Relevant bibliographies by topics / Tumor xenograft

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Academic literature on the topic 'Tumor xenograft'

Author: Grafiati
Published: 3 September 2022
Last updated: 9 March 2023

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Journal articles on the topic "Tumor xenograft"

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Siu, I.-Mei, Vafi Salmasi, Brent A. Orr, Qi Zhao, Zev A. Binder, Christine Tran, Masaru Ishii, Gregory J. Riggins, Christine L. Hann, and Gary L. Gallia. "Establishment and characterization of a primary human chordoma xenograft model." Journal of Neurosurgery 116, no. 4 (April 2012): 801–9. http://dx.doi.org/10.3171/2011.12.jns111123.

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Object Chordomas are rare tumors arising from remnants of the notochord. Because of the challenges in achieving a complete resection, the radioresistant nature of these tumors, and the lack of effective chemotherapeutics, the median survival for patients with chordomas is approximately 6 years. Reproducible preclinical model systems that closely mimic the original patient's tumor are essential for the development and evaluation of effective therapeutics. Currently, there are only a few established chordoma cell lines and no primary xenograft model. In this study, the authors aimed to develop a primary chordoma xenograft model. Methods The authors implanted independent tumor samples from 2 patients into athymic nude mice. The resulting xenograft line was characterized by histopathological analysis and immunohistochemical staining. The patient's tumor and serial passages of the xenograft were genomically analyzed using a 660,000 single-nucleotide polymorphism array. Results A serially transplantable xenograft was established from one of the 2 patient samples. Histopathological analysis and immunohistochemical staining for S100 protein, epithelial membrane antigen, and cytokeratin AE1/AE3 of the primary patient sample and the xenografts confirmed that the xenografts were identical to the original chordoma obtained from the patient. Immunohistochemical staining and western blot analysis confirmed the presence of brachyury, a recently described marker of chordomas, in the tumor from the patient and each of the xenografts. Genome-wide variation was assessed between the patient's tumor and the xenografts and was found to be more than 99.9% concordant. Conclusions To the best of their knowledge, the authors have established the first primary chordoma xenograft that will provide a useful preclinical model for this disease and a platform for therapeutic development.
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Sicklick, Jason Keith, Stephanie Yvette Leonard, Evangeline Mose, Randall P. French, Michele Criscuoli, Dawn V. Jaquish, Karly Maruyama, Richard B. Schwab, David Cheresh, and Andrew M. Lowy. "A novel xenograft model of gastrointestinal stromal tumors." Journal of Clinical Oncology 30, no. 4_suppl (February 1, 2012): 202. http://dx.doi.org/10.1200/jco.2012.30.4_suppl.202.

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202 Background: GIST treatment with imatinib has served as the prototype for targeted molecular therapy. However, patients frequently acquire drug resistance to imatinib and this has prompted the development of additional multi-kinase inhibitors. To date, preclinical testing of novel agents has predominantly been performed using cell line based subcutaneous xenografts that may overestimate drug activity in the clinic. This suggests that novel in vivo models are needed to improve prediction of clinical efficacy. We hypothesized that human GISTs could be intra-peritoneally xenografted into immunodeficient mice in order to better recapitulate the microenvironment and biology of GIST. Methods: Tumor acquisition was performed under an IRB-approved protocol. Following tumor resection, we anesthetized NOD-scid (NS) or NS gamma (NSG) mice and performed a midline laparotomy. 2′2 mm tumor fragments were sutured into the abdominal viscera of NS (N=10) or NSG (N=15) mice. Tumors were imaged every 3-4 wks with ultrasound (US). 2 mice were also evaluated with PET scan. Results: We have xenografted GISTs from 3 patients into 25 mice with an 80% success rate and 4% perioperative mortality. We observed tumor progression in the liver (9/10), renal capsule (8/10), lesser sac (2/3), or gastric wall (1/2) of mice. This included 14 primary xenografts and 11 passaged xenografts. At 21-196 d (median 46 d), tumor size averaged 473±736 mm3 (median 104 mm3, range 2.2-2683 mm3) by US. In addition, 30% (6/20) of mice developed metastatic disease based upon US, necropsy, histology and/or KIT immunostaining. We also determined that 2/2 tumors were FDG-avid on PET. Conclusions: To our knowledge, we report the first intra-peritoneal xenograft model of human GIST using patient-derived tumor tissue. This novel in vivo approach is a reproducible model of human GIST that replicates the tumor microenvironment, heterogeneity, and metastatic potential of a human GI sarcoma. As compared to current research tools/models, this approach may allow researchers to better predict chemotherapeutic responses, further understand the tumor biology of GIST, and serve as a means to propagate additional tumor tissue for subsequent experimental analyses.
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Davies, Jason M., Aaron E. Robinson, Cynthia Cowdrey, Praveen V. Mummaneni, Gregory S. Ducker, Kevan M. Shokat, Andrew Bollen, Byron Hann, and Joanna J. Phillips. "Generation of a patient-derived chordoma xenograft and characterization of the phosphoproteome in a recurrent chordoma." Journal of Neurosurgery 120, no. 2 (February 2014): 331–36. http://dx.doi.org/10.3171/2013.10.jns13598.

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Object The management of patients with locally recurrent or metastatic chordoma is a challenge. Preclinical disease models would greatly accelerate the development of novel therapeutic options for chordoma. The authors sought to establish and characterize a primary xenograft model for chordoma that faithfully recapitulates the molecular features of human chordoma. Methods Chordoma tissue from a recurrent clival tumor was obtained at the time of surgery and implanted subcutaneously into NOD-SCID interleukin-2 receptor gamma (IL-2Rγ) null (NSG) mouse hosts. Successful xenografts were established and passaged in the NSG mice. The recurrent chordoma and the derived human chordoma xenograft were compared by histology, immunohistochemistry, and phospho-specific immunohistochemistry. Based on these results, mice harboring subcutaneous chordoma xenografts were treated with the mTOR inhibitor MLN0128, and tumors were subjected to phosphoproteome profiling using Luminex technology and immunohistochemistry. Results SF8894 is a novel chordoma xenograft established from a recurrent clival chordoma that faithfully recapitulates the histopathological, immunohistological, and phosphoproteomic features of the human tumor. The PI3K/Akt/mTOR pathway was activated, as evidenced by diffuse immunopositivity for phospho-epitopes, in the recurrent chordoma and in the established xenograft. Treatment of mice harboring chordoma xenografts with MLN0128 resulted in decreased activity of the PI3K/Akt/mTOR signaling pathway as indicated by decreased phospho-mTOR levels (p = 0.019, n = 3 tumors per group). Conclusions The authors report the establishment of SF8894, a recurrent clival chordoma xenograft that mimics many of the features of the original tumor and that should be a useful preclinical model for recurrent chordoma.
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Dong, Yiyu, Brandon Manley, A. Ari Hakimi, Jonathan A. Coleman, Paul Russo, and James Hsieh. "Comparing surgical tissue versus biopsy tissue in the development of a clear cell renal cell carcinoma xenograft model." Journal of Clinical Oncology 34, no. 2_suppl (January 10, 2016): 519. http://dx.doi.org/10.1200/jco.2016.34.2_suppl.519.

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519 Background: The use of xenograft tumor models is considered the ideal platform to investigate the effects and toxicities of novel drugs in primary human tumors. The establishment of a personalized xenograft model using preoperative or pretherapy biopsy for patients with metastatic or high risk disease could improve selection of targeted therapy. We report on our xenograft model using various tissue sources including biopsies and correlation with patient’s clinical features. Methods: 56 specimens from primary and metastatic ccRCC from 48 patients were collected. After surgery (n=35) or biopsy (n=21) the specimen was transplanted either subcutaneously or after cell culture to immunodeficient mice. Tumor engraftment was followed for up to 4 months. Successfully engrafted patient-derived tumors were passaged to further mice. Conformation of xenograft tumors with formalin-fixed, paraffin-embedded and Hematoxylin and eosin stained tumor sections was done to assure morphological concordance with the patients tumor. We used a two-tailed two proportion z-test to compare the number of successful xenografts harvested from surgical tissue or biopsy tissue. Results: Overall 25 of the 56 specimens were successful in growing tumor in our immunodeficient mice. The frequency of success based on the type and site of tissue harvest may be seen in Table 1. We found biopsy tissue to be significantly more successful compared to surgical tissue, 61.9% compared to 34.2% (p-value=0.044). Conclusions: We believe our xenograft model, using biopsy tissue, demonstrates the feasibility of a real time personalized in vivo model to aid in the selection of targeted treatments for systemic therapy in ccRCC patients. [Table: see text]
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Lukbanova, E. A., M. V. Mindar, E. A. Dzhenkova, A. Yu Maksimov, A. S. Goncharova, Yu S. Shatova, A. A. Maslov, A. V. Shaposhnikov, E. V. Zaikina, and Yu N. Lazutin. "Experimental approach to obtaining subcutaneous xenograft of non-small cell lung cancer." Research and Practical Medicine Journal 9, no. 2 (May 4, 2022): 65–76. http://dx.doi.org/10.17709/2410-1893-2022-9-2-5.

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Purpose of the study. Was was the creation of a Patient Derived Xenograft (PDX) model of non‑small cell lung cancer in immunodeficient mice adapted to growth in immunodeficient mice.Materials and methods. The study was performed using the tumor material from 14 donors implanted subcutaneously to 132 immunodeficient Balb/c Nude mice. Xenografts were maintained until the third passage. PDXs in the third passage from 3 patients were used to assess the model sensitivity to cisplatin. A histological analysis and genetic tests for the presence of EGFR mutations were performed for donor tumors from 3 patients and the corresponding xenografts in the third passage.Results. We observed a noticeable PDX growth already on the 8th day after the tumor material implantation. Successful xenograft engraftment was noted in 21 of 42 mice (50 %), which were rather successful results. A comparative histological analysis of tumor material from 3 patients showed that the PDX models retained the original histotype. We also demonstrated the identity of the EGFR mutations in the established xenografts from 3 patients and the donor tumors, which proved the value of these PDX models for preclinical studies of substances with potential antitumor activity. The analysis of the xenograft sensitivity to cytostatic cisplatin showed a statistically significant decrease in the growth rate in the xenografts obtained from 2 out of 3 patients, in comparison with the control.Conclusions. The created PDX models can be recommended as test systems for preclinical studies of the effectiveness of new pharmacological substances with potential antitumor activity.
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Breij, Esther CW, David Satijn, Sandra Verploegen, Bart de Goeij, Danita Schuurhuis, Wim Bleeker, Mischa Houtkamp, and Paul Parren. "Use of an antibody-drug conjugate targeting tissue factor to induce complete tumor regression in xenograft models with heterogeneous target expression." Journal of Clinical Oncology 31, no. 15_suppl (May 20, 2013): 3066. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.3066.

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3066 Background: Tissue factor (TF) is the main initiator of coagulation, that starts when circulating factor VII(a) (FVII(a)) binds membrane bound TF. In addition, the TF:FVIIa complex can initiate a pro-angiogenic signaling pathway by activation of PAR-2. TF is aberrantly expressed in many solid tumors, and expression has been associated with poor prognosis. TF-011-vcMMAE, an antibody-drug conjugate (ADC) under development for the treatment of solid tumors, is composed of a human TF specific antibody (TF-011), a proteaseEcleavable valine-citrulline (vc) linker and the microtubule disrupting agent monomethyl auristatin E (MMAE). Methods: TF-011 and TF-011-vcMMAE were functionally characterized using in vitro assays. In vivo anti-tumor activity of TF-011-vcMMAE was assessed in human biopsy derived xenograft models, which genetically and histologically resemble human tumors. TF expression in xenografts was assessed using immunohistochemistry. Results: TF-011 inhibited TF:FVIIa induced intracellular signaling and efficiently killed tumor cells by antibody dependent cell-mediated cytoxicity in vitro, but showed only minor inhibition of TF procoagulant activity. TF-011 was rapidly internalized and targeted to the lysosomes, a prerequisite for intracellular MMAE release and subsequent tumor cell killing by the ADC. Indeed, TF-011-vcMMAE efficiently and specifically killed TF-positive tumors in vitro and in vivo. Importantly, TF-011-vcMMAE showed excellent anti-tumor activity in human biopsyEderived xenograft models derived from bladder, lung, pancreas, prostate, ovarian and cervical cancer (n=7). TF expression in these models was heterogeneous, ranging from 25-100% of tumor cells. Complete tumor regression was observed in all models, including cervical and ovarian cancer xenografts that showed only 25-50% TF positive tumor cells. Conclusions: TF-011-vcMMAE is a promising new ADC with potent anti-tumor activity in xenograft models that represent the heterogeneity of human tumors, including heterogeneous TF expression. The functional characteristics of TF-011-vcMMAE allow efficient tumor targeting, with minimal impact on coagulation.
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Dougherty, Mark, Eric Taylor, and Marlan Hansen. "TMET-34. RADIATION METABOLOMICS IN PRIMARY HUMAN MENINGIOMA AND SCHWANNOMA: EARLY EXPERIENCE AND INITIAL RESULTS." Neuro-Oncology 24, Supplement_7 (November 1, 2022): vii269. http://dx.doi.org/10.1093/neuonc/noac209.1039.

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Abstract Introduction Meningiomas and schwannomas account for 45% of primary CNS tumors. Yet when surgery and radiation fail, no further treatments exist. Metabolomics has been used to discover new cancer therapies; however, to date few have used metabolomics to study meningiomas and schwannomas. Here we present initial results and lessons learned from this novel endeavor. METHODS Primary tumors were obtained from patients during surgery and immediately taken for culturing or xenograft implantation. Upon reaching >90% confluence, cultures were treated with 0gy, 3gy, 10gy, or 20gy gamma radiation, then flash frozen 6 or 72 hours post-treatment. Xenograft tumors were implanted in nude mice. MRI 4 weeks post-implantation confirmed tumor viability. Mice were then given 10gy, 20gy, or sham radiation treatment. Xenografts were harvested 72 hours post-treatment. Metabolites were measured with a ThermoISQ gas chromatography-mass spectrometer. RESULTS Eleven meningiomas and nine schwannomas were successfully cultured. Unsupervised hierarchical clustering of cultures demonstrated greater influence from tumor of origin than from radiation. Univariate analysis of schwannoma xenografts demonstrated elevated ornithine following radiation (fold change 1.62; P = 0.008). However, principal component analysis did not show significant between-group differentiation. Orthotopic meningioma xenografts did not produce sufficient tissue for metabolomics; however, subsequent subcutaneous implants have been successful (data forthcoming). CONCLUSION Standard cell cultures did not reveal significant metabolic changes following radiation; it is unclear whether this was due to culture technique or inter-tumor heterogeneity. In radiated schwannoma xenografts, elevated ornithine may implicate related pathways such as ornithine decarboxylase-mediated polyamide synthesis for DNA double-strand break repair. Compared to other ‘-omics’ studies, metabolomics requires more tissue per sample ( >10mg) and is more sensitive to environmental conditions. Thus, large sample sizes are needed to detect significant changes, and xenografts are likely superior to cell culture. Future plans include increased xenograft sample size and stable isotope tracing for pathway analysis.
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Jeuken, Judith W. M., Sandra H. E. Sprenger, Pieter Wesseling, Hans J. J. A. Bernsen, Ron F. Suijkerbuijk, Femke Roelofs, Merryn V. E. Macville, H. Jacobus Gilhuis, Jacobus J. van Overbeeke, and Rudolf H. Boerman. "Genetic reflection of glioblastoma biopsy material in xenografts: characterization of 11 glioblastoma xenograft lines by comparative genomic hybridization." Journal of Neurosurgery 92, no. 4 (April 2000): 652–58. http://dx.doi.org/10.3171/jns.2000.92.4.0652.

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Object. Human tumors implanted as subcutaneous xenografts in nude mice are widely used for the study of tumor biology and therapy. Validation of these models requires knowledge of the genetic makeup of the xenografts. The aim of this study was to establish whether chromosomal imbalances in 11 xenograft lines derived from human glioblastomas multiforme (x-GBMs) are similar to those found in GBM biopsy samples. The authors also studied genetic stability during serial passaging of three xenograft lines.Methods. Chromosomal imbalances in x-GBMs were detected using comparative genomic hybridization (CGH). The authors compared the CGH results in x-GBMs with those in the original GBMs (o-GBMs) that were used to establish three of the xenograft lines and with the GBM biopsy results reported in the literature (l-GBMs). In three xenograft lines two different passages were analyzed.Conclusions. The results show that the chromosomal imbalances in x-GBMs are similar to those in o-GBMs and l-GBMs, indicating that the GBM xenograft lines used were valid models from a genetic point of view. The CGH analysis of two different passages of three xenograft lines indicates that x-GBMs (like l-GBMs) show intratumoral genetic heterogeneity and do not acquire chromosomal imbalances as a result of serial passaging.
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Singh, Kanika, Negar Jamshidi, Roby Zomer, Terrence J. Piva, and Nitin Mantri. "Cannabinoids and Prostate Cancer: A Systematic Review of Animal Studies." International Journal of Molecular Sciences 21, no. 17 (August 29, 2020): 6265. http://dx.doi.org/10.3390/ijms21176265.

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Prostate cancer is a major cause of death among men worldwide. Recent preclinical evidence implicates cannabinoids as powerful regulators of cell growth and differentiation, as well as potential anti-cancer agents. The aim of this review was to evaluate the effect of cannabinoids on in vivo prostate cancer models. The databases searched included PubMed, Embase, Scopus, and Web of Science from inception to August 2020. Articles reporting on the effect of cannabinoids on prostate cancer were deemed eligible. We identified six studies that were all found to be based on in vivo/xenograft animal models. Results: In PC3 and DU145 xenografts, WIN55,212-2 reduced cell proliferation in a dose-dependent manner. Furthermore, in LNCaP xenografts, WIN55,212-2 reduced cell proliferation by 66–69%. PM49, which is a synthetic cannabinoid quinone, was also found to result in a significant inhibition of tumor growth of up to 90% in xenograft models of LNCaP and 40% in xenograft models of PC3 cells, respectively. All studies have reported that the treatment of prostate cancers in in vivo/xenograft models with various cannabinoids decreased the size of the tumor, the outcomes of which depended on the dose and length of treatment. Within the limitation of these identified studies, cannabinoids were shown to reduce the size of prostate cancer tumors in animal models. However, further well-designed and controlled animal studies are warranted to confirm these findings.
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Dobbin, Zachary C., Ashwini A. Katre, Angela Ziebarth, Monjri Shah, Adam D. Steg, Ronald David Alvarez, Michael G. Conner, and Charles N. Landen. "Use of an optimized primary ovarian cancer xenograft model to mimic patient tumor biology and heterogeneity." Journal of Clinical Oncology 30, no. 15_suppl (May 20, 2012): 5036. http://dx.doi.org/10.1200/jco.2012.30.15_suppl.5036.

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5036 Background: Current xenograft and transgenic models of ovarian cancer are mainly homogeneous and poorly predict response to therapy. Use of patient tumors may represent a better model for tumor biology and offer potential to test personalized medicine approaches, but poor take rates and questions of recapitulation of patient tumors have limited this approach. We have developed a protocol for improved feasibility of such a model and examined its similarity to the patient tumor. Methods: Under IRB and IACUC approval, 23 metastatic ovarian cancer samples were collected at the time of tumor reductive surgery. Samples were implanted either subcutaneously (SQ), intraperitoneally (IP), in the mammary fat pad (MFP), or in the subrenal capsule (SRC) and monitored for tumor growth. Cohorts from 8 xenolines were treated with combined carboplatin and paclitaxel or vehicle, and response to therapy compared between xenografts and patients. Expression of tumor-initiating cell (TIC) markers ALDH1, CD133, and CD44 was assessed by immunohistochemistry in tumors from patients and treated and untreated xenografts. Results: At least one SQ implanted tumor developed in 91.3% of xenografts, significantly higher than in the MFP (63.6%), IP (23.5%), or SRC (8%). Xenografts were similar in expression of putative TIC’s compared to patient tumors. The patients and the xenografts also have similar responses to chemotherapy in that xenografts from patients with a partial response responded more slowly than those from patients achieving a complete response (45 vs 21 days, p=.004). Treated xenografts were more densely composed of TICs. ALDH1 increased to 36.1% from 16.2% (p=0.002) and CD133 increased to 33.8% from 16.2% (p=0.026). Conclusions: Xenoline development can be achieved at a high rate when tumors collected from metastatic sites are implanted SQ. These xenografts are similar to patient tumors with regard to chemotherapy response and TIC expression.. This model may be a more accurate model for in vivo pre-clinical studies as compared to current models. Also, as treated xenografts become chemoresistant, this model is well positioned to evaluate targeted therapies aimed at the most aggressive populations in a heterogeneous tumor.
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Dissertations / Theses on the topic "Tumor xenograft"

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Williams, K. J., M. R. Albertella, B. Fitzpatrick, Paul M. Loadman, Steven D. Shnyder, E. C. Chinje, B. A. Telfer, C. R. Dunk, P. A. Harris, and I. J. Stratford. "In vivo activation of the hypoxia-targeted cytotoxin AQ4N in human tumor xenograft." AACR Publications, 2009. http://hdl.handle.net/10454/4561.

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AQ4N (banoxantrone) is a prodrug that, under hypoxic conditions, is enzymatically converted to a cytotoxic DNA-binding agent, AQ4. Incorporation of AQ4N into conventional chemoradiation protocols therefore targets both oxygenated and hypoxic regions of tumors, and potentially will increase the effectiveness of therapy. This current pharmacodynamic and efficacy study was designed to quantify tumor exposure to AQ4 following treatment with AQ4N, and to relate exposure to outcome of treatment. A single dose of 60 mg/kg AQ4N enhanced the response of RT112 (bladder) and Calu-6 (lung) xenografts to treatment with cisplatin and radiation therapy. AQ4N was also given to separate cohorts of tumor-bearing mice 24 hours before tumor excision for subsequent analysis of metabolite levels. AQ4 was detected by high performance liquid chromatography/mass spectrometry in all treated samples of RT112 and Calu-6 tumors at mean concentrations of 0.23 and 1.07 microg/g, respectively. These concentrations are comparable with those shown to be cytotoxic in vitro. AQ4-related nuclear fluorescence was observed in all treated tumors by confocal microscopy, which correlated with the high performance liquid chromatography/mass spectrometry data. The presence of the hypoxic marker Glut-1 was shown by immunohistochemistry in both Calu-6 tumors and RT112 tumors, and colocalization of AQ4 fluorescence and Glut-1 staining strongly suggested that AQ4N was activated in these putatively hypoxic areas. This is the first demonstration that AQ4N will increase the efficacy of chemoradiotherapy in preclinical models; the intratumoral levels of AQ4 found in this study are comparable with tumor AQ4 levels found in a recent phase I clinical study, which suggests that these levels could be potentially therapeutic.
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Tin, Man Ying. "Study of the anticarcinogenic mechanisms of astragalus membranaceus in colon cancer cells and tumor xenograft." HKBU Institutional Repository, 2006. http://repository.hkbu.edu.hk/etd_ra/777.

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Tabassum, Doris Priscilla. "Exploring Intra-tumor Cooperation in Metastasis and Drug Resistance using Heterogeneous Xenograft Models of Breast Cancer." Thesis, Harvard University, 2016. http://nrs.harvard.edu/urn-3:HUL.InstRepos:33493472.

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Breast cancer is a highly heterogeneous disease, having not only several intrinsic sub-types but also significant sub-clonal heterogeneity within tumors. Intra-tumor heterogeneity can have profound impact on tumor evolution, disease progression and response to therapy. Furthermore, these phenomena can also be influenced by interactions of cancer cells with those of the microenvironment, thereby adding an extra layer of complexity to the study of tumor biology. To investigate the impact of sub-clonal heterogeneity on tumor phenotypes, we developed a heterogeneous mouse xenograft model of breast cancer. Our model revealed that tumor growth can be driven by a minor clone, expressing IL11, in a non-cell autonomous fashion mediated through the microenvironment. We also found that non-cell autonomous driving and clonal interference stabilizes sub-clonal heterogeneity, thereby enabling inter-clonal interactions leading to new phenotypic traits. Utilizing the same model, we identified cooperative interactions between IL11- and FIGF- expressing sub-clones that enhance the metastatic behavior of the tumor as a whole. We found that metastatic cooperation between these two populations result in larger and heterogeneous lung metastasis. Using expression profiles from primary tumors and corresponding metastatic lesions, we identified several key immune-regulatory and extracellular matrix (ECM) remodeling pathways that promote metastasis in our model system. Lastly, we examined heterotypic interactions between tumor cells and cancer associated fibroblasts (CAFs) to understand the mechanism of resistance to lapatinib. Using a 3D co-culture model, we identified significant sub-type-specific changes in gene expression, metabolic, and therapeutic sensitivity profiles of breast cancer cells induced by CAFs. We identified JAK2/STAT3 pathway and CAF-secreted hyaluronan as major factors contributing to CAF-mediated protection. We also found that close spatial proximity to CAFs impacts therapeutic responses by affecting proliferation rates of cancer cells. In summary, we have used in vitro and in vivo models systems to identify key interactions within populations of tumors cells, as well as between tumor microenvironmental components and cancer cells, to identify mechanisms that influence tumorigenesis, metastasis and drug response. We believe that these findings will increase our understanding of breast cancer heterogeneity and enable us to design better therapeutic regimens to eradicate the disease.
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Volk, Lisa Danielle. "The Combination of Nab-Paclitaxel and Bevacizumab Therapy Synergistically Improves Tumor Response in Xenograft Breast Cancer Models." Available to subscribers only, 2008. http://proquest.umi.com/pqdweb?did=1674100511&sid=1&Fmt=2&clientId=1509&RQT=309&VName=PQD.

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Thesis (M.S.)--Southern Illinois University Carbondale, 2008.
"Department of Medical Microbiology, Immunology, and Cell Biology." Includes bibliographical references (p. 86-119). Also available online.
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Maekawa, Hisatsugu. "A Chemosensitivity Study of Colorectal Cancer Using Xenografts of Patient-Derived Tumor Initiating Cells." Kyoto University, 2018. http://hdl.handle.net/2433/235985.

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Yoshida, Toru. "Antiandrogen bicalutamide promotes tumor growth in a novel androgen-dependent prostate cancer xenograft model derived from a bicalutamide-treated patient." Kyoto University, 2006. http://hdl.handle.net/2433/135622.

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Maftei, Constantin Alin Verfasser], Christine [Akademischer Betreuer] Bayer, Peter [Akademischer Betreuer] [Vaupel, and Gabriele [Akademischer Betreuer] Multhoff. "Determination of the dynamics of tumor hypoxia during radiation therapy using biological imaging on mouse xenograft tumors / Constantin Alin Maftei. Gutachter: Peter Vaupel ; Gabriele Multhoff. Betreuer: Christine Bayer." München : Universitätsbibliothek der TU München, 2013. http://d-nb.info/1034134779/34.

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Liwschitz, Maxim [Verfasser]. "Wirkungen einer kombinierten Hemmung von Angiopoetin 2 und VEGF auf die Tumor-Angiogenese in einem Xenograft-Maus-Modell des kolonrektalen Karzinoms / Maxim Liwschitz." Köln : Deutsche Zentralbibliothek für Medizin, 2016. http://d-nb.info/1084240637/34.

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Tanaka, Kuniaki. "Direct Delivery of piggyBac CD19 CAR T Cells Has Potent Anti-tumor Activity against ALL Cells in CNS in a Xenograft Mouse Model." Kyoto University, 2021. http://hdl.handle.net/2433/261609.

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Huang, Yingbo. "Intrapulmonary Inoculation of Multicellular Tumor Spheroids to Construct an Orthotopic Lung Cancer Xenograft Model that Mimics Four Clinical Stages of Non-small Cell Lung Cancer." Scholarly Commons, 2019. https://scholarlycommons.pacific.edu/uop_etds/3596.

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Lung cancer leads in mortality among all types of cancer in the US and Non-small cell lung cancer (NSCLC) is the major type of lung cancer. Immuno-compromised mice bearing xenografts of human lung cancer cells represent the most common animal models for studying lung cancer biology and for evaluating potential anticancer agents. However, orthotopic lung cancer models based on intrapulmonary injection of suspended cancer cells feature premature leakage of the cancer cells to both sides of the lung within five days, which generates a quick artifact of metastasis and thus belies the development and progression of lung cancer as seen in the clinic. Based on intrapulmonary inoculation of multicellular spheroids (MCS), we have developed the first orthotopic xenograft model of lung cancer that simulates all four clinical stages of NSCLC progression in mice over one month: Stage 1 localized tumor at the inoculation site; Stage 2 multiple tumor nodules or larger tumor nodule on the same side of the lung; Stage 3 cancer growth on heart surface; and Stage 4 metastatic cancer on both sides of the lung. The cancer development was monitored conveniently by in vivo fluorescent imaging and validated by open-chest anatomy, ex vivo fluorescent imaging, and histological studies. The model enjoys high rates of postoperative survival (100%) and parenchymal tumor establishment (88.9%). The roughness of the inoculated MCS is associated negatively with the time needed to develop metastatic cancer (p=0.0299). In addition, we have constructed a co-culture MCS that consisted of A549-iRFP lung cancer cells and WI38 normal human fibroblast cells. The pro-proliferation effect and the high expression of α-smooth muscle actin (α-SMA) by the co-cultured WI38 cells indicated their transformation from normal fibroblasts to cancer-associated fibroblasts (CAFs). The morphology of the co-culture MCS features a round shape, a tight internal structure, and quicker development of roughness. The large roughness value of co-culture MCS suggests that small co-culture MCS could be inoculated into mice lung with a small needle to reduce the surgical trauma. Taken together, a new orthotopic model of NSCLC has been developed, which would facilitate future development of medications against lung cancer.
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Books on the topic "Tumor xenograft"

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Winograd, Benjamin, Michael Peckham, and Herbert Michael Pinedo, eds. Human Tumour Xenografts in Anticancer Drug Development. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-73252-2.

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Seminar on Human Tumour Xenografts (1986 Milan, Italy). Human tumour xenografts in anticancer drug development. Berlin: Springer-Verlag, 1988.

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B, Winograd, Peckham Michael J, Pinedo H. M, and European School of Oncology, eds. Human tumour xenografts in anticancer drug development. Berlin: Springer, 1988.

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Patient Derived Tumor Xenograft Models. Elsevier, 2017. http://dx.doi.org/10.1016/c2015-0-00204-0.

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Uthamanthil, Rajesh, Peggy Tinkey, and Elisa de Stanchina. Patient Derived Tumor Xenograft Models: Promise, Potential and Practice. Elsevier Science & Technology Books, 2016.

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Tinkey, Peggy, Elisa de Stanchina, and Rajesh K. Uthamanthil. Patient Derived Tumor Xenograft Models: Promise, Potential and Practice. Elsevier Science & Technology Books, 2016.

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Winograd, Benjamin. Human Tumour Xenografts in Anticancer Drug Development. Springer, 2012.

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Pinedo, Herbert M., Michael Peckham, and Benjamin Winograd. Human Tumour Xenografts in Anticancer Drug Development. Springer London, Limited, 2013.

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(Editor), H. M. Pinedo, ed. Human Tumour Xenografts in Anticancer Drug Development (Eso Monographs (European School of Oncology)). Springer, 1988.

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Book chapters on the topic "Tumor xenograft"

1

Liu, Ming, and Daniel Hicklin. "Human Tumor Xenograft Efficacy Models." In Tumor Models in Cancer Research, 99–124. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-968-0_5.

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Presta, Marco, Giulia De Sena, and Chiara Tobia. "The Zebrafish/Tumor Xenograft Angiogenesis Assay." In The Textbook of Angiogenesis and Lymphangiogenesis: Methods and Applications, 253–68. Dordrecht: Springer Netherlands, 2012. http://dx.doi.org/10.1007/978-94-007-4581-0_16.

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Lin, Dong, Xinya Wang, Peter W. Gout, and Yuzhuo Wang. "Patient-Derived Tumor Xenografts: Historical Background." In Patient-Derived Xenograft Models of Human Cancer, 1–9. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-55825-7_1.

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Annibali, Daniela, Eleonora Leucci, Els Hermans, and Frédéric Amant. "Development of Patient-Derived Tumor Xenograft Models." In Metabolic Signaling, 217–25. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-8769-6_15.

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Dong, Xin, Peter W. Gout, Lu Yi, Yinhuai Wang, Yong Xu, and Kuo Yang. "First-Generation Tumor Xenografts: A Link Between Patient-Derived Xenograft Models and Clinical Disease." In Patient-Derived Xenograft Models of Human Cancer, 155–76. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-55825-7_11.

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Alley, Michael C., Melinda G. Hollingshead, Donald J. Dykes, and William R. Waud. "Human Tumor Xenograft Models in NCI Drug Development." In Anticancer Drug Development Guide, 125–52. Totowa, NJ: Humana Press, 2004. http://dx.doi.org/10.1007/978-1-59259-739-0_7.

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Suarez, Christopher D., and Laurie E. Littlepage. "Patient-Derived Tumor Xenograft Models of Breast Cancer." In Methods in Molecular Biology, 211–23. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3444-7_19.

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Plowman, Jacqueline, Donald J. Dykes, Melinda Hollingshead, Linda Simpson-Herren, and Michael C. Alley. "Human Tumor Xenograft Models in NCI Drug Development." In Anticancer Drug Development Guide, 101–25. Totowa, NJ: Humana Press, 1997. http://dx.doi.org/10.1007/978-1-4615-8152-9_6.

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Davies, Alastair H., Fraser Johnson, Kirsi Ketola, and Amina Zoubeidi. "The Plasticity of Stem-Like States in Patient-Derived Tumor Xenografts." In Patient-Derived Xenograft Models of Human Cancer, 71–91. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-55825-7_6.

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Lukiewicz, Stanislaw, Przemyslaw Plonka, Beata Plonka, Jolanta Raczek, Stanislawa Pajak, and Krystyna Cieszka. "Animal EPR Studies on Allo- and Xenograft Rejection." In Nitric Oxide in Transplant Rejection and Anti-Tumor Defense, 157–87. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-5081-5_10.

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Conference papers on the topic "Tumor xenograft"

1

Singh, Nagendra S., and Irving W. Wainer. "Abstract B32: GRP55 antagonists alter tumor microenvironment and inhibit tumor growth in a pancreatic tumor xenograft model." In Abstracts: AACR Special Conference on Pancreatic Cancer: Advances in Science and Clinical Care; May 12-15, 2016; Orlando, FL. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.panca16-b32.

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Roy, Somdutta, Kevin Martinez, Arturo Ramirez, Daniel Campton, Joshua Nordberg, Eric Kaldjian, Scott J. Dylla, and Holger Karsunky. "Abstract 646: Feasibility of assessing circulating tumor cells in patient-derived xenograft tumor models." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-646.

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Park, Gyeongsin, Byunghoo Song, Seonghak Lee, Chan Kwon Jung Jung, Ahwon Lee, Yang-Guk Chung, Yeong-Jin Choi, Kyo-Young Lee, and Chang Suk Kang. "Abstract 5164: Mesenchymal stromal cells promote tumor engraftment and progression in tumor xenograft model." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-5164.

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Ibrahimov, Emin, Nhu-An Pham, Fannong Meng, Mayleen Sukhram, Dianne Chadwick, Stefano Serra, Patricia Shaw, et al. "Abstract B91: Primary tumor xenograft establishment from pancreatic resection specimens." In Abstracts: AACR Special Conference on Pancreatic Cancer: Progress and Challenges; June 18-21, 2012; Lake Tahoe, NV. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.panca2012-b91.

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Ferenci, Tamas, Johanna Sapi, and Levente Kovacs. "Modelling xenograft tumor growth under antiangiogenic inhibitation with mixed-effects models." In 2016 IEEE International Conference on Systems, Man, and Cybernetics (SMC). IEEE, 2016. http://dx.doi.org/10.1109/smc.2016.7844845.

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Basel, Matthew T., Sanjeev Narayanan, Chanran Ganta, Tej B. Shrestha, Marla Pyle, Stefan H. Bossmann, and Deryl L. Troyer. "Abstract 4820: Developing a xenograft human tumor model in immunocompetent mice." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-4820.

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Liu, Haoyan, Nagma Vohra, Keith Bailey, Magda El-Shenawee, and Alexander Nelson. "Semantic Segmentation of Xenograft Tumor Tissues Imaged with Pulsed Terahertz Technology." In 2022 IEEE International Symposium on Antennas and Propagation and USNC-URSI Radio Science Meeting (AP-S/USNC-URSI). IEEE, 2022. http://dx.doi.org/10.1109/ap-s/usnc-ursi47032.2022.9887166.

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Siu, I.-Mei, Peter C. Burger, Qi Zhao, Jacob Ruzevick, Nick Connis, Christine L. Hann, and Gary L. Gallia. "Abstract 360: Erlotinib inhibits growth of a patient derived chordoma tumor xenograft." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-360.

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Wulf-Goldenberg, Annika, Maria Stecklum, Iduna Fichtner, and Jens Hoffmann. "Abstract 5200: Preclinical model of patient-derived tumor xenograft in humanized mice." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-5200.

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Schueler, Julia, Mariette Heins, Artem Shatillo, Kimmo Lehtimäki, Anne-Lise Peille, Taina-Kaisa Stenius, Timo Bragge, Jussi Rytkönen, Diana Miszczuk, and Tuulia Huhtala. "Abstract 2774: Longitudinal characterization of patient-derived orthotopic xenograft brain tumor models." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-2774.

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Reports on the topic "Tumor xenograft"

1

Li, Xiao-Nan. Harnessing Autopsied DIPG Tumor Tissues for Orthotopic Xenograft Model Development in the Brain Stems of SCID Mice. Fort Belvoir, VA: Defense Technical Information Center, September 2012. http://dx.doi.org/10.21236/ada568355.

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