironment akin to that found in humans. However, to monitor the disease course, animal models require consistent and noninvasive surveillance. In vivo bioluminescent imaging has become a mainstay imaging modality due to its flexibility and ease of use. However, with some orthotopic prostate tumor models, bioluminescence fails to describe disease progression due to optical scattering and signal attenuation. CT scanning, in addition to its utility in human cancer diagnosis and surveillance, can be applied to mouse models with improved results. However, CT imaging has poor definition when imaging soft tissues and is not routinely used in prostate cancer models. Using an orthotopic prostate cancer model, our results demonstrate that, when compared to bioluminescent imaging, CT imaging correlates more closely to orthotopic prostate tumor growth in mice. Based on the data from this study, we conclude that CT imaging can be used as an alternative to the more commonly used bioluminescent imaging for measuring orthotopic prostate cancer growth over time.

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Dharmadhikari, Sayali, Cameron A. Best, Nakesha King, Michaela Henderson, Jed Johnson, Christopher K. Breuer, and Tendy Chiang. "Mouse Model of Tracheal Replacement With Electrospun Nanofiber Scaffolds." Annals of Otology, Rhinology & Laryngology 128, no. 5 (January 30, 2019): 391–400. http://dx.doi.org/10.1177/0003489419826134.

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Objectives: The clinical experience with tissue-engineered tracheal grafts (TETGs) has been fraught with graft stenosis and delayed epithelialization. A mouse model of orthotopic replacement that recapitulates the clinical findings would facilitate the study of the cellular and molecular mechanisms underlying graft stenosis. Methods: Electrospun nanofiber tracheal scaffolds were created using nonresorbable (polyethylene terephthalate + polyurethane) and co-electrospun resorbable (polylactide-co-caprolactone/polyglycolic acid) polymers (n = 10/group). Biomechanical testing was performed to compare load displacement of nanofiber scaffolds to native mouse tracheas. Mice underwent orthotopic tracheal replacement with syngeneic grafts (n = 5) and nonresorbable (n = 10) and resorbable (n = 10) scaffolds. Tissue at the anastomosis was evaluated using hematoxylin and eosin (H&E), K5+ basal cells were evaluated with the help of immunofluorescence testing, and cellular infiltration of the scaffold was quantified. Micro computed tomography was performed to assess graft patency and correlate radiographic and histologic findings with respiratory symptoms. Results: Synthetic scaffolds were supraphysiologic in compression tests compared to native mouse trachea ( P < .0001). Nonresorbable scaffolds were stiffer than resorbable scaffolds ( P = .0004). Eighty percent of syngeneic recipients survived to the study endpoint of 60 days postoperatively. Mean survival with nonresorbable scaffolds was 11.40 ± 7.31 days and 6.70 ± 3.95 days with resorbable scaffolds ( P = .095). Stenosis manifested with tissue overgrowth in nonresorbable scaffolds and malacia in resorbable scaffolds. Quantification of scaffold cellular infiltration correlated with length of survival in resorbable scaffolds (R2 = 0.95, P = .0051). Micro computed tomography demonstrated the development of graft stenosis at the distal anastomosis on day 5 and progressed until euthanasia was performed on day 11. Conclusion: Graft stenosis seen in orthotopic tracheal replacement with synthetic tracheal scaffolds can be modeled in mice. The wide array of lineage tracing and transgenic mouse models available will permit future investigation of the cellular and molecular mechanisms underlying TETG stenosis.

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Siolas, Despina, Orlando Aristizabal, Kate Byrne, Lawrence P. Leichman, Robert H. Vonderheide, and Dafna Bar-Sagi. "Preclinical immunotherapy studies using an orthotopic pancreatic cancer mouse model." Journal of Clinical Oncology 33, no. 3_suppl (January 20, 2015): 324. http://dx.doi.org/10.1200/jco.2015.33.3_suppl.324.

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324 Background: Pancreatic cancer is well known for its aggressive clinical course and resistance to chemotherapy. The advent of new mouse models of pancreatic cancer have accelerated our understanding of tumorigenesis and enabled preclinical testing of experimental therapeutics with a desire to translate these findings into meaningful clinical treatments. Methods: We have developed a model where pancreatic cells obtained from a KrasG12D;Trp53R172H genetically engineered mouse can be cultivated in two dimensional cell culture and implanted into the pancreas of a immunocompetent syngeneic mouse allowing for tumor formation in situ. In addition, we are using this model to study the effectiveness of new drug combination therapy such as gemcitabine, albumin-bound paclitaxel and CD40 agonist immunotherapy using overall survival as a primary endpoint. Results: These cells generate tumors of five millimeter diameter within two weeks of implantation with 100% efficiency. Because cancer cells are seeded in the context of normal surrounding pancreatic tissue, this model is not hampered by the genetic field effect of expressing cancer mutations in the entire pancreatic organ, allowing for the study of the tumor microenviroment. Responses to therapeutic interventions can be non-invasively monitored through small animal high resolution ultrasound. Conclusions: Our orthotopic pancreatic cancer mouse system is an effective model for pre-clinical studies of tumorigenesis, immunotherapy and examination of the tumor microenvironment. Future experiments will focus on exploiting this system for identifying potent immunotherapy and chemotherapy combinations and for detecting biomarkers of efficiency.

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18

Zhang, Guan-Meng, Di Jiao, Shao-Chen Nie, Zhao-Yuan Xu, Xiaoyan Zhang, Yanmei Dai, Mai-Ning Jiao, Hanlin Ou, Ying-Bin Yan, and Dan Ding. "Near-infrared aggregation-induced emission nanodots for early diagnosis of tongue squamous cell carcinoma and sentinel lymph node mapping." Biomaterials Science 10, no. 8 (2022): 1929–35. http://dx.doi.org/10.1039/d1bm01976g.

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By developing DPA-TPE-DCM with intense near-infrared fluorescence emission in the aggregation state, AIE materials were used for the first time in the early diagnosis of orthotopic TSCC and SLN mapping in an orthotopic TSCC-bearing mouse model.

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Zhang, Ying, Li Luo, Xueling Zheng, and Tinghe Yu. "An Advanced Orthotopic Ovarian Cancer Model in Mice for Therapeutic Trials." BioMed Research International 2016 (2016): 1–4. http://dx.doi.org/10.1155/2016/2585787.

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A nude mouse received subcutaneous injection of human ovarian cancer cells HO-8910PM to form a tumor, and then the tumor fragment was surgically transplanted to the ovary of a recipient mouse to establish an orthotopic cancer model. Tumors occurred in 100% of animals. A mouse displayed an ovarian mass, ascites, intraperitoneal spread, and lung metastasis at natural death. The mean survival time was34.1±17.2days, with median survival time of 28.5 days. The findings indicated that the present mouse model can reflect the biological behavior of advanced human ovarian cancers. This in vivo model can be used to explore therapeutic means against chemoresistance and metastasis, and an effective treatment would prolong the survival time.

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Reeb, Ashley N., Andrea Ziegler, and Reigh-Yi Lin. "Characterization of human follicular thyroid cancer cell lines in preclinical mouse models." Endocrine Connections 5, no. 2 (March 2016): 47–54. http://dx.doi.org/10.1530/ec-15-0114.

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Follicular thyroid cancer (FTC) is the second most common type of thyroid cancers. In order to develop more effective personalized therapies, it is necessary to thoroughly evaluate patient-derived cell lines in in vivo preclinical models before using them to test new, targeted therapies. This study evaluates the tumorigenic and metastatic potential of a panel of three human FTC cell lines (WRO, FTC-238, and TT1609-CO2) with defined genetic mutations in two in vivo murine models: an orthotopic thyroid cancer model to study tumor progression and a tail vein injection model to study metastasis. All cell lines developed tumors in the orthotopic model, with take rates of 100%. Notably, WRO-derived tumors grew two to four times faster than tumors arising from the FTC-238 and TT2609-CO2 cell lines. These results mirrored those of a tail vein injection model for lung metastasis: one hundred percent of mice injected with WRO cells in the tail vein exhibited aggressive growth of bilateral lung metastases within 35 days. In contrast, tail vein injection of FTC-238 or TT2609-CO2 cells did not result in lung metastasis. Together, our work demonstrates that these human FTC cell lines display highly varied tumorigenic and metastatic potential in vivo with WRO being the most aggressive cell line in both orthotopic and lung metastasis models. This information will be valuable when selecting cell lines for preclinical drug testing.

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Latteyer, S., S. Christoph, S. Theurer, G. S. Hönes, K. W. Schmid, D. Führer, and L. C. Moeller. "Thyroxine promotes lung cancer growth in an orthotopic mouse model." Endocrine-Related Cancer 26, no. 6 (June 2019): 565–74. http://dx.doi.org/10.1530/erc-18-0353.

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Thyroid hormones are important for physiology and homeostasis. In addition to nuclear thyroid hormone receptors, the plasma membrane protein integrin αvβ3 has been recognized as a receptor for both thyroxine (T4) and triiodothyronine (T3). Here, we studied whether thyroid hormone promotes growth of murine lung cancer via αvβ3 in vivo. Murine Lewis lung carcinoma cells (3LL), stably transfected with luciferase, were injected into mouse lungs. Tumor growth in untreated mice was compared to hypothyroid mice and hypothyroid mice treated with T3 or T4 with or without the αvβ3 inhibitor 3,5,3′,5′-tetraiodothyroacetic acid (Tetrac). Tumor progression was determined by serial in vivo imaging of bioluminescence emitted from the tumor. Tumor weight was recorded at the end of the experiment. Neoangiogenesis was determined by immunohistochemistry for CD31. Tumor growth was reduced in hypothyroidism and increased by T4 treatment. Strikingly, only T4 but not T3 treatment promoted tumor growth. This T4 effect was abrogated by the αvβ3 inhibitor Tetrac. Tumor weight and neoangiogenesis were also significantly increased only in T4-treated mice. The T4 effect on tumor weight and neoangiogenesis was abolished by Tetrac. In vitro, T4 did not stimulate 3LL cell proliferation or signaling pathway activation. We conclude that T4 promotes lung cancer growth in this orthotopic mouse model. The tumor-promoting effect is mediated via the plasma membrane integrin αvβ3 and increased neoangiogenesis rather than direct stimulation of 3LL cells. These data suggest that such effects of levothyroxine may need to be considered in cancer patients on T4 substitution.

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Nucera, Carmelo, Matthew A. Nehs, Michal Mekel, Xuefeng Zhang, Richard Hodin, Jack Lawler, Vânia Nose, and Sareh Parangi. "A Novel Orthotopic Mouse Model of Human Anaplastic Thyroid Carcinoma." Thyroid 19, no. 10 (October 2009): 1077–84. http://dx.doi.org/10.1089/thy.2009.0055.

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23

Chan, Eddie S. Y., Amit R. Patel, Armine K. Smith, John B. Klein, Anil A. Thomas, Warren D. Heston, and William A. Larchian. "Optimizing Orthotopic Bladder Tumor Implantation in a Syngeneic Mouse Model." Journal of Urology 182, no. 6 (December 2009): 2926–31. http://dx.doi.org/10.1016/j.juro.2009.08.020.

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24

Li, Bo, Artour Torossian, Wenyan Li, Stephen Schleicher, Kathy Niu, Nicholas J. Giacalone, Sung June Kim, et al. "A Novel Bioluminescence Orthotopic Mouse Model for Advanced Lung Cancer." Radiation Research 176, no. 4 (October 2011): 486–93. http://dx.doi.org/10.1667/rr2565.1.

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Vandewynckel, Yves-Paul, Riet De Rycke, Eliene Bogaerts, and Hans Van Vlierberghe. "Intestinal metaplasia in an orthotopic mouse model for hepatocellular carcinoma." Digestive and Liver Disease 46, no. 12 (December 2014): e17. http://dx.doi.org/10.1016/j.dld.2014.07.003.

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Hwang, K., K. M. Nam, J. E. Kwon, S. Y. Ji, J. H. Han, T. W. Seo, Y. N. Choi, et al. "P06.02.B Advanced CAR-T cell against orthotopic glioblastoma mouse model." Neuro-Oncology 24, Supplement_2 (September 1, 2022): ii37—ii38. http://dx.doi.org/10.1093/neuonc/noac174.126.

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Abstract Background The adoptive and engineered chimeric antigen receptor (CAR) T cells have demonstrated remarkable success in treating hematologic cancers; however, this success has yet to be extrapolated to solid tumors such as glioblastoma multiforme (GBM). The purpose of this study was to evaluate the survival efficacy using advanced CAR-T cells in orthotopic GBM mouse model. Material and Methods Advanced CAR-T cell, which reprograms the patient’s T-cells with a transgene encoding part of interleukin-7 receptor-α (ΔIL7Rα) domain in addition to the CD3ζ signaling domain and 4-1BB costimulatory domain in the advanced CAR gene to exhibit excellent in vivo persistence and anti-tumor effect of advanced CAR-T cells. In addition to the advanced CAR gene, TGF-beta converter is introduced, which converts the inhibitory signal of TGF-beta, an immunosuppressive cytokine overexpressed in the hostile tumor microenvironment, into the activation signal of the cytokine IL-18 in advanced CAR-T cells.DAY9 NSG mice bearing orthotopically xenografted GBM cell lines (1 × 105 U251MG expressing IL13Rα2) were randomized to 8 experimental groups. Each experimental group was intravenously injected with only once with different subtype advanced CAR-T cells (Td ~ 47.3% of 5 × 106) and monitored for survival. Results Among treatment groups, mice treated with advanced CAR-T cells of TGF-β converter subtype demonstrated a statistically significant increase in survival (p=0.042, 95%CI, 0.375-0.981) compared with other subtypes. In DAY9 orthotopic GBM mouse model, we showed that a single I.V. injection of advanced CAR-T cells targeting IL13Rα2-specific tumor achieved survival benefit. Conclusion This study is the first report to show statistically significant survival benefit in DAY9 orthotopic GBM mouse model using a single I.V. injection of advanced CAR-T cells, yet merits further clinical trials in real world of clinical setting.

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Ni, Jie, Andre Bongers, Uphar Chamoli, Joseph Bucci, Peter Graham, and Yong Li. "In Vivo 3D MRI Measurement of Tumour Volume in an Orthotopic Mouse Model of Prostate Cancer." Cancer Control 26, no. 1 (January 1, 2019): 107327481984659. http://dx.doi.org/10.1177/1073274819846590.

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Prostate cancer (CaP) is the most commonly diagnosed cancer in males in western countries. Orthotopic implantation is considered as an ideal xenograft model for CaP study, and noninvasive measurement of tumor volume changes is important for monitoring responses to anticancer therapies. In this study, the T2-weighted fast spin echo sequence magnetic resonance imaging (MRI) was performed on a CaP orthotopic non-obese diabetic/severe combined immunodeficiency (NOD/SCID) mouse model weekly for 6 weeks post PC-3 CaP cell inoculation, and the fat signal was suppressed using a chemical shift-selective pulse. Subsequently, the MRI data were imported into the image processing software Avizo Standard and stacked into three-dimensional (3D) volumes. Our results demonstrate that MRI, combined with 3D reconstruction, is a feasible and sensitive method to assess tumor growth in a PC-3 orthotopic CaP mouse model and this established monitoring approach is promising for longitudinal observation of CaP xenograft development after anticancer therapy in vivo. Further investigation is needed to validate this protocol in a larger cohort of mice to generate enough statistical power.

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Tan, Xiaotian, Luke J. Broses, Menglian Zhou, Kathleen C. Day, Wenyi Liu, Ziqi Li, Alon Z. Weizer, et al. "Multiparameter urine analysis for quantitative bladder cancer surveillance of orthotopic xenografted mice." Lab on a Chip 20, no. 3 (2020): 634–46. http://dx.doi.org/10.1039/c9lc01006h.

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Chen, Hengkai, Zhenli Li, Liman Qiu, Xiuqing Dong, Geng Chen, Yingjun Shi, Linsheng Cai, et al. "Personalized neoantigen vaccine combined with PD-1 blockade increases CD8⁺ tissue-resident memory T-cell infiltration in preclinical hepatocellular carcinoma models." Journal for ImmunoTherapy of Cancer 10, no. 9 (September 2022): e004389. http://dx.doi.org/10.1136/jitc-2021-004389.

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BackgroundPersonalized neoantigen vaccine could induce a robust antitumor immune response in multiple cancers, whose efficacy could be further enhanced by combining with programmed cell death 1 blockade (α-PD-1). However, the corresponding immune response and synergistic mechanisms remain largely unclear. Here, we aimed to develop clinically available combinational therapeutic strategy and further explore its potential antitumor mechanisms in hepatocellular carcinoma (HCC).MethodsNeoantigen peptide vaccine (NeoVAC) for murine HCC cell line Hepa1-6 was developed and optimized by neoantigen screening and adjuvant optimization. Then the synergistic efficacy and related molecular mechanisms of NeoVAC combined with α-PD-1 in HCC were evaluated by orthotopic HCC mouse model, single-cell RNA sequencing, tetramer flow cytometry, immunofluorescence, etc. The tumor-killing capacity of CD8+ tissue-resident memory T cells (CD8+ TRMs) was assessed by orthotopic HCC mouse model, and autologous patient-derived cells.ResultsNeoVAC, which consisted of seven high immunogenic neoantigen peptides and clinical-grade Poly(I:C), could generate a strong antitumor immune response in HCC mouse models. Significantly, its efficacy could be further improved by combining with α-PD-1, with 80% of durable tumor regression and long-term immune memory in orthotopic HCC models. Moreover, in-depth analysis of the tumor immune microenvironment showed that the percentage of CD8+ TRMs was remarkedly increased in NeoVAC plus α-PD-1 treatment group, and positively associated with the antitumor efficacy. In vitro and in vivo T-cell cytotoxicity assay further confirmed the strong tumor-killing capacity of CD8+ TRMs sorting from orthotopic mouse HCC or patient’s HCC tissue.ConclusionsThis study showed that NeoVAC plus α-PD-1 could induce a strong antitumor response and long-term tumor-specific immune memory in HCC by increasing CD8+ TRMs infiltration, which might serve as a potential immune-therapeutic target for HCC.

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Linxweiler, Johannes, Turkan Hajili, Philip Zeuschner, Michael D. Menger, Michael Stöckle, Kerstin Junker, and Matthias Saar. "Primary Tumor Resection Decelerates Disease Progression in an Orthotopic Mouse Model of Metastatic Prostate Cancer." Cancers 14, no. 3 (January 31, 2022): 737. http://dx.doi.org/10.3390/cancers14030737.

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Radical prostatectomy in oligometastatic prostate cancer is a matter of intense debate. Besides avoiding local complications, it is hypothesized that primary tumor resection may result in better oncological outcomes. The aim of our study was to analyze the effect of primary tumor resection on disease progression in an orthotopic prostate cancer mouse model. First, the optimal time point for primary tumor resection, when metastases have already occurred, but the primary tumor is still resectable, was determined as 8 weeks after inoculation of 5 × 105 LuCaP136 cells. In a second in vivo experiment, 64 mice with metastatic prostate cancer were randomized into two groups, primary tumor resection or sham operation, and disease progression was followed up for 10 weeks. The technique of orthotopic primary tumor resection was successfully established. Compared with the sham operation group, mice with primary tumor resection showed a significantly longer survival (p < 0.001), a significantly slower PSA increase (p < 0.01), and a lower number of lung metastases (p = 0.073). In conclusion, primary tumor resection resulted in slower disease progression and longer survival in an orthotopic mouse model of metastatic prostate cancer. In future studies, this model will be used to unravel the molecular mechanisms of primary tumor/metastasis interaction in prostate cancer.

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Zhang, Liwen, and Pengcheng Bu. "Generation of an orthotopic mouse model to study colorectal cancer metastasis." STAR Protocols 2, no. 4 (December 2021): 100792. http://dx.doi.org/10.1016/j.xpro.2021.100792.

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Kovar, Joy L., Mark A. Johnson, William M. Volcheck, Jiyan Chen, and Melanie A. Simpson. "Hyaluronidase Expression Induces Prostate Tumor Metastasis in an Orthotopic Mouse Model." American Journal of Pathology 169, no. 4 (October 2006): 1415–26. http://dx.doi.org/10.2353/ajpath.2006.060324.

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KANG, YUN, MOTOKO OMURA, AKIKO SUZUKI, CHUMPOL THEERALADANON, TAKASHI OKA, YOSHIHIRO NAKAGAMI, ATSUSHI SUZUKI, YOJI NAGASHIMA, and TOMIO INOUE. "Proliferation of human lung cancer in an orthotopic transplantation mouse model." Experimental and Therapeutic Medicine 1, no. 3 (2010): 471–75. http://dx.doi.org/10.3892/etm_00000073.

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Nicolas, Adele M., Marina Pesic, Franz Rödel, Emmanouil Fokas, and Florian R. Greten. "Image-guided radiotherapy in an orthotopic mouse model of rectal cancer." STAR Protocols 3, no. 4 (December 2022): 101749. http://dx.doi.org/10.1016/j.xpro.2022.101749.

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CHAFFER, C. L., J. SLAVIN, C. TEMELCOS, J. GOAD, and E. D. WILLIAMS. "Patterns of spread in an orthotopic mouse model of bladder cancer." BJU International 97 (March 2006): 9. http://dx.doi.org/10.1111/j.1464-410x.2006.06085_31.x.

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Reiberger, Thomas, Yunching Chen, Rakesh R. Ramjiawan, Tai Hato, Christopher Fan, Rekha Samuel, Sylvie Roberge, et al. "An orthotopic mouse model of hepatocellular carcinoma with underlying liver cirrhosis." Nature Protocols 10, no. 8 (July 23, 2015): 1264–74. http://dx.doi.org/10.1038/nprot.2015.080.

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Zhu, Ping. "Effects of gamboge in an orthotopic mouse model of colon cancer." World Chinese Journal of Digestology 22, no. 4 (2014): 476. http://dx.doi.org/10.11569/wcjd.v22.i4.476.

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Zhang, Xuepeng, Xuguang Zheng, Feng Jiang, Zheng Gang Zhang, Mark Katakowski, and Michael Chopp. "Dual-color fluorescence imaging in a nude mouse orthotopic glioma model." Journal of Neuroscience Methods 181, no. 2 (July 2009): 178–85. http://dx.doi.org/10.1016/j.jneumeth.2009.05.004.

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Märten, Angela, Nina Zeiss, Susanne Serba, Stefan Mehrle, Marie von Lilienfeld-Toal, and Jan Schmidt. "Bortezomib is ineffective in an orthotopic mouse model of pancreatic adenocarcinoma." Molecular Cancer Therapeutics 7, no. 11 (November 2008): 3624–31. http://dx.doi.org/10.1158/1535-7163.mct-08-0393.

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Wang, Xiaoen, Zili An, Jack Geller, and Robert M. Hoffman. "High-malignancy orthotopic nude mouse model of human prostate cancer LNCaP." Prostate 39, no. 3 (May 15, 1999): 182–86. http://dx.doi.org/10.1002/(sici)1097-0045(19990515)39:3<182::aid-pros6>3.0.co;2-b.

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Rodriguez, Carlos J., Nicholas Griffin Battaglia, Scott A. Gerber, and Edith M. Lord. "Development of an Orthotopic Colorectal Cancer Mouse Model for Radiation Therapy Studies." Journal of Immunology 200, no. 1_Supplement (May 1, 2018): 178.29. http://dx.doi.org/10.4049/jimmunol.200.supp.178.29.

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Abstract Radiation is commonly used before surgery to reduce tumor burden in rectal cancer. It has been suggested that radiation therapy induces an immune response against the tumor. Previous work using mice ectopic models has shown a correlation between tumor regression and the production of IFN-g and the induction of cytotoxic T cells after radiotherapy. Ectopic models, such as the use of colon cell lines in leg muscle, provide us with some information about the response to radiation, but this response may differ if the tumor is grown orthotopically in the tissue from which it originates. To assess this difference in response, we have developed an orthotopic model to study the growth of colorectal cancer in mice and the response to radiation treatment. In our model, MC38 adenocarcinoma murine cells expressing luciferase are implanted in the rectal wall of C57BL/6 mice through the serous membrane. Tumor growth, assessed using IVIS, revealed tumor masses that steadily increase in size reaching approximately 1 gram 21 days post-injection of 50,000 cells. Importantly, tumor growth in most mice was limited to the site of injection, as mesenteric and omental sites were free of tumor burden. The cellular composition and the morphology of these tumors is being examined using flow cytometry and immunohistochemistry, respectively. Furthermore, studies are underway to determine the response of these tumors to fractionated radiation and to determine if there are differences from the ectopic models of colon cancer. This more clinically relevant model will improve our understanding of response to radiotherapy in colorectal cancer and help develop more effective treatments for this disease.

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Karlsson, Johan, Yuan Rui, Kristen L. Kozielski, Amanda L. Placone, Olivia Choi, Stephany Y. Tzeng, Jayoung Kim, et al. "Engineered nanoparticles for systemic siRNA delivery to malignant brain tumours." Nanoscale 11, no. 42 (2019): 20045–57. http://dx.doi.org/10.1039/c9nr04795f.

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Bioreducible nanoparticles were engineered for safe and effective systemic siRNA delivery, including crossing the blood–brain barrier to achieve in vivo gene silencing in an orthotopic glioblastoma mouse model.

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Chen, Chen, Jens Neumann, Florian Kühn, Serene M. L. Lee, Moritz Drefs, Joachim Andrassy, Jens Werner, Alexandr V. Bazhin, and Tobias S. Schiergens. "Establishment of an Endoscopy-Guided Minimally Invasive Orthotopic Mouse Model of Colorectal Cancer." Cancers 12, no. 10 (October 16, 2020): 3007. http://dx.doi.org/10.3390/cancers12103007.

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Open orthotopic mouse models of colorectal cancer have disadvantages such as the requirement for advanced surgical skills or the trauma caused by laparotomy. To overcome these drawbacks, this study aimed to evaluate the establishment of a minimally invasive model using murine colonoscopy. CT26 and MC38 CRC cells of different concentrations were injected into BALB/C and C57BL/6J mice, respectively. Follow-up endoscopies were performed to assign an endoscopic score to tumor growth. Gross autopsy, histologic and immuno-histochemical evaluation, and immune scoring were performed. To describe the learning curve of the procedures, a performance score was given. Local tumor growth with colorectal wall infiltration, luminal ulceration, the presence of tumor-infiltrating lymphocytes, lympho-vascular invasion, and early spontaneous lymph node, peritoneal, and hepatic metastases were observed. The tumors showed cytoplasmic immuno-staining for CK20. Compared to the MC38/C57BL/6J model, tumorigenicity and immunogenicity of the CT26/BALB/C model were higher. Tumor volume correlated with the endoscopic score. This endoscopy-guided orthotopic mouse model is easy to learn and quick to establish. It features early metastasis and enables the study of interactions with the immune system. When specific cell concentrations and cell lines are applied, controlled local tumor growth and metastasis can be achieved within short observation periods.

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Song, Yurong, Shaneen S. Baxter, Lisheng Dai, Chelsea Sanders, Sandra Burkett, Ryan N. Baugher, Stephanie D. Mellott, et al. "Mesothelioma Mouse Models with Mixed Genomic States of Chromosome and Microsatellite Instability." Cancers 14, no. 13 (June 24, 2022): 3108. http://dx.doi.org/10.3390/cancers14133108.

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Malignant mesothelioma (MMe) is a rare malignancy originating from the linings of the pleural, peritoneal and pericardial cavities. The best-defined risk factor is exposure to carcinogenic mineral fibers (e.g., asbestos). Genomic studies have revealed that the most frequent genetic lesions in human MMe are mutations in tumor suppressor genes. Several genetically engineered mouse models have been generated by introducing the same genetic lesions found in human MMe. However, most of these models require specialized breeding facilities and long-term exposure of mice to asbestos for MMe development. Thus, an alternative model with high tumor penetrance without asbestos is urgently needed. We characterized an orthotopic model using MMe cells derived from Cdkn2a+/−;Nf2+/− mice chronically injected with asbestos. These MMe cells were tumorigenic upon intraperitoneal injection. Moreover, MMe cells showed mixed chromosome and microsatellite instability, supporting the notion that genomic instability is relevant in MMe pathogenesis. In addition, microsatellite markers were detectable in the plasma of tumor-bearing mice, indicating a potential use for early cancer detection and monitoring the effects of interventions. This orthotopic model with rapid development of MMe without asbestos exposure represents genomic instability and specific molecular targets for therapeutic or preventive interventions to enable preclinical proof of concept for the intervention in an immunocompetent setting.

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Borzov, A. A., A. A. Оvsepyan, E. I. Katorkina, E. O. Anisimova, and M. V. Lykov. "Development of a Mouse Glioblastoma Orthotopic Model Using the GLi-261 Cell Line." BIOpreparations. Prevention, Diagnosis, Treatment 19, no. 4 (December 11, 2019): 242–50. http://dx.doi.org/10.30895/2221-996x-2019-19-4-242-250.

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Glioblastoma is the most common and most aggressive type of brain tumor, with an almost 100 % mortality rate over 5 years. The search for new effective approaches to the treatment of this disease requires the development of adequate experimental models.Objective: to develop and put into practice an orthotopic model of mouse glioblastoma.Materials and methods: GLi-261 mouse glioma cells were orthotopically inoculated into the putamen of C57Bl/6 mice brain. Tumor dynamics was investigated by Preclinical MRI System 7.0T/17cm (Flexiscan) highfield magnetic resonance imager (MR Solutions, UK). Temcital® (temozolomide) was used as a positive control in the treatment of experimental glioblastoma. The neurological status of animals in the course of tumour development was assessed by specific tests.Results: a GLi-261 cell-based mouse glioblastoma orthotopic model was developed using stereotactic equipment for accurate inoculation of tumour cells, magnetic resonance imaging for non-invasive determination of tumour volume and dynamics, and special tests for determination of the neurological status of the biological test systems. This model was used to demonstrate the effectiveness of temozolomide (the «gold standard» for glioblastoma treatment).Conclusions: this model has been introduced into practice at the IBC Generium, LLC, and can be used as an in vivo test system for preclinical evaluation of efficacy of new antitumour drugs being developed, as well as brain cancer treatment regimens using combination therapy.

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46

Vincent-Chong, Vui King, and Mukund Seshadri. "Development and Radiation Response Assessment in A Novel Syngeneic Mouse Model of Tongue Cancer: 2D Culture, 3D Organoids and Orthotopic Allografts." Cancers 12, no. 3 (March 2, 2020): 579. http://dx.doi.org/10.3390/cancers12030579.

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Oral squamous cell carcinoma (OSCC) are aggressive cancers that contribute to significant morbidity and mortality in humans. Although numerous human xenograft models of OSCC have been developed, only a few syngeneic models of OSCC exist. Here, we report on a novel murine model of OSCC, RP-MOC1, derived from a tongue tumor in a C57Bl/6 mouse exposed to the carcinogen 4-nitroquinoline-1-oxide. Phenotypic characterization and credentialing (STR profiling, exome sequencing) of RP-MOC1 cells was performed in vitro. Radiosensitivity was evaluated in 2D culture, 3D organoids, and in vivo using orthotopic allografts. RP-MOC1 cells exhibited a stable epithelial phenotype with proliferative, migratory and invasive properties. Exome sequencing identified several mutations commonly found in OSCC patients. The LD50 for RP-MOC1 cells in 2D culture and 3D organoids was found to be 2.4 Gy and 12.6 Gy, respectively. Orthotopic RP-MOC1 tumors were pan-cytokeratin+ and Ki-67+. Magnetic resonance imaging of orthotopic RP-MOC1 tumors established in immunocompetent mice revealed marked growth inhibition following 10 Gy and 15 Gy fractionated radiation regimens. This radiation response was completely abolished in tumors established in immunodeficient mice. This novel syngeneic model of OSCC can serve as a valuable platform for the evaluation of combination strategies to enhance radiation response against this deadly disease.

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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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Song, Xiaodong, Zili Shao, Menglin Han, and Huihong Liang. "A novel mouse model of orthotopic extrahepatic cholangiocarcinoma confirmed with molecular imaging." Translational Cancer Research 8, no. 2 (April 2019): 583–91. http://dx.doi.org/10.21037/tcr.2019.03.19.

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Nakano, Tomoyuki, Kenji Fujimoto, Arata Tomiyama, Masamichi Takahashi, Takamune Achiha, Hideyuki Arita, Daisuke Kawauchi, et al. "Eribulin prolongs survival in an orthotopic xenograft mouse model of malignant meningioma." Cancer Science 113, no. 2 (December 8, 2021): 697–708. http://dx.doi.org/10.1111/cas.15221.

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Li, Ting, Zheng Hu, Lei Wang, and Guo-Yue Lv. "Details determining the success in establishing a mouse orthotopic liver transplantation model." World Journal of Gastroenterology 26, no. 27 (July 21, 2020): 3889–98. http://dx.doi.org/10.3748/wjg.v26.i27.3889.

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