Journal articles: 'Mouse xenograft models'

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

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

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Sari, Gulce, Gertine W. van Oord, Martijn D. B. van de Garde, Jolanda J. C. Voermans, Andre Boonstra, and Thomas Vanwolleghem. "Sexual Dimorphism in Hepatocyte Xenograft Models." Cell Transplantation 30 (January 1, 2021): 096368972110061. http://dx.doi.org/10.1177/09636897211006132.

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Humanized liver mouse models are crucial tools in liver research, specifically in the fields of liver cell biology, viral hepatitis and drug metabolism. The livers of these humanized mouse models are repopulated by 3-dimensional islands of fully functional primary human hepatocytes (PHH), which are notoriously difficult to maintain in vitro. As low efficiency and high cost hamper widespread use, optimization is of great importance. In the present study, we analyzed experimental factors associated with Hepatitis E virus (HEV) infection and PHH engraftment in 2 xenograft systems on a Nod-SCID-IL2Ry-/- background: the alb-urokinase plasminogen activator mouse model (uPA-NOG, n=399); and the alb-HSV thymidine kinase model (TK-NOG, n = 198). In a first analysis, HEV fecal shedding in liver humanized uPA-NOG and TK-NOG mice with comparable human albumin levels was found to be similar irrespective of the mouse genetic background. In a second analysis, sex, mouse age at transplantation and hepatocyte donor were the most determinant factors for xenograft success in both models. The sexual imbalance for xenograft success was related to higher baseline ALT levels and lower thresholds for ganciclovir induced liver morbidity and mortality in males. These data call for sexual standardization of human hepatocyte xenograft models, but also provide a platform for further studies on mechanisms behind sexual dimorphism in liver diseases.

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Richmond, A., and Y. Su. "Mouse xenograft models vs GEM models for human cancer therapeutics." Disease Models and Mechanisms 1, no. 2-3 (2008): 78–82. http://dx.doi.org/10.1242/dmm.000976.

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

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Abstract The model systems available for studying human hematopoiesis, malignant hematopoiesis, and hematopoietic stem cell (HSC) function in vivo have improved dramatically over the last decade, primarily due to improvements in xenograft mouse strains. Several recent reviews have focused on the historic development of immunodeficient mice over the last 2 decades, as well as their use in understanding human HSC and leukemia stem cell (LSC) biology and function in the context of a humanized mouse. However, in the intervening time since these reviews, a number of new mouse models, technical approaches, and scientific advances have been made. In this review, we update the reader on the newest and best models and approaches available for studying human malignant and normal HSCs in immunodeficient mice, including newly developed mice for use in chemotherapy testing and improved techniques for humanizing mice without laborious purification of HSC. We also review some relevant scientific findings from xenograft studies and highlight the continued limitations that confront researchers working with human HSC and LSC in vivo.

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Guihard, Soizic, Pauline Peyrouze, and Meyling H. Cheok. "Pharmacogenomic considerations of xenograft mouse models of acute leukemia." Pharmacogenomics 13, no. 15 (2012): 1759–72. http://dx.doi.org/10.2217/pgs.12.158.

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

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

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

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Meningiomas are the most frequent primitive central nervous system tumors found in adults. Mouse models of cancer have been instrumental in understanding disease mechanisms and establishing preclinical drug testing. Various mouse models of meningioma have been developed over time, evolving in light of new discoveries in our comprehension of meningioma biology and with improvements in genetic engineering techniques. We reviewed all mouse models of meningioma described in the literature, including xenograft models (orthotopic or heterotopic) with human cell lines or patient derived tumors, and genetically engineered mouse models (GEMMs). Xenograft models provided useful tools for preclinical testing of a huge range of innovative drugs and therapeutic options, which are summarized in this review. GEMMs offer the possibility of mimicking human meningiomas at the histological, anatomical, and genetic level and have been invaluable in enabling tumorigenesis mechanisms, including initiation and progression, to be dissected. Currently, researchers have a range of different mouse models that can be used depending on the scientific question to be answered.

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Gamble, John T., Daniel J. Elson, Juliet A. Greenwood, Robyn L. Tanguay, and Siva K. Kolluri. "The Zebrafish Xenograft Models for Investigating Cancer and Cancer Therapeutics." Biology 10, no. 4 (2021): 252. http://dx.doi.org/10.3390/biology10040252.

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In order to develop new cancer therapeutics, rapid, reliable, and relevant biological models are required to screen and validate drug candidates for both efficacy and safety. In recent years, the zebrafish (Danio rerio) has emerged as an excellent model organism suited for these goals. Larval fish or immunocompromised adult fish are used to engraft human cancer cells and serve as a platform for screening potential drug candidates. With zebrafish sharing ~80% of disease-related orthologous genes with humans, they provide a low cost, high-throughput alternative to mouse xenografts that is relevant to human biology. In this review, we provide background on the methods and utility of zebrafish xenograft models in cancer research.

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Bobbs, Alexander S., Jennifer M. Cole, and Karen D. Cowden Dahl. "Emerging and Evolving Ovarian Cancer Animal Models." Cancer Growth and Metastasis 8s1 (January 2015): CGM.S21221. http://dx.doi.org/10.4137/cgm.s21221.

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

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Shen, Yen Ting, Rashi Asthana, Casper Peeters, Christine Allen, Carlo DeAngelis, and Micheline Piquette-Miller. "Potential Limitations of Bioluminescent Xenograft Mouse Models: A Systematic Review." Journal of Pharmacy & Pharmaceutical Sciences 23 (May 13, 2020): 177–99. http://dx.doi.org/10.18433/jpps30870.

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Purpose: Bioluminescent imaging (BLI) is a versatile technique that offers non-invasive and real-time monitoring of tumor development in preclinical cancer research. However, the technique may be limited by several factors that can lead to misinterpretation of the data. This review aimed to investigate the validity of current BLI tumor models and provide recommendations for future model development. Methods: Two major databases, MedLine and EMBASE, were searched from inception to July 2018 inclusively. Studies utilizing mouse xenograft models with demonstration of linear correlations between bioluminescent signal and tumor burden were included. Coefficients of correlation and determination were extracted along with data relating to animal model parameters. Results: 116 studies were included for analysis. It was found that the majority of models demonstrate good correlation regardless of the model type. Selection of a single cell clone with highest luciferase expression resulted in a significantly better correlation. Lastly, appropriate tumor measurement techniques should be utilized when validating the BLI model. Conclusions: In general, BLI remains a valid tool for pre-clinical assessment of tumor burden. While no single factor may be identified as a general limitation, data should be interpreted with caution.

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Xie, M., and C. He. "Antitumor Activity of Foretinib in Breast Cancer Xenograft Mouse Models." Annals of Oncology 24 (May 2013): iii47. http://dx.doi.org/10.1093/annonc/mdt088.1.

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DAI, LEI, CAIDE LU, XI YU, LONG-JUN DAI, and JEFF X. ZHOU. "Construction of orthotopic xenograft mouse models for human pancreatic cancer." Experimental and Therapeutic Medicine 10, no. 3 (2015): 1033–38. http://dx.doi.org/10.3892/etm.2015.2642.

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van Weerden, Wytske M., and Johannes C. Romijn. "Use of nude mouse xenograft models in prostate cancer research." Prostate 43, no. 4 (2000): 263–71. http://dx.doi.org/10.1002/1097-0045(20000601)43:4<263::aid-pros5>3.0.co;2-i.

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Futami, Kazunobu, Emi Kumagai, Hiroshi Makino, et al. "Anticancer activity of RecQL1 helicase siRNA in mouse xenograft models." Cancer Science 99, no. 6 (2008): 1227–36. http://dx.doi.org/10.1111/j.1349-7006.2008.00794.x.

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Hicks, William H., Cylaina E. Bird, Jeffrey I. Traylor, et al. "Contemporary Mouse Models in Glioma Research." Cells 10, no. 3 (2021): 712. http://dx.doi.org/10.3390/cells10030712.

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Despite advances in understanding of the molecular pathogenesis of glioma, outcomes remain dismal. Developing successful treatments for glioma requires faithful in vivo disease modeling and rigorous preclinical testing. Murine models, including xenograft, syngeneic, and genetically engineered models, are used to study glioma-genesis, identify methods of tumor progression, and test novel treatment strategies. Since the discovery of highly recurrent isocitrate dehydrogenase (IDH) mutations in lower-grade gliomas, there is increasing emphasis on effective modeling of IDH mutant brain tumors. Improvements in preclinical models that capture the phenotypic and molecular heterogeneity of gliomas are critical for the development of effective new therapies. Herein, we explore the current status, advancements, and challenges with contemporary murine glioma models.

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Zhang, Huiyuan, Lin Qi, Yuchen Du, et al. "Patient-Derived Orthotopic Xenograft (PDOX) Mouse Models of Primary and Recurrent Meningioma." Cancers 12, no. 6 (2020): 1478. http://dx.doi.org/10.3390/cancers12061478.

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Background. Meningiomas constitute one-third of all primary brain tumors. Although typically benign, about 20% of these tumors recur despite surgery and radiation, and may ultimately prove fatal. There are currently no effective chemotherapies for meningioma. We, therefore, set out to develop patient-derived orthotopic xenograft (PDOX) mouse models of human meningioma using tumor. Method. Of nine patients, four had World Health Organization (WHO) grade I tumors, five had WHO grade II tumors, and in this second group two patients also had recurrent (WHO grade III) meningioma. We also classified the tumors according to our recently developed molecular classification system (Types A, B, and C, with C being the most aggressive). We transplanted all 11 surgical samples into the skull base of immunodeficient (SCID) mice. Only the primary and recurrent tumor cells from one patient—both molecular Type C, despite being WHO grades II and III, respectively—led to the formation of meningioma in the resulting mouse models. We characterized the xenografts by histopathology and RNA-seq and compared them with the original tumors. We performed an in vitro drug screen using 60 anti-cancer drugs followed by in vivo validation. Results. The PDOX models established from the primary and recurrent tumors from patient K29 (K29P-PDOX and K29R-PDOX, respectively) replicated the histopathology and key gene expression profiles of the original samples. Although these xenografts could not be subtransplanted, the cryopreserved primary tumor cells were able to reliably generate PDOX tumors. Drug screening in K29P and K29R tumor cell lines revealed eight compounds that were active on both tumors, including three histone deacetylase (HDAC) inhibitors. We tested the HDAC inhibitor Panobinostat in K29R-PDOX mice, and it significantly prolonged mouse survival (p < 0.05) by inducing histone H3 acetylation and apoptosis. Conclusion. Meningiomas are not very amenable to PDOX modeling, for reasons that remain unclear. Yet at least some of the most malignant tumors can be modeled, and cryopreserved primary tumor cells can create large panels of tumors that can be used for preclinical drug testing.

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Pimentel, Muriel M. L., Fernanda A. Santos, Ana C. G. Teixeira, et al. "Biochemical, thermographic, and follicular responses of murine models of hormone-treated bovine ovarian renal capsule xenografts." Pesquisa Veterinária Brasileira 37, no. 5 (2017): 425–31. http://dx.doi.org/10.1590/s0100-736x2017000500001.

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ABSTRACT: This study aimed to evaluate the characteristics of two different murine models of hormone-treated renal-encapsulated bovine ovarian tissue xenotransplantation. Two immunodeficient mouse models (BALB/c Nude and C57BL6 SCID) were xenografted with ovarian pieces from heifers and each group was subjected to two hormonal treatments of eCG or a combination of FSH+LH. Donor ovaries and recipients were evaluated by histology and infrared thermography at different times. At the time of xenograft collection, animals were evaluated for alterations in hepatorenal biochemistry. The statistical test used in the study was ANOVA, followed by Tukey’s test. Among the strains, 80% of C57BL6 SCID and 77% of BALB/c Nude mice showed development and vascularization of the transplanted tissue, which acquired cyclicity at 19 and 9 days post-transplant, respectively. Hemorrhagic follicles in xenografts induced with FSH+LH were found in the C57BL6 SCID strain. Infrared thermography was insufficient to distinguish the tissue donor recipient. In conclusion, the C57BL6 SCID strain appears to be the best host for ovarian xenografts, since the transplants in these mice were viable and showed robust follicular development. This work will aid future choices of immunodeficient strains for xenografting procedures.

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Murayama, Takahiko, and Noriko Gotoh. "Patient-Derived Xenograft Models of Breast Cancer and Their Application." Cells 8, no. 6 (2019): 621. http://dx.doi.org/10.3390/cells8060621.

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Recently, patient-derived xenograft (PDX) models of many types of tumors including breast cancer have emerged as a powerful tool for predicting drug efficacy and for understanding tumor characteristics. PDXs are established by the direct transfer of human tumors into highly immunodeficient mice and then maintained by passaging from mouse to mouse. The ability of PDX models to maintain the original features of patient tumors and to reflect drug sensitivity has greatly improved both basic and clinical study outcomes. However, current PDX models cannot completely predict drug efficacy because they do not recapitulate the tumor microenvironment of origin, a failure which puts emphasis on the necessity for the development of the next generation PDX models. In this article, we summarize the advantages and limitations of current PDX models and discuss the future directions of this field.

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Inkoom, Andriana, Nkafu Ndemazie, Kevin Affram, et al. "Enhancing efficacy of gemcitabine in pancreatic patient-derived xenograft mouse models." International Journal of Pharmaceutics: X 2 (December 2020): 100056. http://dx.doi.org/10.1016/j.ijpx.2020.100056.

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Rea, Domenica, Vitale del Vecchio, Giuseppe Palma, et al. "Mouse Models in Prostate Cancer Translational Research: From Xenograft to PDX." BioMed Research International 2016 (2016): 1–11. http://dx.doi.org/10.1155/2016/9750795.

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Despite the advancement of clinical and preclinical research on PCa, which resulted in the last five years in a decrement of disease incidence by 3-4%, it remains the most frequent cancer in men and the second for mortality rate. Based on this evidence we present a brief dissertation on numerous preclinical models, comparing their advantages and disadvantages; among this we report the PDX mouse models that show greater fidelity to the disease, in terms of histopathologic features of implanted tumor, gene and miRNA expression, and metastatic pattern, well describing all tumor progression stages; this characteristic encourages the translation of preclinical results. These models become particularly useful in meeting the need of new treatments identification that eradicate PCa bone metastases growing, clarifying pathway of angiogenesis, identifying castration-resistant stem-like cells, and studying the antiandrogen therapies. Also of considerable interest are the studies of 3D cell cultures derived from PDX, which have the ability to maintain PDX cell viability with continued native androgen receptor expression, also showing a differential sensitivity to drugs. 3D PDX PCa may represent a diagnostic platform for the rapid assessment of drugs and push personalized medicine. Today the development of preclinical models in vitro and in vivo is necessary in order to obtain increasingly reliable answers before reaching phase III of the drug discovery.

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Park, Jun Won, Hyejin Um, Hanna Yang, Joo Young Cha, Kyoung-June Lee та Hark K. Kim. "CWP232291, a Wnt/β-catenin inhibitor, to suppress the growth and development of gastrointestinal cancers." Journal of Clinical Oncology 35, № 15_suppl (2017): e15534-e15534. http://dx.doi.org/10.1200/jco.2017.35.15_suppl.e15534.

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e15534 Background: CWP232291 (JW Pharmaceutical Corp, Seoul, Korea) is a potent β-catenin inhibitor currently tested in phase I trials for AML and MM. We evaluated the preclinical efficacy of CWP232291 for gastrointestinal cancers using xenograft and genetically-engineered mouse (GEM) models. Methods: For xenograft experiments, we intraperitoneally administered 150 mg/kg of CWP232291 twice a week to 14 heterotopic and 2 orthotopic xenografts of human gastric cancer cell lines formed in NOD/SCID mice. For GEM experiments, we intraperitoneally administered 100 mg/kg of CWP232291 (n = 19) or vehicle (n = 27) twice a week for 17 weeks to 3-week-old Villin-Cre;Smad4 F/F;Trp53F/F GEM mice that spontaneously form intestinal tumors with the β-catenin signaling activation. Results: CWP232291 exhibited in vivo activity in human gastric cancer xenografts. Activity of CWP232291 was more prominent in human gastric cancer cell lines harboring mutations in the β-catenin signaling pathway, such as APC, and in the 5-FU-resistant derivative of SNU-620, than in the other xenografts (P = 0.028, t-test). In the MKN-45 orthotopic xenograft, we noted a decrease in luciferase signal intensity after 4 weeks of CWP232291 treatment. CWP232291 demonstrated synergistic activity with paclitaxel and irinotecan in the SNU-484 heterotopic xenograft. In GEM experiments, CWP232291 treatment significantly suppressed the spontaneous development of intestinal tumors (56.3% vs. 91.3% with vehicle) in Villin-Cre;Smad4 F/F;Trp53F/F mice. Furthermore, CWP232291 treatment significantly reduced the number of mice that develop intestinal adenocarcinomas (37.5% vs. 78.3% with vehicle). Immunohistochemistry revealed CD8 T cell activation within the mouse intestinal tumors. Conclusions: CWP232291 demonstrated significant preclinical efficacy in gastrointestinal tumors, especially in cancers with the β-catenin signaling activation.

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Davies, Jason M., Aaron E. Robinson, Cynthia Cowdrey, et al. "Generation of a patient-derived chordoma xenograft and characterization of the phosphoproteome in a recurrent chordoma." Journal of Neurosurgery 120, no. 2 (2014): 331–36. http://dx.doi.org/10.3171/2013.10.jns13598.

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Object The management of patients with locally recurrent or metastatic chordoma is a challenge. Preclinical disease models would greatly accelerate the development of novel therapeutic options for chordoma. The authors sought to establish and characterize a primary xenograft model for chordoma that faithfully recapitulates the molecular features of human chordoma. Methods Chordoma tissue from a recurrent clival tumor was obtained at the time of surgery and implanted subcutaneously into NOD-SCID interleukin-2 receptor gamma (IL-2Rγ) null (NSG) mouse hosts. Successful xenografts were established and passaged in the NSG mice. The recurrent chordoma and the derived human chordoma xenograft were compared by histology, immunohistochemistry, and phospho-specific immunohistochemistry. Based on these results, mice harboring subcutaneous chordoma xenografts were treated with the mTOR inhibitor MLN0128, and tumors were subjected to phosphoproteome profiling using Luminex technology and immunohistochemistry. Results SF8894 is a novel chordoma xenograft established from a recurrent clival chordoma that faithfully recapitulates the histopathological, immunohistological, and phosphoproteomic features of the human tumor. The PI3K/Akt/mTOR pathway was activated, as evidenced by diffuse immunopositivity for phospho-epitopes, in the recurrent chordoma and in the established xenograft. Treatment of mice harboring chordoma xenografts with MLN0128 resulted in decreased activity of the PI3K/Akt/mTOR signaling pathway as indicated by decreased phospho-mTOR levels (p = 0.019, n = 3 tumors per group). Conclusions The authors report the establishment of SF8894, a recurrent clival chordoma xenograft that mimics many of the features of the original tumor and that should be a useful preclinical model for recurrent chordoma.

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Iwami, Kenichiro, Hiroyuki Momota, Atsushi Natsume, Sayano Kinjo, Tetsuya Nagatani, and Toshihiko Wakabayashi. "A novel method of intracranial injection via the postglenoid foramen for brain tumor mouse models." Journal of Neurosurgery 116, no. 3 (2012): 630–35. http://dx.doi.org/10.3171/2011.10.jns11852.

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Object Mouse models have been widely used in developing therapies for human brain tumors. However, surgical techniques such as bone drilling and skin suturing to create brain tumors in adult mice are still complicated. The aim of this study was to establish a simple and accurate method for intracranial injection of cells or other materials into mice. Methods The authors performed micro CT scans and skull dissection to assess the anatomical characteristics of the mouse postglenoid foramen. They then used xenograft and genetically engineered mouse models to evaluate a novel technique of percutaneous intracranial injection via the postglenoid foramen. They injected green fluorescent protein–labeled U87MG cells or virus-producing cells into adult mouse brains via the postglenoid foramen and identified the location of the created tumors by using bioluminescence imaging and histological analysis. Results The postglenoid foramen was found to be a well-conserved anatomical structure that allows percutaneous injection into the cerebrum, cerebellum, brainstem, and basal cistern in mice. The mean (± SD) time for the postglenoid foramen injection technique was 88 ± 15 seconds. The incidence of in-target tumor formation in the xenograft model ranged from 80% to 100%, depending on the target site. High-grade gliomas were successfully developed by postglenoid foramen injection in the adult genetically engineered mouse using virus-mediated platelet-derived growth factor B gene transfer. There were no procedure-related complications. Conclusions The postglenoid foramen can be used as a needle entry site into the brain of the adult mouse. Postglenoid foramen injection is a less invasive, safe, precise, and rapid method of implanting cells into the adult mouse brain. This method can be applied to both orthotopic xenograft and genetically engineered mouse models and may have further applications in mice for the development of therapies for human brain tumors.

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Liaw, Tracy T. Y. E., Patricia P. A. Burke, X. Chen, Theresa T. M. LaVallee, Richard Lock, and Maria Kavallaris. "ENMD-1198 in Combination with Vincristine Shows Synergistic Activity in Leukemia Cells and Prolonged Mouse Survival in Human Leukemia Xenografts." Blood 110, no. 11 (2007): 859. http://dx.doi.org/10.1182/blood.v110.11.859.859.

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Abstract ENMD-1198 (2-methoxyestra-1, 3, 5, (10), 16-tetraene-3-carboxamide), an analogue of 2 methoxyestradiol (2ME2 or Panzem®), is a microtubule destabilizing agent that binds to the colchicine-binding site of β-tubulin. ENMD-1198 has shown anti-angiogenic and anti-proliferative activities in several tumour models and is currently being evaluated in a Phase 1 clinical trial. To date however, the efficacy and mechanisms of action of ENMD-1198 in leukemia are not well-studied or fully understood. Hence, in order to assess the efficacy of ENMD-1198 in leukemia, a clinically relevant model of primary human ALL cells xenografted into immuno-deficient (NOD/SCID) mice was used (1). Three human ALL xenografts (ALL3, ALL7 and ALL19) that exhibit intrinsic differences in response to vincristine (VCR) (1) were treated with 100 mg/kg ENMD-1198 by gavage (daily for 28 days), commencing treatment when engraftment rates reached 1% human CD45+ in mouse peripheral blood. Treatment with ENMD-1198 significantly increased the mouse survival rates compared to vehicle control in all three xenografts (Leukemia Growth Delay (LGD) for ALL3 = 17.3 days, p < 0.005; ALL7 = 21.5 days, p < 0.005; ALL19 = 16.7 days, p < 0.005). Interestingly, ALL7, the least sensitive xenograft to vincristine, showed the best response to ENMD-1198 with a growth delay factor of 21 days. To determine whether the combination of ENMD-1198 and VCR has therapeutic advantages in leukemia, anti-proliferative studies of the drug combination in CCRF-CEM leukemia cells were carried out. A synergistic effect was observed when ENMD-1198 and VCR were combined. The effect of this drug combination was further examined in the ALL human xenograft mouse model. Mice inoculated with ALL7 xenograft were treated with 50 mg/kg ENMD-1198 (daily for 28 days) and 0.5 mg/kg VCR (weekly for 4 weeks) by intraperitoneal injection. The drug combination significantly prolonged mouse survival rates compared to single ENMD-1198 and VCR treatments (LGD 35.19days; p < 0.005). Functional analysis of the drug combination treatment in CCRF-CEM cells in vitro showed that the cells arrested at G2/M followed by sub-G1 (apoptosis) phase, with decreased HIF-1α and JAK-2 proteins. Apoptosis in vitro was associated with increased DR5, active caspase 3 and cleaved PARP proteins in CCRF-CEM cells treated with the combination. In summary, ENMD-1198 alone, and in combination with VCR, has shown promising results in the treatment of preclinical models of leukemia.

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Ye, Shiming, Melvin I. Fox, Nicole A. Belmar, et al. "Enavatuzumab, a Humanized Anti-TWEAK Receptor Monoclonal Antibody, Exerts Antitumor Activity through Attracting and Activating Innate Immune Effector Cells." Journal of Immunology Research 2017 (2017): 1–14. http://dx.doi.org/10.1155/2017/5737159.

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Enavatuzumab is a humanized IgG1 anti-TWEAK receptor monoclonal antibody that was evaluated in a phase I clinical study for the treatment of solid malignancies. The current study was to determine whether and how myeloid effector cells were involved in postulated mechanisms for its potent antitumor activity in xenograft models. The initial evidence for a role of effector cells was obtained in a subset of tumor xenograft mouse models whose response to enavatuzumab relied on the binding of Fc of the antibody to Fcγ receptor. The involvement of effector cells was further confirmed by immunohistochemistry, which revealed strong infiltration of CD45+ effector cells into tumor xenografts in responding models, but minimal infiltration in nonresponders. Consistent with the xenograft studies, human effector cells preferentially migrated toward in vivo-responsive tumor cells treated by enavatuzumab in vitro, with the majority of migratory cells being monocytes. Conditioned media from enavatuzumab-treated tumor cells contained elevated levels of chemokines, which might be responsible for enavatuzumab-triggered effector cell migration. These preclinical studies demonstrate that enavatuzumab can exert its potent antitumor activity by actively recruiting and activating myeloid effectors to kill tumor cells. Enavatuzumab-induced chemokines warrant further evaluation in clinical studies as potential biomarkers for such activity.

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LIN, KEVIN Y., ALEXANDER F. BAGLEY, ALEXIA Y. ZHANG, DANIEL L. KARL, SAM S. YOON, and SANGEETA N. BHATIA. "GOLD NANOROD PHOTOTHERMAL THERAPY IN A GENETICALLY ENGINEERED MOUSE MODEL OF SOFT TISSUE SARCOMA." Nano LIFE 01, no. 03n04 (2010): 277–87. http://dx.doi.org/10.1142/s1793984410000262.

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Plasmonic nanomaterials are poised to impact the clinical management of cancer through their ability to convert externally applied energy into localized heat at sites of diseased tissue. However, characterization of plasmonic nanomaterials as cancer therapeutics has been limited to xenograft models, creating a need to extend these findings to more clinically relevant models of cancer. Here, we evaluate the method of photothermal ablation therapy in a genetically engineered mouse model (GEMM) of sarcoma, which more accurately recapitulates the human disease in terms of structure and biology than subcutaneous xenograft models. Using polyethylene glycol (PEG)-coated gold nanorods (PEG-NRs), we quantitatively evaluate the ability of nanoparticles to penetrate and accumulate in sarcomas through passive targeting mechanisms. We demonstrate that PEG-NR–mediated photothermal heating results in significant delays in tumor growth with no progression in some instances. Lastly, by evaluating our photothermal ablation protocol in a GEMM, we observe off-target heating effects that are not detectable in xenograft models and which may be of future clinical interest.

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Yamauchi, Takuji, Katsuto Takenaka, Shingo Urata, et al. "Polymorphic Sirpa is the genetic determinant for NOD-based mouse lines to achieve efficient human cell engraftment." Blood 121, no. 8 (2013): 1316–25. http://dx.doi.org/10.1182/blood-2012-06-440354.

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Li, Jianneng, Michael Berk, Mohammad Alyamani, et al. "Hexose-6-phosphate dehydrogenase blockade reverses prostate cancer drug resistance in xenograft models by glucocorticoid inactivation." Science Translational Medicine 13, no. 595 (2021): eabe8226. http://dx.doi.org/10.1126/scitranslmed.abe8226.

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Prostate cancer resistance to next-generation hormonal treatment with enzalutamide is a major problem and eventuates into disease lethality. Biologically active glucocorticoids that stimulate glucocorticoid receptor (GR) have an 11β-OH moiety, and resistant tumors exhibit loss of 11β-HSD2, the oxidative (11β-OH → 11-keto) enzyme that normally inactivates glucocorticoids, allowing elevated tumor glucocorticoids to drive resistance by stimulating GR. Here, we show that up-regulation of hexose-6-phosphate dehydrogenase (H6PD) protein occurs in prostate cancer tissues of men treated with enzalutamide, human-derived cell lines, and patient-derived prostate tissues treated ex vivo with enzalutamide. Genetically silencing H6PD blocks NADPH generation, which inhibits the usual reductive directionality of 11β-HSD1, to effectively replace 11β-HSD2 function in human-derived cell line models, suppress the concentration of biologically active glucocorticoids in prostate cancer, and reverse enzalutamide resistance in mouse xenograft models. Similarly, pharmacologic blockade of H6PD with rucaparib normalizes tumor glucocorticoid metabolism in human cell lines and reinstates responsiveness to enzalutamide in mouse xenograft models. Our data show that blockade of H6PD, which is essential for glucocorticoid synthesis in humans, normalizes glucocorticoid metabolism and reverses enzalutamide resistance in mouse xenograft models. We credential H6PD as a pharmacologic vulnerability for treatment of next-generation androgen receptor antagonist–resistant prostate cancer by depleting tumor glucocorticoids.

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Özdemir, B., C. Secondini, R. Schwaninger, et al. "279 STROMA REACTION IN MOUSE XENOGRAFT MODELS OF PROSTATE CANCER BONE METASTASIS." European Urology Supplements 9, no. 2 (2010): 115. http://dx.doi.org/10.1016/s1569-9056(10)60278-3.

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Qi, Lin, Patricia Baxter, Mari Kogiso, et al. "PCM-05AUTOPSY-DERIVED ORTHOTOPIC XENOGRAFT MOUSE MODELS OF TERMINAL PEDIATRIC BRAIN TUMORS." Neuro-Oncology 18, suppl 3 (2016): iii140.1—iii140. http://dx.doi.org/10.1093/neuonc/now080.05.

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Yada, Erica, Satoshi Wada, Shintaro Yoshida, and Tetsuro Sasada. "Use of patient-derived xenograft mouse models in cancer research and treatment." Future Science OA 4, no. 3 (2018): FSO271. http://dx.doi.org/10.4155/fsoa-2017-0136.

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Wilson, Thomas, Giacomo Pirovano, Gu Xiao, et al. "PARP-Targeted Auger Therapy in p53 Mutant Colon Cancer Xenograft Mouse Models." Molecular Pharmaceutics 18, no. 9 (2021): 3418–28. http://dx.doi.org/10.1021/acs.molpharmaceut.1c00323.

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Dourado, Keina M. C., June Baik, Vanessa K. P. Oliveira, et al. "Endoglin: a novel target for therapeutic intervention in acute leukemias revealed in xenograft mouse models." Blood 129, no. 18 (2017): 2526–36. http://dx.doi.org/10.1182/blood-2017-01-763581.

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Key Points Leukemia-forming activity is enriched in endoglin-expressing AML and B-ALL blasts using a mouse xenograft model. Inhibition of endoglin function with TRC105 reduces leukemia development and progression.

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Kato, Yukinari, Tomokazu Ohishi, Manabu Kawada, et al. "The mouse–canine chimeric anti-dog podoplanin antibody P38B exerts antitumor activity in mouse xenograft models." Biochemistry and Biophysics Reports 17 (March 2019): 23–26. http://dx.doi.org/10.1016/j.bbrep.2018.11.005.

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Wu, Wei, Su-Ni Tang, Yong Zhang, et al. "Prostate Cancer Xenograft Inhibitory Activity and Pharmacokinetics of Decursinol, a Metabolite of Angelica gigas Pyranocoumarins, in Mouse Models." American Journal of Chinese Medicine 45, no. 08 (2017): 1773–92. http://dx.doi.org/10.1142/s0192415x17500963.

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We have previously shown that the ethanol extract of dried Angelica gigas Nakai (AGN) root exerts anticancer activity against androgen receptor (AR)-negative human DU145 and PC-3 prostate cancer xenografts and primary carcinogenesis in the transgenic adenocarcinoma of mouse prostate (TRAMP) model. The major pyranocoumarin isomers decursin (D) and decursinol angelate (DA), when provided at equi-molar intake to that provided by AGN extract, accounted for the inhibitory efficacy against precancerous epithelial lesions in TRAMP mice. Since we and others have shown in rodents and humans that D and DA rapidly and extensively convert to decursinol, here we tested whether decursinol might be an in vivo active compound for suppressing xenograft growth of human prostate cancer cells expressing AR. In SCID-NSG mice carrying subcutaneously inoculated human LNCaP/AR-Luc cells overexpressing the wild type AR, we compared the efficacy of 4.5[Formula: see text]mg decursinol per mouse with equi-molar dose of 6[Formula: see text]mg D/DA per mouse. The result showed that decursinol decreased xenograft tumor growth by 75% and the lung metastasis, whereas D/DA exerted a much less effect. Measurement of plasma decursinol concentration, at 3[Formula: see text]h after the last dose of respective dosing regimen, showed higher circulating level in the decursinol-treated NSG mice than in the D/DA-treated mice. In a subsequent single-dose pharmacokinetic experiment, decursinol dosing led to 3.7-fold area under curve (AUC) of plasma decursinol over that achieved by equi-molar D/DA dosing. PK advantage notwithstanding, decursinol represents an active compound to exert in vivo prostate cancer growth and metastasis inhibitory activity in the preclinical model.

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Antonelli, Antonella, Willy A. Noort, Jenny Jaques, et al. "Establishing human leukemia xenograft mouse models by implanting human bone marrow–like scaffold-based niches." Blood 128, no. 25 (2016): 2949–59. http://dx.doi.org/10.1182/blood-2016-05-719021.

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Key Points Humanized niche xenograft mouse models were generated that enabled engraftment of patients’ leukemia cells covering all risk groups. Self-renewal was better maintained in the humanized niches as determined by serial transplantation and genome-wide transcriptome studies.

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Yin, Lei, Zhenglin Yao, Yue Wang, Julius Huang, Michelle Mazuranic, and Ang Yin. "Preclinical evaluation of novel CDK4/6 inhibitor GLR2007 in glioblastoma models." Journal of Clinical Oncology 39, no. 15_suppl (2021): e14023-e14023. http://dx.doi.org/10.1200/jco.2021.39.15_suppl.e14023.

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e14023 Background: Glioblastoma multiforme (GBM) is characterized by a high frequency of cyclin-dependent kinase (CDK)4 and CDK6 pathway dysregulation. CDK4/6 inhibitors palbociclib and abemaciclib are approved for the treatment of breast cancer, but poor blood–brain barrier (BBB) penetration limits their efficacy in GBM. GLR2007 is a novel CDK4/6 inhibitor with potential for improved penetration across the BBB. Here, we report on the activity of GLR2007 in GBM cell lines and its anti-tumor efficacy in mouse xenograft models. Methods: Three in vitro assays were used to assess the activity of GLR2007. Inhibition of CDK4/6 enzymatic activity by GLR2007 or palbociclib was calculated, and cell cycle stages were analyzed in U87-MG cells treated with vehicle control or GLR2007 for 24 h. Cell viability was evaluated in U87-MG and U118-MG cell lines after culture for 72 h with GLR2007 or abemaciclib. In vivo evaluation of the anti-tumor efficacy of GLR2007 versus vehicle, abemaciclib, and/or palbociclib was performed in BALB/c nude mouse GBM xenograft models. Quantitative whole-body autoradiography was used to determine the distribution of [14C]GLR2007 in the tissues of Sprague Dawley rats. Results: GLR2007 potency toward CDK4 and CDK6 was 33.1 and 3.8 times that of palbociclib, respectively. At concentrations >13.72 nM, GLR2007 caused G1 arrest of U87-MG cells. GLR2007 inhibited proliferation in U87-MG cells (IC50 15.6±2.4 nM) and U118-MG cells (IC50 23.2±5.2 nM). Anti-tumor efficacy of GLR2007 versus vehicle control was observed in two mouse GBM xenograft models (Table). Studies performed in rats demonstrated the distribution of [14C]GLR2007 in whole brain tissue following a single oral dose, with total radioactivity levels in the brain exceeding those in plasma by 2.3–4.5-fold from 2–6 h after dosing. Conclusions: These preclinical studies demonstrate the potential of GLR2007 as a novel CDK4/6 inhibitor for treatment of GBM. GLR2007 showed numerically greater anti-tumor efficacy than approved CDK4/6 inhibitors in xenograft models, and evidence of substantial central nervous system penetration. [Table: see text]

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Cho, Kyungjoo, Simon Weonsang Ro, Sang Hyun Seo, et al. "Genetically Engineered Mouse Models for Liver Cancer." Cancers 12, no. 1 (2019): 14. http://dx.doi.org/10.3390/cancers12010014.

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Liver cancer is the fourth leading cause of cancer-related death globally, accounting for approximately 800,000 deaths annually. Hepatocellular carcinoma (HCC) is the most common type of liver cancer, comprising approximately 80% of cases. Murine models of HCC, such as chemically-induced models, xenograft models, and genetically engineered mouse (GEM) models, are valuable tools to reproduce human HCC biopathology and biochemistry. These models can be used to identify potential biomarkers, evaluate potential novel therapeutic drugs in pre-clinical trials, and develop molecular target therapies. Considering molecular target therapies, a novel approach has been developed to create genetically engineered murine models for HCC, employing hydrodynamics-based transfection (HT). The HT method, coupled with the Sleeping Beauty transposon system or the CRISPR/Cas9 genome editing tool, has been used to rapidly and cost-effectively produce a variety of HCC models containing diverse oncogenes or inactivated tumor suppressor genes. The versatility of these models is expected to broaden our knowledge of the genetic mechanisms underlying human hepatocarcinogenesis, allowing the study of premalignant and malignant liver lesions and the evaluation of new therapeutic strategies. Here, we review recent advances in GEM models of HCC with an emphasis on new technologies.

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Hoseini, Sayed Shahabuddin, Madelyn Espinosa-Cotton, Hong-fen Guo, and Nai-Kong V. Cheung. "Overcoming leukemia heterogeneity by combining T cell engaging bispecific antibodies." Journal for ImmunoTherapy of Cancer 8, no. 2 (2020): e001626. http://dx.doi.org/10.1136/jitc-2020-001626.

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BackgroundLeukemia represents about 5% of all human cancers. Despite advances in therapeutics, a substantial number of patients succumb to the disease. Several subtypes of leukemia are inherently more resistant to treatment despite intensive chemotherapy or targeted therapy.MethodsHere we describe the generation of T cell engaging (CD3) bispecific antibodies (BsAbs) built on humanized IgG frameworks using the IgG(L)-scFv format against two targets expressed on acute lymphoblastic leukemia (ALL) and on acute myeloid leukemia (AML).ResultsEach BsAb mediated potent anti-leukemia effect against ALL (CD19) and AML (CD33) in vitro and in xenograft models. Importantly, the CD19-specific BsAb (BC250) was effective against hematogenous spread preventing metastases to liver and kidney in mice bearing ALL and Burkitt’s lymphoma xenografts. BC250 was more potent than the The Food and Drug Administration (FDA)-approved BsAb blinatumomab against ALL xenografts in vivo as measured by tumor bioluminescence and mouse survival. Furthermore, the combination of the CD19 and CD33 BsAbs in two xenograft models of mixed phenotype acute leukemia (biphenotypic and bilineal leukemia) was far superior than monotherapy with either of the BsAbs alone.ConclusionsSelective combinations of these leukemia-specific BsAb offer the potential to overcome tumor heterogeneity or clonal escape in the modern era of antibody-based T cell-driven immunotherapy.

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Knoblaugh, Sue E., and Lauren E. Himmel. "Keeping Score: Semiquantitative and Quantitative Scoring Approaches to Genetically Engineered and Xenograft Mouse Models of Cancer." Veterinary Pathology 56, no. 1 (2018): 24–32. http://dx.doi.org/10.1177/0300985818808526.

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There is a growing need to quantitate or “score” lesions in mouse models of human disease, for correlation with human disease and to establish their clinical relevance. Several standard semiquantitative scoring schemes have been adapted for nonneoplastic lesions; similarly, the pathologist must carefully select an approach to score mouse models of cancer. Genetically engineered mouse models with a continuum of precancerous and cancerous lesions and xenogeneic models of various derivations present unique challenges for the pathologist. Important considerations include experimental design, understanding of the human disease being modeled, standardized classification of lesions, and approaches for semiquantitative and/or quantitative scoring in the model being evaluated. Quantification should be considered for measuring the extent of neoplasia and expression of tumor biomarkers. Semiquantitative scoring schemes have been devised that include severity, frequency, and distribution of lesions. Although labor-intensive, scoring mouse models of cancer provides numerical data that enable statistical analysis and greater translational impact.

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Tejeda, M., D. Gaál, I. Szűcs, and A. Telekes. "Avemar inhibits the growth of mouse and human xenograft mammary carcinomas comparable to endocrine treatments." Journal of Clinical Oncology 25, no. 18_suppl (2007): 21132. http://dx.doi.org/10.1200/jco.2007.25.18_suppl.21132.

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21132 Background: An in vitro study demonstrated that Avemar increased the effect of Tamoxifen on MCF7 (ER+) mammary carcinoma cells. Methods: MXT (ER+) mouse mammary tumor tissue was transplanted s.c. into BDF1 mice. The tumor bearing animals were treated p.o. with Avemar. Then the most effective Avemar dose (3.0 g/kg), Tamoxifen (0.5 mg/kg s.c.), Examestane (10 mg/kg i.p.) and Anastrasol (5 mg/kg i.p.) monotherapies and their combinations with Avemar was compared. All treatments were given once daily, for 10 days, starting 7 days after the tumor transplantation. The same experimental schedule was repeated using T47/D (ER+) human breast carcinoma cell lines transplanted into C.B-17/Icr-scid/scid mouse. Finally, the growth of T47/D and MDA-MB-231 (ER-) xenografts treated by Avemar was compared. Tumor volume was measured up to 25 days after transplantation in MXT and 55 days in xenograft. Results: In MXT model all monotherapies and combinations led to retardation of tumor growth. Combination of Avemar with any of the endocrine treatment enhanced the efficacy compared to endocrine monotherapy. Out of the four monotherapies the best result was achieved by Avemar (50% inhibition). The combination of Avemar with Examestane increased the tumor growth inhibition to 60.4% compared to control. The other treatments did not exceed the effect of Avemar monotherapy. In xenograft model Avemar produced 50% tumor growth inhibition compared to control and was more effective than the other treatments Examestane (26%), Anastrasol (25%) or Tamoxifen (42%). Combined treatment with Avemar always improved efficacy within the range of 3–10%. Avemar showed similar efficacy when T47/D (49%) and MDA-MB-231 (52%) xenografts were compared. Conclusions: The tumor growth inhibitory effect of Avemar on ER positive MXT mouse breast carcinoma as well as in T47/D xenograft models are comparable (equal or better) to standard endocrine treatments. Avemar certainly did not reduce the effect of endocrine treatments. The antitumor activity of Avemar did not depend on the estrogen receptor status. No significant financial relationships to disclose.

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Licha, David, Silvia Vidali, Sepideh Aminzadeh-Gohari, et al. "Untargeted Metabolomics Reveals Molecular Effects of Ketogenic Diet on Healthy and Tumor Xenograft Mouse Models." International Journal of Molecular Sciences 20, no. 16 (2019): 3873. http://dx.doi.org/10.3390/ijms20163873.

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The application of ketogenic diet (KD) (high fat/low carbohydrate/adequate protein) as an auxiliary cancer therapy is a field of growing attention. KD provides sufficient energy supply for healthy cells, while possibly impairing energy production in highly glycolytic tumor cells. Moreover, KD regulates insulin and tumor related growth factors (like insulin growth factor-1, IGF-1). In order to provide molecular evidence for the proposed additional inhibition of tumor growth when combining chemotherapy with KD, we applied untargeted quantitative metabolome analysis on a spontaneous breast cancer xenograft mouse model, using MDA-MB-468 cells. Healthy mice and mice bearing breast cancer xenografts and receiving cyclophosphamide chemotherapy were compared after treatment with control diet and KD. Metabolomic profiling was performed on plasma samples, applying high-performance liquid chromatography coupled to tandem mass spectrometry. Statistical analysis revealed metabolic fingerprints comprising numerous significantly regulated features in the group of mice bearing breast cancer. This fingerprint disappeared after treatment with KD, resulting in recovery to the metabolic status observed in healthy mice receiving control diet. Moreover, amino acid metabolism as well as fatty acid transport were found to be affected by both the tumor and the applied KD. Our results provide clear evidence of a significant molecular effect of adjuvant KD in the context of tumor growth inhibition and suggest additional mechanisms of tumor suppression beyond the proposed constrain in energy supply of tumor cells.

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Schmid, T. E., O. Zlobinskaya, D. Michalski, et al. "80 SERUM HSP70 – A SOLUBLE, TUMOR-SPECIFIC MARKER IN XENOGRAFT TUMOR MOUSE MODELS." Radiotherapy and Oncology 102 (March 2012): S28—S29. http://dx.doi.org/10.1016/s0167-8140(12)70057-9.

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Teichman, Jennifer, Lorin Dodbiba, Henry Thai, et al. "Hedgehog inhibition mediates radiation sensitivity in mouse xenograft models of human esophageal adenocarcinoma." PLOS ONE 13, no. 5 (2018): e0194809. http://dx.doi.org/10.1371/journal.pone.0194809.

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Meyer, Lüder Hinrich, and Klaus-Michael Debatin. "Diversity of Human Leukemia Xenograft Mouse Models: Implications for Disease Biology: Figure 1." Cancer Research 71, no. 23 (2011): 7141–44. http://dx.doi.org/10.1158/0008-5472.can-11-1732.

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Michelucci, A., A. Golebiewska, A. Oudin, A. Schuster, R. Balling, and S. P. Niclou. "P04.01 Characterization of microglia/macrophage phenotypes in glioma patient-derived xenograft mouse models." Neuro-Oncology 18, suppl_4 (2016): iv23. http://dx.doi.org/10.1093/neuonc/now188.079.

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Zhang, Tianwei, Lin Zhang, Shuqiong Fan, et al. "Patient-Derived Gastric Carcinoma Xenograft Mouse Models Faithfully Represent Human Tumor Molecular Diversity." PLOS ONE 10, no. 7 (2015): e0134493. http://dx.doi.org/10.1371/journal.pone.0134493.

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Yalcin, M., E. Dyskin, L. Lansing, et al. "Tetraiodothyroacetic Acid (Tetrac) and Nanoparticulate Tetrac Arrest Growth of Medullary Carcinoma of the Thyroid." Journal of Clinical Endocrinology & Metabolism 95, no. 4 (2010): 1972–80. http://dx.doi.org/10.1210/jc.2009-1926.

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Abstract Context: Tetraiodothyroacetic acid (tetrac) blocks angiogenic and tumor cell proliferation actions of thyroid hormone initiated at the cell surface hormone receptor on integrin αvβ3. Tetrac also inhibits angiogenesis initiated by vascular endothelial growth factor and basic fibroblast growth factor. Objective: We tested antiangiogenic and antiproliferative efficacy of tetrac and tetrac nanoparticles (tetrac NP) against human medullary thyroid carcinoma (h-MTC) implants in the chick chorioallantoic membrane (CAM) and h-MTC xenografts in the nude mouse. Design: h-MTC cells were implanted in the CAM model (n = 8 per group); effects of tetrac and tetrac NP at 1 μg/CAM were determined on tumor angiogenesis and tumor growth after 8 d. h-MTC cells were also implanted sc in nude mice (n = 6 animals per group), and actions on established tumor growth of unmodified tetrac and tetrac NP ip were determined. Results: In the CAM, tetrac and tetrac NP inhibited tumor growth and tumor-associated angiogenesis. In the nude mouse xenograft model, established 450–500 mm3 h-MTC tumors were reduced in size over 21 d by both tetrac formulations to less than the initial cell mass (100 mm3). Tumor tissue hemoglobin content of xenografts decreased by 66% over the course of administration of each drug. RNA microarray and quantitative real-time PCR of tumor cell mRNAs revealed that both tetrac formulations significantly induced antiangiogenic thrombospondin 1 and apoptosis activator gene expression. Conclusions: Acting via a cell surface receptor, tetrac and tetrac NP inhibit growth of h-MTC cells and associated angiogenesis in CAM and mouse xenograft models.

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Ma, Hayley S., Sarah M. Greenblatt, Courtney M. Shirley, et al. "All-trans retinoic acid synergizes with FLT3 inhibition to eliminate FLT3/ITD+ leukemia stem cells in vitro and in vivo." Blood 127, no. 23 (2016): 2867–78. http://dx.doi.org/10.1182/blood-2015-05-646786.

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Key Points ATRA and FLT3 TKIs have synergistic activity against FLT3/ITD+ AML cell lines and patient samples. Combination reduces the leukemia stem cell population and improves survival in genetic and xenograft AML mouse models.

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Journal articles on the topic 'Mouse xenograft models'

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