Relevant bibliographies by topics / Xenograft tumors

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Academic literature on the topic 'Xenograft tumors'

Author: Grafiati
Published: 6 September 2023

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Journal articles on the topic "Xenograft tumors"

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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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Pham, Khoa, Allison R. Hanaford, Brad A. Poore, Micah J. Maxwell, Heather Sweeney, Akhila Parthasarathy, Jesse Alt, et al. "Comprehensive Metabolic Profiling of MYC-Amplified Medulloblastoma Tumors Reveals Key Dependencies on Amino Acid, Tricarboxylic Acid and Hexosamine Pathways." Cancers 14, no. 5 (March 3, 2022): 1311. http://dx.doi.org/10.3390/cancers14051311.

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Reprograming of cellular metabolism is a hallmark of cancer. Altering metabolism allows cancer cells to overcome unfavorable microenvironment conditions and to proliferate and invade. Medulloblastoma is the most common malignant brain tumor of children. Genomic amplification of MYC defines a subset of poor-prognosis medulloblastoma. We performed comprehensive metabolic studies of human MYC-amplified medulloblastoma by comparing the metabolic profiles of tumor cells in three different conditions—in vitro, in flank xenografts and in orthotopic xenografts in the cerebellum. Principal component analysis showed that the metabolic profiles of brain and flank high-MYC medulloblastoma tumors clustered closely together and separated away from normal brain and in vitro MYC-amplified cells. Compared to normal brain, MYC-amplified medulloblastoma orthotopic xenograft tumors showed upregulation of the TCA cycle as well as the synthesis of nucleotides, hexosamines, amino acids and glutathione. There was significantly higher glucose uptake and usage in orthotopic xenograft tumors compared to flank xenograft tumors and cells in culture. In orthotopic tumors, glucose was the main carbon source for the de novo synthesis of glutamate, glutamine and glutathione through the TCA cycle. In vivo, the glutaminase II pathway was the main pathway utilizing glutamine. Glutathione was the most abundant upregulated metabolite in orthotopic tumors compared to normal brain. Glutamine-derived glutathione was synthesized through the glutamine transaminase K (GTK) enzyme in vivo. In conclusion, high MYC medulloblastoma cells have different metabolic profiles in vitro compared to in vivo, and key vulnerabilities may be missed by not performing in vivo metabolic analyses.
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Kijima, Noriyuki, Yoshikazu Nakajima, Daisuke Kanematsu, Tomoko Shofuda, Yuichiro Higuchi, Hiroshi Suemizu, Kanji Mori, et al. "TMOD-29. ESTABLISHMENT OF PATIENT-DERIVED XENOGRAFTS FROM RARE PRIMARY BRAIN TUMORS." Neuro-Oncology 22, Supplement_2 (November 2020): ii234. http://dx.doi.org/10.1093/neuonc/noaa215.979.

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Abstract Patient derived xenografts are essential tools for translational research and preclinical development of novel therapeutic strategies of primary brain tumors. Recent advances in genomics of primary brain tumors revealed molecular classification of primary brain tumors, thus establishment of patient derived xenografts from each subtype of primary brain tumors is urgently needed. However, currently available patient derived xenografts are limited and are from specific subtype of primary brain tumors such as glioblastoma IDH wild type. In this study, we aim to establish patient derived xenografts from primary brain tumors with various molecular characteristics, especially rare primary brain tumors. We got primary brain tumor tissues from patients, dissociated those tissue into single cells, and orthotopically injected those cells into NOD/Shi-scid IL2Rγ KO mouse. We successfully established rare patient-derived xenografts from atypical teratoid rhabdoid tumor and CNS Ewing sarcoma family tumor with CIC alteration, which is recently described as new entity of primitive neuroectodermal tumors of the CNS. We also analyzed histopathological characteristics of these xenografts and found that each xenograft well recapitulated histopathological features of original patients’ resected tumors. These xenografts have advantages for translational research and preclinical development of novel therapeutic strategies for rare primary brain tumors. In addition, further efforts are needed to establish other types of rare primary brain tumors.
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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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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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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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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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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 "Xenograft tumors"

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Cataldo, A. "ANTI-TUMOR ACTIVITY OF CPG-ODN IN OVARIAN XENOGRAFT TUMORS." Doctoral thesis, Università degli Studi di Milano, 2014. http://hdl.handle.net/2434/229558.

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Synthetic oligodeoxynucleotides expressing CpG motifs (CpG-ODN), Toll-like receptor 9 (TLR9) agonists, are able to induce innate/adaptive immune responses and can enhance the antitumor activity of DNA-damaging chemotherapy and radiation therapy in preclinical mouse models. It was recently reported that peritumoral CpG-ODN treatment in preclinical models of ovarian cancer, activating TLR-9 expressing cells in tumor microenvironment, induces modulation of DNA repair genes and sensitizes cancer cells to DNA-damaging Cisplatin treatment. In this thesis we investigated whether this treatment induces modulation of miRNAs in tumor cells and their relevance to chemotherapy response. Array analysis identified 20 differentially expressed miRNAs (16 down- and 4 up-regulated) in human IGROV-1 ovarian tumor cells from CpG-ODN-treated mice versus controls. Evaluation of the role of the 3 most differentially expressed miRNAs on sensitivity to Cisplatin of IGROV-1 cells revealed significant increased Cisplatin cytotoxicity upon ectopic expression of hsa-miR-302b (up-modulated in our array), but no increased effect upon reduced expression of hsa-miR-424 or hsa-miR-340 (down-modulated in our array). The impact of expression levels of all 20 differentially expressed miRNAs were associated with time to replase and overall survival probability in two data sets of ovarian cancer patients treated with platinum. It was found that hsa-miR-302b expression was significantly associated with time to relapse or overall survival in these patients. Use of bio-informatics tools identified 19 mRNAs potentially targeted by hsa-miR-302b, including HDAC4 gene, which has been reported to mediate Cisplatin sensitivity in ovarian cancer. Both HDAC4 mRNA and protein levels were significantly reduced in IGROV-1 cells overexpressing hsa-miR-302b. Altogether, these findings indicate that hsa-miR-302b acts as a ‘‘chemosensitizer’’ in human ovarian carcinoma cells and may represent a biomarker able to predict response to Cisplatin treatment. Moreover, the identification of miRNAs that improve sensitivity to chemotherapy provides the experimental underpinning for their possible future clinical use. In the second part of this thesis we tested the efficacy of CpG-ODN in combination with other possible therapeutic agents in ovarian carcinoma ascites-bearing athymic mice, to mimic clinical treatment situations in advanced human ovarian disease. Mice injected i.p. with IGROV-1 ovarian cancer cells were treated at different stages of ascites progression for 4 weeks with CpG-ODN alone or in combination with Bevacizumab, Polyinosinic:Polycytidylic acid (Poly(I):Poly(C)), Gefitinib, Cetuximab and Cisplatin. In mice treated when ascitic fluid began to accumulate, CpG-ODN combined with Bevacizumab, Poly(I): Poly(C) or Gefitinib did not significantly increase Median Survival Times (MST), as compared with that using CpG-ODN alone, whereas MST in mice treated with CpG-ODN plus Cetuximab was significantly increased (>103 days for combination vs 62 days for CpG alone; P = 0.0008), with 4/8 mice alive at the end of the experiment. In mice showing evident and established ascites, evaluated with increase of abdominal volume and body weight (27.9 ± 0.8 g after vs 23 ± 1.1 g before tumor cell injection), treatment with Cisplatin in addition to CpG-ODN/Cetuximab led to significantly increased MST (105.5 days; P = 0.001), with all mice still alive at 85 days, over that using CpG ODN/Cetuximab (66 days), Cetuximab/Cisplatin (18.5 days), Cisplatin (23 days) or saline (16 days). At a very advanced stage of disease (body weight: 31.4 ± 0.9 g), when more than half of control mice had to be sacrificed 6 days after starting treatments, the triple-combination therapy still increased MST (45 days; P = 0.0089) vs controls. These data indicated that CpG-ODN combination therapies that enhance the immune response in the tumor microenvironment and concomitantly target tumor cells are highly efficacious even in experimental advanced malignancies. Although differences in the distribution of TLR9 in mice and humans and the enrichment of this receptor on innate immune cells of athymic mice must be considered, our results indicate a promising strategy to treat ovarian cancer patients with bulky ascites.
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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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Pfeffer, Nils Christian Verfasser], and Udo [Akademischer Betreuer] [Schumacher. "Expression of HIF-1alpha and GLUT-1 in human xenograft tumors in immundeficient mice / Nils Christian Pfeffer. Betreuer: Udo Schumacher." Hamburg : Staats- und Universitätsbibliothek Hamburg, 2013. http://d-nb.info/1038789192/34.

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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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Carpenter, Kent James. "Inhibition of PIM and AXL Kinases As Potential Treatments for a Variety of Hematological Malignancies and Solid Tumors." BYU ScholarsArchive, 2014. https://scholarsarchive.byu.edu/etd/3842.

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This thesis is divided into three chapters. In each case, the goal is to achieve inhibition of a growth kinase (PIM or AXL) and subsequent arrest of cell growth and induction of apoptosis (in vitro cell culture models) or decrease in tumor volume (in vivo xenograft studies). Chapter one and chapter two discuss inhibition of proviral integration site for Moloneymurine leukemia virus (PIM) kinases. The three PIM kinases, PIM-1, PIM-2, and PIM-3, are a subfamily of serine/threonine kinases that are known to be involved in signaling pathways as downstream effectors of signal transducer and activator of transcription-5 (STAT5) signaling and inhibitors of apoptosis. PIM kinases are implicated in a large percentage of hematological malignancies and solid tumors. Because they have been shown to correlate with disease progression and poor prognosis in many of these conditions, PIM kinase inhibitors are being developed and investigated for therapeutic use. The aim of this study in chapter one was to evaluate the role of PIM 1, 2 and 3 in urothelial carcinomas, using second generation Pan-PIM kinase inhibitor TP-3654. Retrospective immunohistochemical analysis of bladder cancer specimens found that PIM 1, 2, and 3 was expressed in a significant number of cases. PIM-1 was expressed in 4 bladder cancer cell lines and TP-3654 treatment was able to inhibit BAD phosphorylation to induce apoptosis. The second aim of this study was to investigate the effects of TP-3654 on the interaction of c-MYC with PIM kinase family members. The data indicate that PIM-1 only interacts with c-MYC in the acute myeloid leukemia (AML) and multiple myeloma (MM) cell lines studied, and that PIM-1 siRNA knockdown or treatment with TP-3654 is able to decrease this interaction. The third chapter discusses inhibition of the receptor tyrosine kinase Axl. Pancreatic cancer is a highly lethal disease characterized by malignant cells that rapidly disseminate from the primary tumor to form local and distant metastases. Axl is overexpressed in over 50% of pancreatic cancers and expression of Axl in these cancers is highly associated with a poor prognostic outcome for patients. Small molecule inhibitors of AXL are currently under investigation, as AXL is associated with cell migration mediated by epithelial-mesenchymal transition (EMT). The aim of this study was to investigate the effects of a small molecule inhibitor of AXL, TP-0903, on pancreatic cancer cell lines. Consistent with the known function of Axl, TP-0903 inhibited Gas6-induced migration and invasion of pancreatic cancer cells invitro and potently induced apoptosis. Additionally, we found that inhibition of AXL decreased expression of EMT marker genes and induced mesenchymal pancreatic cancer cell lines to take on an epithelial phenotype. TP-0903 also significantly inhibited the growth of pancreatic cancer cell lines grown in xenograft tumor mouse model and taken together, the results suggest Axl is a potential therapeutic target in pancreatic cancer and TP-0903 as a potential therapeutic agent.
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SARONNI, DAVIDE. "TYROSINE KINASE INHIBITORS IN NEUROENDOCRINE TUMORS: FROM IN VITRO TO ZEBRAFISH MODEL." Doctoral thesis, Università degli Studi di Milano, 2022. http://hdl.handle.net/2434/917967.

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(1) Background: Neuroendocrine neoplasms (NENs) are a group of tumors that arise from neuroendocrine cells throughout the body, with the lungs and gastrointestinal tract being the most common sites of origin. In patients with NENs and distant metastases, surgery is generally not curative. Although well-differentiated and low-grade NENs, classified as neuroendocrine tumors (NETs), are usually less aggressive than poorly-differentiated NENs, they can develop distant metastases in about 15% of cases. These patients require chronic medical management. However, the clinical efficacy of these treatments is limited by the low objective response rate, due to the occurrence of tumor resistance and the high biological heterogeneity of these neoplasms. (2) Research problem: We addressed this study on two rare NETs: lung neuroendocrine tumors (LNETs) and medullary thyroid carcinoma (MTC). LNETs represent about 2% of lung tumors, while MTCs are rare thyroid tumors caused by mutations in the RET proto-oncogene. Both NETs are well-differentiated neoplasms and are known to be highly vascularized. Therefore, they represent a potential target for tyrosine kinase inhibitors (TKIs) selective for receptors involved in angiogenesis. The aim of this project was to evaluate the antitumor activity of several new TKIs both in vitro, using LNETs (NCI-H727, UMC-11 and NCI-H835) and MTC (TT and MZ-CRC-1) cell lines, and in vivo, adopting a novel zebrafish xenograft model to study angiogenesis. In LNETs we tested: sulfatinib, a small molecule that inhibits the Vascular Endothelial Growth Factor Receptor (VEGFR) 1, 2, and 3, and the Fibroblast Growth Factor Receptor type 1 (FGFR1); cabozantinib, a multi-target inhibitor selective for VEGFR2, c-Met, Kit, Axl and Flt3; and axitinib, a multi-target TKI of VEGFR1, 2, 3 and Platelet-Derived Growth Factor Receptor-beta (PDGFRβ). In MTC we tested: sulfatinib; SPP86, a RET-specific inhibitor; and SU5402, an inhibitor of the FGFR1 and VEGFR2. (3) Methodology: In LNETs and MTC cells the effects of selected TKIs have been evaluated in vitro through: MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) and MTS (3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium) assays, for assessing cell viability; flow-cytometer analysis, for the evaluation of cell cycle and apoptosis; and wound-healing assay, to study cell migration. In vivo we took advantage of the transgenic zebrafish line of Tg(fli1a:EGFP)y1. Through the xenotransplantation of NET cells in the subperidermal space near the subintestinal vein, we assessed the effects of TKIs on tumor-induced angiogenesis and cancer dissemination. (4) Key Results: In LNET cell lines we observed a dose-dependent decrease in cell viability after incubation with all TKIs. This effect seems to be related to the perturbation of the cell cycle and induction in apoptosis. In NCI-H727 wound healing assay showed a significant reduction in cell migration only after incubation with cabozantinib. In the zebrafish model, we found a significant reduction of the tumor-induced angiogenesis in implanted LNET cell lines after treatment with all TKIs. Cabozantinib and axitinib were more potent than sulfatinib in inhibition of angiogenesis, while cabozantinib was the most efficient in reducing cell migration from the transplantation site to the tail. In MTC cell lines, sulfatinib, SU5402 and SPP86 showed a decrease in cell viability, confirmed by the significant reduction in S phase cell population. Moreover, sulfatinib and SPP86 showed for both cell lines a significant induction of apoptosis. Sulfatinib and SPP86 inhibited the migration of TT and MZCRC-1 cells, evaluated through the wound healing assay, while SU5402 was able to inhibit migration only in TT cells. In vivo we observed a significant reduction of TT cells-induced angiogenesis in zebrafish embryos after treatment with sulfatinib and SPP86. (5) Conclusions: Despite sulfatinib resulted the most potent compound in terms of inhibition of LNET cell proliferation, cabozantinib showed in vivo the most effective impact in reducing tumor-induced angiogenesis. Cabozantinib was the only TKI able to inhibit in vivo the dissemination of implanted LNET cells. According to these data, cabozantinib could represent a potential candidate in the therapy of patients with highly vascularized LNET. In MTC cell lines, SPP86 and sulfatinib displayed a similar antitumor activity both in vitro and in vivo, suggesting a good efficacy of specific RET inhibitors (SPP86) with potentially less adverse effects than multitarget TKIs (sulfatinib). In addition, this study showed that the zebrafish model for NETs represents an innovative tool for drug screening with several advantages compared with rodent models: rapidity of procedure, animal immune suppression is not required, lower number of tumor cells for implant and the optical transparency provides a real-time monitoring of cell-stromal interactions and cancer progression in living animals.
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Walter, Thomas. "Métastases hépatiques de tumeurs endocrines digestives : développement de modèles animaux pour l’étude des mécanismes biologiques et l’évaluation préclinique des thérapeutiques." Thesis, Lyon 1, 2010. http://www.theses.fr/2010LYO10241.

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Les métastases hépatiques de tumeurs endocrines digestives sont hypervasculaires et hétérogènes. Les mécanismes de développement de ces métastases hépatiques, en particulier le rôle de l’angiogenèse tumorale associée à ces tumeurs, sont complexes. Ceci explique la difficulté de prédire le profil évolutif de ces tumeurs et de trouver des facteurs prédictifs de réponses aux traitements médicaux utilisés. L’objectif de notre travail a été de mieux comprendre : le rôle de l’angiogenèse dans le développement des métastases hépatiques de tumeurs endocrines digestives ; les mécanismes d’actions et en particulier leur activité anti-angiogénique, de deux types de molécules (analogue de la somatostatine et inhibiteur de mTOR). Nos résultats nous ont permis à travers une double approche expérimentale, in vitro et in vivo de : (a) montrer la complexité de la régulation de la synthèse et de la sécrétion du VEGF par les cellules endocrines néoplasiques ; (b) confirmer expérimentalement la dissociation entre expression du VEGF et capacités angiogéniques d’une part, propriétés invasives et métastatiques d’autre part, dans les tumeurs endocrines digestives ; (c) montrer expérimentalement que l’inhibition de l’angiogenèse peut contribuer à l’effet anti-tumoral de substances d’intérêt thérapeutique dans les tumeurs endocrines digestives
Liver metastases of digestive endocrine tumors are hypervascular and heterogeneous. The mechanisms of development of these metastases, especially the role of angiogenesis, are complex. This explains the difficulty to predict the natural history of these tumors and to find predictive factors of response to medical treatments. Our aim was to evaluate: the role of angiogenesis in the development of liver metastasis from digestive endocrine tumors; mechanisms of action, especially antiangiogenic activity, of two drugs (somatostatin analogues and mTOR inhibitor). We were able to demonstrate through an in vitro and in vivo experimental approach that: (a) the regulation of VEGF synthesis and secretion is complex, with different roles according to the cell studied; (b) there is a dissociation between VEGF expression and angiogenic capacities, on one hand, and invasive and metastatic properties, on the other hand; (c) the inhibition of angiogenesis may contribute to the anti-tumoral effect of several drugs of therapeutic interest in digestive endocrine tumors
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9

Faizi, M. A. H. P. "The effect of hyperthermia and irradiation on a human ovary tumour xenograft." Thesis, Bucks New University, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.380292.

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Huang, Ting [Verfasser], and Aladár [Gutachter] Szalay. "Vaccinia Virus-mediated Therapy of Solid Tumor Xenografts: Intra-tumoral Delivery of Therapeutic Antibodies / Ting Huang. Gutachter: Aladar Szalay." Würzburg : Universität Würzburg, 2015. http://d-nb.info/1108780555/34.

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Books on the topic "Xenograft tumors"

1

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

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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 "Xenograft tumors"

1

O’Hara, Julia A., Rosalyn D. Blumenthal, Oleg Y. Grinberg, Stalina Grinberg, Carmen Wilmot, David M. Goldenberg, and Harold M. Swartz. "Tumor pO2 Assessments in Human Xenograft Tumors Measured by EPR Oximetry: Location of Paramagnetic Materials." In Oxygen Transport to Tissue XXIV, 205–14. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4615-0075-9_20.

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

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Qazi, Maleeha, Aneet Mann, Randy van Ommeren, Chitra Venugopal, Nicole McFarlane, Parvez Vora, and Sheila K. Singh. "Generation of Murine Xenograft Models of Brain Tumors from Primary Human Tissue for In Vivo Analysis of the Brain Tumor-Initiating Cell." In Stem Cells and Tissue Repair, 37–49. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1435-7_4.

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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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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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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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Kopper, L., P. Nagy, J. Rajnay, and K. Lapis. "Xenografted Human Tumors in Preclinical Drug Design." In Human Tumour Xenografts in Anticancer Drug Development, 138. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-73252-2_31.

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Green, Colin, Hakim Djeha, Gail Rowlinson-Busza, Christina Kousparou, and Agamemnon A. Epenetos. "Xenograft Mouse Models for Tumour Targeting." In Antibody Engineering, 463–76. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-01147-4_35.

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Sharma, Surinder K., and R. Barbara Pedley. "Xenograft Mouse Models for Tumour Targeting." In Antibody Engineering, 477–90. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-01147-4_36.

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Conference papers on the topic "Xenograft tumors"

1

Singh-Gupta, Vinita, Fulvio Lonardo, Joseph Rakowski, Christopher Yunker, Shirish Gadgeel, and Gilda Hillman. "Abstract LB-264: Axitinib improves radiotherapy for murine xenograft lung tumors." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-lb-264.

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Samkoe, Kimberley S., Alina Chen, Imran Rizvi, Julia A. O'Hara, P. Jack Hoopes, Tayyaba Hasan, and Brian W. Pogue. "Magnetic resonance image-guided photodynamic therapy of xenograft pancreas tumors with verteporfin." In SPIE BiOS: Biomedical Optics, edited by David H. Kessel. SPIE, 2009. http://dx.doi.org/10.1117/12.809857.

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Nguyen, Uyen, Johanna Webb, Rebecca Schmitz, Kelsey Tweed, Anna Huttenlocher, Melissa C. Skala, and Alex J. Walsh. "Optical imaging of zebrafish xenograft tumors for a high throughput drugs screen." In Multiscale Imaging and Spectroscopy II, edited by Kristen C. Maitland, Darren M. Roblyer, and Paul J. Campagnola. SPIE, 2021. http://dx.doi.org/10.1117/12.2577637.

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Saito, Tomoki, Shinya Ohashi, Ayaka Mizumoto, Osamu Kikuchi, Kotaro Matsumoto, Aoi Komatsu, Seiji Naganuma, et al. "Abstract 1670: Characterization of the chick chorioallantoic membrane tumor model in comparison with various xenograft mouse tumors." 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.am2020-1670.

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Chou, Ting-Chao, Xiuguo Zhang, Huajin Dong, and Samuel J. Danishefsky. "Abstract 3527: Therapeutic cure against five human xenograft tumors and strongly suppressed drug-resistant and refractory xenograft tumors in nude mice by the third generation epothilone: Iso-oxazole fludelone." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-3527.

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Brabetz, Sebastian, Huriye Seker-Cin, Susanne N. Gröbner, Norman L. Mack, Volker Hovestadt, David T. W. Jones, Till Milde, et al. "Abstract A07: Molecular characterization of patient-derived xenograft models of pediatric brain tumors." In Abstracts: Patient-Derived Cancer Models: Present and Future Applications from Basic Science to the Clinic; February 11-14, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1557-3265.pdx16-a07.

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Garmendia, Irati, Cristina Bértolo, Irene Ferrer, María J. Pajares, Daniel Ajona, Luis Paz-Ares, Ruben Pio, Luis M. Montuenga, and Jackeline Agorreta. "Abstract LB-084: Dasatinib reduces tumor growth in xenograft models derived from human lung tumors with YES1 overexpression." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-lb-084.

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Qi, Lin, Baxter A. Patricia, Kogiso Mari, Du Yuchen, Lindsay Holly, Liu Zhigang, Xiumei Zhao, et al. "Abstract 1450: Autopsy derived orthotopic xenograft (ADOX) mouse models for terminal pediatric brain tumors." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-1450.

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Olson, Devra J., Anita Kulukian, Janelle D. Taylor, Margo C. Zaval, Albina Nesterova, Kelly M. Hensley, Michelle L. Ulrich, Nicole S. Stevens, and Scott R. Peterson. "Abstract 1962: Preclinical characterization of tucatinib in HER2-amplified xenograft and CNS implanted tumors." 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.am2020-1962.

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Brabetz, Sebastian, Susanne N. Gröbner, Huriye Seker-Cin, Florian Selt, Till Milde, David T. Jones, Madison T. Wise, et al. "Abstract 1935: Molecular characterization of orthotopic patient-derived xenograft models of pediatric brain tumors." 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.am2017-1935.

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Reports on the topic "Xenograft tumors"

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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