Bibliografias temáticas / Preclinical oncology

Literatura científica selecionada sobre o tema "Preclinical oncology"

Autor: Grafiati

Publicado: 20 de julho de 2024

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Artigos de revistas sobre o assunto "Preclinical oncology"

Kahn, Jenna, Philip J. Tofilon e Kevin Camphausen. "Preclinical models in radiation oncology". Radiation Oncology 7, n.º 1 (2012): 223. http://dx.doi.org/10.1186/1748-717x-7-223.

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Kumari, Rajendra. "Refining Preclinical Modeling in Oncology". Genetic Engineering & Biotechnology News 33, n.º 19 (novembro de 2013): 34–35. http://dx.doi.org/10.1089/gen.33.19.14.

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Ibarrola-Villava, Maider, Andrés Cervantes e Alberto Bardelli. "Preclinical models for precision oncology". Biochimica et Biophysica Acta (BBA) - Reviews on Cancer 1870, n.º 2 (dezembro de 2018): 239–46. http://dx.doi.org/10.1016/j.bbcan.2018.06.004.

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Gardner, Eric E., e Charles M. Rudin. "Preclinical oncology — reporting transparency needed". Nature Reviews Clinical Oncology 13, n.º 1 (15 de dezembro de 2015): 8–9. http://dx.doi.org/10.1038/nrclinonc.2015.216.

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Clézardin, Philippe, Ismahène Benzaïd e Peter I. Croucher. "Bisphosphonates in preclinical bone oncology". Bone 49, n.º 1 (julho de 2011): 66–70. http://dx.doi.org/10.1016/j.bone.2010.11.017.

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Thöni, C. "Preclinical research in oncology: Gender aspects". memo - Magazine of European Medical Oncology 4, n.º 4 (dezembro de 2011): 217–20. http://dx.doi.org/10.1007/s12254-011-0295-y.

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BOULEFTOUR, WAFA, BENOITE MERY, ELISE ROWINSKI, CHARLENE RIVIER, ELISABETH DAGUENET e NICOLAS MAGNE. "Cardio-Oncology Preclinical Models: A Comprehensive Review". Anticancer Research 41, n.º 11 (novembro de 2021): 5355–64. http://dx.doi.org/10.21873/anticanres.15348.

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Wittenburg, Luke A., e Daniel L. Gustafson. "Optimizing preclinical study design in oncology research". Chemico-Biological Interactions 190, n.º 2-3 (abril de 2011): 73–78. http://dx.doi.org/10.1016/j.cbi.2011.01.029.

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Zumberg, Marc S., Virginia C. Broudy, Elizabeth M. Bengtson e Scott D. Gitlin. "Preclinical Medical Student Hematology/Oncology Education Environment". Journal of Cancer Education 30, n.º 4 (31 de janeiro de 2015): 711–18. http://dx.doi.org/10.1007/s13187-014-0778-8.

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Hormuth, David A., Anna G. Sorace, John Virostko, Richard G. Abramson, Zaver M. Bhujwalla, Pedro Enriquez‐Navas, Robert Gillies et al. "Translating preclinical MRI methods to clinical oncology". Journal of Magnetic Resonance Imaging 50, n.º 5 (29 de março de 2019): 1377–92. http://dx.doi.org/10.1002/jmri.26731.

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Teses / dissertações sobre o assunto "Preclinical oncology"

Loskog, Angelica. "Immunogene Therapy of Bladder Carcinoma : A Preclinical Study". Doctoral thesis, Uppsala universitet, Enheten för onkologi, 2002. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-2637.

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This thesis comprises studies on murine and human models of bladder carcinoma with the aim to develop novel immunogene therapies. On the basis of the results presented in this thesis, a clinical trial is underway. The potential of activating the immune system to combat cancer has long intrigued immunologists. Research has now been intensified and clinically effective treatments are beginning to materialize. We evaluated the induction of anti-tumor responses by inserting immunomodulating genes into tumor cells with adenovectors. Human biopsies and cell lines were positive for adenovirus attachment receptors, and cell lines were easily transduced. CD40L modified cells efficiently induced maturation of dendritic cell (DC). Phenotypical changes of AdCD40L transduced cells, such as increased apoptotic rate, upregulated MHC-I, Fas and TNFR may further strengthen the anti-tumor response. CD40L modified murine bladder cancer cells activated systemic immunity upon vaccination and in situ injections of AdCD40L inhibited tumor progression. Cytotoxic assays revealed the presence of cytotoxic T cells (CTLs) in vaccinated mice. Many tumors have developed ways to evade the immune system. Bladder carcinoma is associated with immune escape mechanisms like IL10 production. We demonstrated that immunosuppression by IL10 inhibited CTL function and that IL10 suppression may be reverted by AdCD40L therapy. In conclusion, AdCD40L therapy induces systemic immunity and inhibits tumor progression in murine models. The immunological mechanisms involve maturation of nearby DCs and CTL induction. AdCD40L therapy is effective despite immune escape mechanisms, e.g. IL10 secretion. The thesis argues for using AdCD40L immunogene therapy as a treatment of bladder carcinoma.

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Chaffee, Beth K. "Preclinical Modeling of Musculoskeletal Cancer". The Ohio State University, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=osu1376844544.

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Venugopal, Balaji. "Preclinical evaluation of a novel drug delivery system for cisplatin". Thesis, University of Glasgow, 2012. http://theses.gla.ac.uk/4198/.

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The aim of this body of work was to characterise a novel cisplatin drug delivery system and to develop new tools based on biophotonic imaging that could be used to enhance studies of drug delivery in vivo. Cucurbiturils (CB) are macrocycles which are formed by acid catalysed condensation of glycoluril and formaldehyde. The internal cavity of CB[7] encapsulates a single molecule of cisplatin and the hypothesis was that encapsulation would reduce thiol degradation of the drug. Drug sensitivity studies in vitro with the cisplatin-sensitive human ovarian cancer cell line, A2780, and a cisplatin-resistant derivative, A2780/cp70, showed that the CB[7] encapsulated cisplatin retained activity but that this encapsulation drug delivery system was not able to overcome resistance to platinum. However, when these cell lines were grown as subcutaneous xenografts in nu/nu mice, the encapsulated cisplatin was able to reduce the growth of A2780/cp70 tumours which are resistant to the maximum tolerated dose of cisplatin in vivo. One possible explanation of this observation is that encapsulation might alter the pharmacokinetics of cisplatin and a method for the detection of platinum in biological samples by ICP-MS was established and validated. This assay was sufficiently sensitive to detect the low levels of platinum present in mouse plasma 24 hours after administration of either free or encapsulated cisplatin. Plasma and tissue pharmacokinetics show that encapsulation had no effect on the peak plasma concentration of cisplatin but did reduce the rate at which cisplatin was cleared from the plasma. The increased plasma AUC of cisplatin resulted in a non-selective increase in the delivery of cisplatin to both tumour and normal tissues. However, there was no apparent increase in toxicity which could be explained by the fact that encapsulation, unlike an increase in the dose of free cisplatin, had no effect on the peak plasma concentration. Subcutaneous xenografts lack critical features of human tumours. The development of more complex models for use in drug development has been limited due to lack of a method for monitoring tumour growth. Biophotonic imaging was, therefore, investigated to determine whether it is sufficiently sensitive and reproducible to be able to evaluate growth of disseminated tumours in mice. The bioluminescent signal is dependent on the metabolism of luciferin by luciferase. Subcutaneous injection of luciferin was shown to produce a consistent signal in all injected mice. The bioluminescent signal was transient but reached a maximum intensity 6 minutes after injection and remained stable for about 4 minutes which defined the window during which measurements were taken. Sensitivity was shown to be dependent on the level of expression of luciferase by the cells. Injection of commercially available HCT116Luc cells, where the luciferase gene was inserted by a lentiviral system, was shown to allow detection of 10,000 cells in the lungs of mice. This sensitivity was about 10 fold greater than was obtained by lipofectamine based gene transfection. When HCT116Luc cells were grown as subcutaneous xenografts in mice, an exponential growth pattern was easily detected by bioluminescence imaging and the reproducibility between mice was comparable to that routinely obtained by calliper measurements. Activity of encapsulated cisplatin was determined in a model of disseminated ovarian cancer. Rab25, a member of the RAS oncoprotein superfamily, is up-regulated in around 80% of ovarian cancer samples compared to normal ovarian epithelium. Rab25 contributes to tumour progression by enabling the tumour cells to invade the extracellular matrix by altering the trafficking of integrin. Transfection of Rab25 into A2780 cells results in cells that can grow in the peritoneal cavity of mice. A2780-Rab25 cells were 4 fold resistant to cisplatin in vitro which confirms a previous observation that Rab25 expression in A2780 makes them less sensitive to the induction of apoptosis in response to stress. A2780-Rab25 cells that express the luciferase gene (A2780-Rab25Luc) were injected into the peritoneal cavity of mice and growth was measured by biophotonic imaging. Exponential growth was clearly apparent at a stage at which no obvious abdominal distension was apparent. The disseminated A2780-Rab25Luc tumour xenografts were less sensitive to cisplatin than are subcutaneous xenografts of A2780. This is the first study that suggests that Rab25 over-expression results in reduced drug sensitivity in vivo. In contrast, a very significant growth inhibition was observed when mice were treated with an equivalent dose of encapsulated cisplatin regardless of whether it was administered by the intraperitoneal or subcutaneous route. These results are very encouraging since they confirm the enhanced activity of encapsulated cisplatin and also demonstrate the value of biophotonic imaging for measurement of tumour growth in vivo. Pharmacodynamic measures of drug activity in vivo in animal models are often based either on measures of surrogate tissue response or on single measures on tumour tissue removed at the end of the experiment. Biophotonic imaging in vivo allows the translation of reporter assays used in cell lines in vitro to studies of tumour response in vivo. A plasmid was prepared that links the p53 transcriptional response element to the luciferase gene and it was then transfected in to A2780 cells which express wild type p53. Stable transfectants of A2780p53Luc were treated with cisplatin, doxorubicin and paclitaxel and induction of p53 determined by bioluminescence and confirmed by Western blotting. A very low bioluminescent signal was present in untreated cells and a clear dose dependent increase in bioluminescence was seen in response to all three drugs. When A2780p53Luc cells were grown as subcutaneous xenografts the bioluminescent signal was significant in untreated tumours but was markedly increased 24 hours after treatment of the mice with cisplatin. Induction of p53 in the tumours was confirmed by immunohistochemistry and this also confirmed significant expression of p53 in untreated tumours. The possible implications of these findings for the improved delivery of cisplatin are discussed.

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Martín, Liberal Juan Jesús. "Combination of cytotoxic agents and targeted therapy for the treatment of advanced sarcomas: preclinical background and early clinical development". Doctoral thesis, Universitat de Barcelona, 2016. http://hdl.handle.net/10803/401753.

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Sarcomas are a group of malignancies characterized by their bad prognosis and the absence of effective treatments. Median survival of advanced sarcoma patients is only one year in spite of treatment. Therefore, it is mandatory to identify new therapeutic strategies. Our hypothesis is that the inhibition of angiogenesis and the mTOR pathway in sarcomas in combination with active cytotoxic agents enhances each strategy alone without increase in toxicity. To confirm such hypothesis, we conducted two phase I trials with associated preclinical studies which have been published in international scientific journals. Article 1: Phase I trial of sorafenib in combination with ifosfamide in patients with advanced sarcoma: a Spanish group for research on sarcomas (GEIS) study. Background: This phase I trial assessed safety, pharmacokinetics (PK), dose limiting toxicity (DLT), maximum tolerated dose and recommended dose (RD) of the combination of sorafenib plus ifosfamide in patients with advanced sarcoma. Methods: Twelve sarcoma patients (9 soft-tissue, 3 bone sarcoma) were treated with sorafenib plus ifosfamide (starting doses 200 mg bid and 6 g/m(2) respectively). A 3 + 3 dose escalation design with cohorts of 3-6 patients was used. A study to assess the in vitro efficacy of the combination was also conducted. Results: Three DLTs were observed: fatigue grade 4 with sorafenib 400 mg bid plus ifosfamide 6 g/m(2) and encephalopathy and emesis grade 3 with sorafenib 400 mg bid plus ifosfamide 7.5 g/m(2). Other toxicities included diarrhea, hand-foot syndrome, mucositis, neutropenia, skin rash and thrombocytopenia. There were no relevant effects on PK of sorafenib but an increase in ifosfamide active metabolite 4-hydroxy-ifosfamide was observed. Eight patients achieved stable disease lasting more than 12 weeks. An additive effect was observed in vitro. Conclusions: RD was sorafenib 400 mg bid plus ifosfamide 6 g/m(2), allowing administration of active doses of both agents. Limited preliminary antitumor activity was also observed. A phase II study is currently ongoing.
Los sarcomas son un grupo de tumores caracterizados por su mal pronóstico y la ausencia de tratamientos efectivos. La mediana de supervivencia de los pacientes afectos de sarcoma avanzado es de tan solo 1 año a pesar de recibir tratamiento. Por lo tanto, es necesario encontrar nuevas estrategias terapéuticas efectivas. Nuestra hipótesis es que la inhibición de la angiogénesis y de la vía de mTOR en sarcomas en combinación con agentes citotóxicos activos potencia la actividad anti tumoral de cada una de las estrategias terapéuticas por separado sin toxicidad significativa. Para confirmar dicha hipótesis realizamos dos ensayos clínicos fase I con experimentos preclínicos asociados que han sido publicados en revistas científicas internacionales. Artículo 1: Ensayo clínico fase I de sorafenib en combinación con ifosfamida en pacientes con sarcoma avanzado: un estudio del Grupo Español de Investigación en Sarcomas (GEIS). Este ensayo clínico fase I evaluó la seguridad, la farmacocinética, la toxicidad limitante de dosis, la dosis máxima tolerada y la dosis recomendada de la combinación de sorafenib más ifosfamida en pacientes con sarcoma avanzado. La dosis recomendada fue sorafenib 400 mg bid más ifosfamida 6 g/m2, un esquema que permite la administración de dosis activas de ambos fármacos. También se observaron signos preliminares de actividad antitumoral. Artículo 2: Ensayo clínico fase I y evaluación de la eficacia preclínica del inhibidor de mTOR sirolimus más gemcitabina en pacientes con tumores sólidos avanzados Llevamos a cabo un ensayo clínico fase I en pacientes con tumores sólidos avanzados para identificar la dosis recomendada, evaluar la PK, la actividad farmacodinámica y la eficacia antitumoral preclínica de la combinación de sirolimus y gemcitabina. La dosis recomendada fue sirolimus 5 mg al día más gemcitabina 800 mg/m2. Además, se observó actividad antitumoral en los modelos preclínicos de sarcoma, así como inhibición de la vía de mTOR.

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Sambandam, Vaishnavi. "The Role of Hedgehog signaling in Hepatitis B virus X protein mediated hepatocellular carcinoma". Diss., Temple University Libraries, 2014. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/292349.

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Biology
Ph.D.
Hepatitis B virus encoded X protein (HBx) contributes centrally to the pathogenesis of hepatocellular carcinoma (HCC). Aberrant activation of the Hedgehog (Hh) pathway has been linked to cancer. Thus, experiments were designed to test the hypothesis that HBx contributes to HCC via activation of Hh signaling. HBx expression correlated with up-regulation of Hh markers in human liver cancer cell lines, in HBx transgenic mice that developed HCC and in liver samples from HBV infected patients with HCC. The findings in human samples provide clinical validation of those in the HBx transgenic mice (HBxTg), and underscore the relevance of these transgenic mice to disease pathogenesis. Further, blockade of Hh signaling inhibited HBx stimulation of cell migration, anchorage independent growth, HCC tumorigenesis in HBx transgenic mice and tumor growth in xenograft model. These results suggest that the ability of HBx to promote cancer is at least partially dependent upon Hh activation and that activation of Hh signaling appears to be important for the development of HBx associated HCC. HBx also activates pathways that stimulate downstream Hh signaling, such as PI3K/AKT and Ras/Raf/MEK, also referred as non-canonical Hh signaling. Upon canonical Hh inhibition, compensatory activation of these pathways was seen in the presence of HBx in liver cancer cell lines and in HBxTg mice. Individual inhibition of these pathways also down-regulated Gli2 expression in HBx positive cell lines. These data suggests that in addition to canonical Hh signaling, activation of PI3K/AKT and ERK pathways by HBx leads to up-regulation of Gli2 expression in HBV-mediated HCC. This work identifies Hh pathway inhibition as a therapeutic strategy to slow tumor development and this work could lead to combination therapies that target Hh, AKT and ERK pathways, which may prevent or delay the appearance/progression of HCC.
Temple University--Theses

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Gullbo, Joachim. "Preclinical Development of New Alkylating Oligopeptides for Cancer Therapy". Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2003. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-3785.

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Jeon, Jae Yoon. "Preclinical and clinical development of kinase inhibitors in acute myeloid leukemia". The Ohio State University, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=osu158699311567933.

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Karlsson, Henning. "New preclinical strategies for characterization and development of anticancer drugs". Doctoral thesis, Uppsala universitet, Cancerfarmakologi och beräkningsmedicin, 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-330999.

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Increased understanding of the molecular mechanisms underlying cancer development has shifted drug discovery towards target driven drug development the last decades, but the development of effective cancer drugs has been hampered by the lack of predictive preclinical models. 3-D cultures, considered to more accurately reflect solid tumors in vivo, have been proposed as one way to increase the predictability of clinical efficacy in cancer drug discovery and development. The aims of this thesis were to improve preclinical models for cancer drug development, with focus on colorectal cancer (CRC) and use of multicellular tumor spheroids (MCTS), and also to mechanistically characterize some potentially new anticancer drugs (papers I – IV). The most important technical improvement was the development of direct measurement of green fluorescent protein (GFP) marked cells in spheroids, simplifying live collection of viability data and enabling high-throughput screening (HTS) in the MCTS model (paper I). In paper III and IV, the 3-D model was adapted to enable studies on the interaction between drugs and radiation. Two potentially new anticancer drugs, VLX50 and VLX60, were mechanistically characterized. VLX60, a novel copper containing thiosemicarbazone, induced reactive oxygen species (ROS) formation, was selectively active against BRAF mutated colon cancer cells and exhibited anticancer activity in vivo (paper II). Furthermore, two potentially new anticancer drugs were found suitable for further development for use in combination with radiation (papers III and IV). In paper III, synergy with radiation in spheroids compared to monolayer cultured colon cancer cells was shown with the novel iron-chelating inhibitor of oxidative phosphorylation, VLX600. In paper IV, the antiprotozoal drug nitazoxanide was shown to sensitize quiescent clonogenic colon cancer cells to radiation. In conclusion, introduction of measurement of fluorescence of GFP marked cells in spheroids makes clinically relevant 3-D models feasible for HTS experiments and characterization of candidate drugs and radiosensitizers in early cancer drug discovery and development. VLX60 has several characteristics suitable for further development into a cancer drug, notably against BRAF mutated colorectal cancer cells. VLX600 and nitazoxanide show radiosensitizing properties making them promising for further development for use as cancer drugs in combination with radiation.

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Recasens, Zorzo Clara. "Preclinical evaluation of the antitumor activity of a new CXCR4 inhibitor: a novel therapeutic approach in diffuse large B-cell lymphoma". Doctoral thesis, Universitat de Barcelona, 2018. http://hdl.handle.net/10803/663897.

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Constitutive activation of the chemokine receptor CXCR4 is associated with tumor progression, invasion and resistance to treatment. Overexpression of CXCR4 in diffuse large B-cell lymphoma (DLBCL) confers a reduced prognosis. However, the biological relevance of this receptor in DLBCL progression remains underexplored. In this thesis, the new CXCR4 inhibitor IQS-01.01 has been preclinicaly evaluated in in vitro and in vivo models of DLBCL. It has been concluded that 1) inhibition of CXCR4 presents antitumor properties in DLBCL, 2) that IQS-01.01RS holds better pharmacological properties than the reference CXCR4 inhibitor, AMD3100 3) that treatment with IQS- 01.01RS reduces the levels of the oncogene MYC and 4) that the combinantion of IQS- 01.01RS with the BET-bromodomain inhibitor, CPI203, is synergistic in DLBCL. The results of this doctoral thesis unravel a cooperation between CXCR4 and MYC in DLBCL, and indicate that CXCR4 inhibition in combination with inhibition of MYC is a promising novel therapeutic approach in DLBCL.
La activación constitutiva del receptor de quemocinas CXCR4 está asociada a la progresión tumoral, invasión y resistencia al tratamiento. En el linfoma difuso de células grandes (LDCG) la sobreexpresión de CXCR4 concede un peor pronóstico, pero la relevancia biológica de este receptor no se ha estudiado en profundidad. En esta tesis se ha evaluado un nuevo inhibidor de CXCR4 (IQS-01.01) en modelos preclínicos de LDCG. Usando tanto modelos in vitro como in vivo de LDCG se ha concluido 1) que la inhibición de CXCR4 en LDCG tiene un efecto antitumoral, 2) que IQS-01.01RS tiene mayores propiedades farmacológicas que el inhibidor de referencia, AMD3100 3) que el tratamiento con IQS-01.01RS reduce los niveles del oncogén MYC y 4) que la combinación de IQS-01.01 RS con el inhibido de BET, CPI203, confiere un efecto antitumoral sinérgico. Los resultados de esta tesis doctoral ponen en evidencia una cooperación entre MYC y CXCR4 en LDCG e indican que la inhibición de CXCR4 en combinación con un inhibidor de MYC es una terapia prometedora contra el LDCG.

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Chakupurakal, Geothy. "Preclinical studies of adenovirus-specific T-cells for adoptive transfer to haemopoietic stem cell transplant recipients". Thesis, University of Birmingham, 2011. http://etheses.bham.ac.uk//id/eprint/2883/.

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Allogeneic stem cell transplantation (SCT) is the only curative treatment option for many haematological malignancies. Adenovirus (Ad) infections are a significant cause of morbidity and mortality post SCT. Lack of effective anti-viral treatment for Ad disease has led to the development of adoptive immunotherapy of Ad-specific T-cells as a promising therapeutic option for patients in this setting. The aim of this project was to establish preclinical criteria for the development of a clinical trial comparing two T-cell enrichment methods- multimer selection and cytokine secretion selection to enrich Ad-specific T-cells for the purposes of adoptive transfer directly without the need for in vitro culture. Eight pHLA tetramers containing HLA class I restricted Ad epitopes were generated and their ability to identify and enrich Ad-specific T-cells investigated. HLA A*01 TDL tetramer consistently detected T-cells in all (13/13) healthy adult donors screened. Frequency and enrichement of Ad-specific T-cells by cytokine secretion and selection was also investigated. Despite the low frequency of Ad-specific T-cells, clinical grade enrichment was feasible by both methods. T-cells selected by both methods were then characterised for homing and proliferative potential. Ad-specific T-cells identified by either method had a high proliferative potential, possessed a novel minimally differentiated memory phenotype, were cytotoxic towards Ad species responsible for infections in SCT recipients and capable of limiting virus replication. In conclusion, Ad-specific T-cells enriched by multimer selection or cytokine secretion selection are suitable for adoptive transfer to patients with Ad infection following HSCT. Both methods also allow the monitoring of Ad-specific immune reconstitution after adoptive transfer.

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Mais fontes

Livros sobre o assunto "Preclinical oncology"

1954-, Adams Julian, ed. Proteasome inhibitors in cancer therapy. Totowa, N.J: Humana Press, 2004.

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1954-, Adams Julian, ed. Proteasome inhibitors in cancer therapy. Totowa, N.J: Humana Press, 2004.

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Fiebig, H. H. Revelance Of Tumor Models For Anticancer Drug Development (CONTRIBUTIONS TO ONCOLOGY). Editado por H. H. Fiebig. Karger, 1999.

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Kerr, David J., e Bruce C. Baguley. Anticancer Drug Development. Elsevier Science & Technology Books, 2001.

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Adams, Julian. Proteasome Inhibitors in Cancer Therapy. Humana Press, 2010.

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(Editor), Bruce C. Baguley, e David J. Kerr (Editor), eds. Anticancer Drug Development. Academic Press, 2001.

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Capítulos de livros sobre o assunto "Preclinical oncology"

Nimmagadda, Sridhar, Sagar Shelake e Martin G. Pomper. "Preclinical Experimentation in Oncology". In Radiopharmaceutical Chemistry, 569–82. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-98947-1_33.

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Seo, Youngho, He Jiang e Benjamin L. Franc. "Preclinical SPECT and SPECT/CT". In Molecular Imaging in Oncology, 193–220. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-10853-2_6.

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Kalen, Joseph D., e James L. Tatum. "Small Animal Imaging in Oncology Drug Development". In Image Fusion in Preclinical Applications, 101–15. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-030-02973-9_5.

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Franc, Benjamin L., Youngho Seo, Robert Flavell e Carina Mari Aparici. "Preclinical SPECT and SPECT-CT in Oncology". In Molecular Imaging in Oncology, 359–404. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-42618-7_11.

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Wolf, Gunter, e Nasreddin Abolmaali. "Preclinical Molecular Imaging Using PET and MRI". In Molecular Imaging in Oncology, 257–310. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-10853-2_9.

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Reichardt, Wilfried, e Dominik von Elverfeldt. "Preclinical Applications of Magnetic Resonance Imaging in Oncology". In Molecular Imaging in Oncology, 405–37. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-42618-7_12.

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Zschaeck, S., e M. Beck. "Whole-Body Hyperthermia in Oncology: Renaissance in the Immunotherapy Era?" In Water-filtered Infrared A (wIRA) Irradiation, 107–15. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-92880-3_8.

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AbstractA short introduction to the use of whole-body hyperthermia (WBH) in oncology is provided. The main focus is on fever-range whole-body hyperthermia (FRWBH), since various preclinical studies have shown promising results using this approach. However, FRWBH has not been comprehensively investigated in clinical oncology trials. Having provided an overview on the methods to induce WBH, we will summarize preclinical and clinical data on the mode of action of FRWBH. The latter treatment positively affects the tumor micromilieu, especially by decreasing tumor hypoxia. It has the potential to enhance tumor-directed immune reactions and has proven anti-depressive and potential analgesic effects in patients without cancer. These pleiotropic effects align with good tolerability and high acceptability by patients. Given the available evidence, we argue that FRWBH should be investigated as an adjunct to modern cancer treatments in controlled clinical trials.

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Rojiani, Mumtaz V., e Amyn M. Rojiani. "Morphologic Manifestations of Vascular-disrupting Agents in Preclinical Models". In Vascular-Targeted Therapies in Oncology, 81–94. Chichester, UK: John Wiley & Sons, Ltd, 2006. http://dx.doi.org/10.1002/0470035439.ch5.

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Chopra, Rajesh, e Florence I. Raynaud. "Preclinical Studies to Enable First in Human Clinical Trials". In Phase I Oncology Drug Development, 45–69. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-47682-3_3.

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Buck, Andreas K., Florian Gärtner, Ambros Beer, Ken Herrmann, Sibylle Ziegler e Markus Schwaiger. "Preclinical and Clinical Tumor Imaging with SPECT/CT and PET/CT". In Drug Delivery in Oncology, 247–88. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2011. http://dx.doi.org/10.1002/9783527634057.ch9.

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Trabalhos de conferências sobre o assunto "Preclinical oncology"

Selt, F., J. Kiss, J. Gronych, DTW Jones, T. Brummer, AE Kulozik, SM Pfister, T. Milde e O. Witt. "Preclinical model development for pilocytic astrocytoma". In 26th Annual Meeting of the working group “Experimental Neuro-Oncology”. Georg Thieme Verlag KG, 2017. http://dx.doi.org/10.1055/s-0037-1607402.

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Xue, Jia, Xiaobo Chen, Xiaoyu An, Jingjing Wang, Henry Li e Sheng Guo. "40 NGS-based immunology panel: applications in preclinical immuno-oncology research". In SITC 37th Annual Meeting (SITC 2022) Abstracts. BMJ Publishing Group Ltd, 2022. http://dx.doi.org/10.1136/jitc-2022-sitc2022.0040.

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Vasciaveo, Alessandro, Min Zou, Juan Arriaga, Andrea Califano e Cory Abate-Shen. "Abstract 822: OncoLoop: Closing the loop between patient-centered drug discovery and preclinical testing in precision-oncology". 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.am2020-822.

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Krueger, Sarah, Thomas Dailey, Kevin Guley e Maryland Franklin. "Abstract 4712: Image-guided focal irradiation in syngeneic preclinical oncology mouse models". 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.am2017-4712.

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Stecklum, Maria, Annika Wulf-Goldenberg, Magdalena Paterka, Bernadette Brzezicha, Iduna Fichtner e Jens Hoffmann. "Abstract A006: Preclinical tumor models in humanized mice for translational immuno-oncology research". In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics; October 26-30, 2017; Philadelphia, PA. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1535-7163.targ-17-a006.

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Lee, Joon Sang, Shannon McGrath, Emma Wang, Maximilian Rogers-Grazado, Yu-an Zhang, Natalia Malkova, Jack Pollard e Alexei Protopopov. "Abstract 174: Genomic cytometry characterization of preclinical models for development of immune-oncology therapeutics". 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.am2020-174.

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Sachsenmeier, Kris F., Nazzareno Dimasi, Qihui Huang, Erin Sult, Binyam Bezabeh, Ryan Fleming, Carl Hay et al. "Abstract 4635: The avidity hypothesis: comparing bispecific and monospecific antibodies in preclinical oncology models." 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.am2013-4635.

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Stecklum, Maria, Annika Wulf-Goldenberg, Bernadette Brzezicha, Konrad Klinghammer, Korinna Jöhrens, Wolfgang Walther e Jens Hoffmann. "Abstract 2713: Preclinical models for translational immuno-oncology research: patient-derived xenografts on humanized mice". In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-2713.

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Ibsen, Eric M., e Jeffrey Kumer. "Abstract 3498: A systematic approach to evaluate and select preclinical study workflow software applications for oncology". In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-3498.

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Brzezicha, Bernadette, Michael Becker, Maria Stecklum, Teresia Conrad, Martin Janz, Aitomi Bittner, Clemens Schmitt, Ulrich Keilholz e Jens Hoffmann. "Abstract 1069: New panel of patient derived lymphoma xenografts (PDX) for preclinical research and immune oncology". In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-1069.

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