Academic literature on the topic 'Multicellular tumour spheroids'

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Journal articles on the topic "Multicellular tumour spheroids"

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Molla, Annie, Morgane Couvet, and Jean-Luc Coll. "Unsuccessful mitosis in multicellular tumour spheroids." Oncotarget 8, no. 17 (February 24, 2017): 28769–84. http://dx.doi.org/10.18632/oncotarget.15673.

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Hargrave, P., P. W. Nicholson, D. T. Delpy, and M. Firbank. "Optical properties of multicellular tumour spheroids." Physics in Medicine and Biology 41, no. 6 (June 1, 1996): 1067–72. http://dx.doi.org/10.1088/0031-9155/41/6/010.

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SANTINI, M. T., G. RAINALDI, and P. L. INDOVINA. "Multicellular tumour spheroids in radiation biology." International Journal of Radiation Biology 75, no. 7 (January 1999): 787–99. http://dx.doi.org/10.1080/095530099139845.

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Jamieson, L. E., D. J. Harrison, and C. J. Campbell. "Chemical analysis of multicellular tumour spheroids." Analyst 140, no. 12 (2015): 3910–20. http://dx.doi.org/10.1039/c5an00524h.

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Sheth, Disha B., and Miklόs Gratzl. "Electrochemical mapping of oxygenation in the three-dimensional multicellular tumour hemi-spheroid." Proceedings of the Royal Society A: Mathematical, Physical and Engineering Sciences 475, no. 2225 (May 2019): 20180647. http://dx.doi.org/10.1098/rspa.2018.0647.

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Blood capillaries deliver oxygen and nutrients to surrounding micro-regions of tissue and carry away metabolic waste. In normal tissue, capillaries are close enough to keep all the cells viable. In solid tumours, the capillary system is chaotic and typical inter-capillary distances are larger than in normal tissue. Therefore, hypoxic regions develop. Drug molecules may not reach these areas at concentrations above the lethal level. The combined effect of low drug concentrations and local hypoxia, often exacerbated by acidity, leads to therapy failure. To better understand the interplay between hypoxia and poor drug penetration, oxygenation needs to be assessed in different areas of inter-capillary tissue. The multicellular tumour spheroid is a well-established three-dimensional (3D) in vitro model of the capillary microenvironment. It is used to mimic nascent tumours and micro-metastases as well. In this work, we demonstrate for the first time that dynamic intra-spheroidal oxygen maps can be obtained at the 3D multicellular tumour hemi-spheroid (MCH) using a non-invasive microelectrode array. The same oxygen distributions exist inside the equivalent but less accessible full spheroid. The MCH makes high throughput—high content analysis of spheroids feasible and thus can assist studies on basic cancer biology, drug development and personalized medicine.
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Grimes, David Robert, Catherine Kelly, Katarzyna Bloch, and Mike Partridge. "A method for estimating the oxygen consumption rate in multicellular tumour spheroids." Journal of The Royal Society Interface 11, no. 92 (March 6, 2014): 20131124. http://dx.doi.org/10.1098/rsif.2013.1124.

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Hypoxia occurs when oxygen levels within a tissue drop below normal physiological levels. In tumours, hypoxia is associated with poor prognosis, increased likelihood of metastasis and resistance to therapy. Imaging techniques, for example, positron emission tomography, are increasingly used in the monitoring of tumour hypoxia and have the potential to help in the planning of radiotherapy. For this application, improved understanding of the link between image contrast and quantitative underlying oxygen distribution would be very useful. Mathematical models of tissue hypoxia and image formation can help understand this. Hypoxia is caused by an imbalance between vascular supply and tissue demand. While much work has been dedicated to the quantitative description of tumour vascular networks, consideration of tumour oxygen consumption is largely neglected. Oxidative respiration in standard two-dimensional cell culture has been widely studied. However, two-dimensional culture fails to capture the complexities of growing three-dimensional tissue which could impact on the oxygen usage. In this study, we build on previous descriptions of oxygen consumption and diffusion in three-dimensional tumour spheroids and present a method for estimating rates of oxygen consumption from spheroids, validated using stained spheroid sections. Methods for estimating the local partial pressure of oxygen, the diffusion limit and the extents of the necrotic core, hypoxic region and proliferating rim are also derived. These are validated using experimental data from DLD1 spheroids at different stages of growth. A relatively constant experimentally derived diffusion limit of 232 ± 22 μm and an O 2 consumption rate of 7.29 ± 1.4 × 10 −7 m 3 kg −1 s −1 for the spheroids studied was measured, in agreement with laboratory measurements.
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Chignola, R., A. Schenetti, E. Chiesa, R. Foroni, S. Sartpris, A. Brendolan, G. Tridente, G. Andrighetto, and D. Liberati. "Oscillating growth patterns of multicellular tumour spheroids." Cell Proliferation 32, no. 1 (February 1999): 39–48. http://dx.doi.org/10.1046/j.1365-2184.1999.3210039.x.

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McMillan, Kay S., Anthony G. McCluskey, Annette Sorensen, Marie Boyd, and Michele Zagnoni. "Emulsion technologies for multicellular tumour spheroid radiation assays." Analyst 141, no. 1 (2016): 100–110. http://dx.doi.org/10.1039/c5an01382h.

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St-Georges-Robillard, Amélie, Maxime Cahuzac, Benjamin Péant, Hubert Fleury, Muhammad Abdul Lateef, Alexis Ricard, Alexandre Sauriol, Frédéric Leblond, Anne-Marie Mes-Masson, and Thomas Gervais. "Long-term fluorescence hyperspectral imaging of on-chip treated co-culture tumour spheroids to follow clonal evolution." Integrative Biology 11, no. 4 (April 1, 2019): 130–41. http://dx.doi.org/10.1093/intbio/zyz012.

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Abstract Multicellular tumour spheroids are an ideal in vitro tumour model to study clonal heterogeneity and drug resistance in cancer research because different cell types can be mixed at will. However, measuring the individual response of each cell population over time is challenging: current methods are either destructive, such as flow cytometry, or cannot image throughout a spheroid, such as confocal microscopy. Our group previously developed a wide-field fluorescence hyperspectral imaging system to study spheroids formed and cultured in microfluidic chips. In the present study, two subclones of a single parental ovarian cancer cell line transfected to express different fluorophores were produced and co-culture spheroids were formed on-chip using ratios forming highly asymmetric subpopulations. We performed a 3D proliferation assay on each cell population forming the spheroids that matched the 2D growth behaviour. Response assays to PARP inhibitors and platinum-based drugs were also performed to follow the clonal evolution of mixed populations. Our experiments show that hyperspectral imaging can detect spheroid response before observing a decrease in spheroid diameter. Hyperspectral imaging and microfluidic-based spheroid assays provide a versatile solution to study clonal heterogeneity, able to measure response in subpopulations presenting as little as 10% of the initial spheroid.
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Kerr, David J., Thomas E. Wheldon, Sharyn Hydns, and Stanley B. Kaye. "Cytotoxic drug penetration studies in multicellular tumour spheroids." Xenobiotica 18, no. 6 (January 1988): 641–48. http://dx.doi.org/10.3109/00498258809041702.

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Dissertations / Theses on the topic "Multicellular tumour spheroids"

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Monazzam, Azita. "Multicellular Tumour Spheroids in a Translational PET Imaging Strategy." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2007. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-8196.

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Tindall, Marcus John. "Modelling cell movement and the cell cycle in multicellular tumour spheroids." Thesis, University of Southampton, 2002. https://eprints.soton.ac.uk/50618/.

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The work presented in this thesis is concerned with modelling the effects of cell movement on the growth and formation of cell cycle phase specific regions within solid tumours. A model is proposed in the context of multicellular tumour spheroids (MCTS) and includes a simple model of the cell cycle, where cells move between each cell cycle phase depending on the availability of extracellular nutrient, as well as cell movement via chemotaxis, which varies depending upon the respective cell cycle phase of the cell. Numerical and asymptotic solutions show the model re-produces the well known MCTS structure of an internal quiescent cell region surrounded by a rim of proliferating cells. A further, more interesting result, describes a tumour surrounded by a rim of quiescent cells, with an inner quiescent and an interim proliferating cell region. The resultant solutions are a result of the different cell velocity profiles along with the effects of the cell cycle kinetics in different regions of the tumour. The non-linear form of the conservation equations describing the movement of cells means that solutions with spatial discontinuities in the cell concentrations (shocks) are observed for specific parameter values. Analysis of the effects of the chemotactic response and the cell cycle kinetics, both spatial and temporal, provide insight in to the model's behaviour and shows an understanding of cell cycle kinetics, cell movement and the spatial structure of tumours is important in assisting therapeutic strategies. The effectiveness of apoptosis, as an anti-cancer strategy, is shown to be dependent upon the concentration and spatial organisation of proliferating cells within the respective tumour. Comparison with the experimentally verified model of tumour growth developed by Gompertz allows specific model parameters to be expressed in terms of experimentally known variables. Such analysis shows that Gompertz's model is good at predicting the growth of solid tumours with a proliferating rim, but other models are required to understand the growth of non-uniform, heterogeneous tumours. Experimental justification of the model is provided by considering the observed internalisation of H3 Thymidine labelled cells and inert microspheres within MCTS. Here experimental results show that following adherence to the spheroid edge, the microspheres were all advected towards the centre of the spheroids whilst the labelled cells were spread throughout the proliferating and quiescent outer regions. The cell cycle model which is developed is, unlike previous models, able to account for this observed behaviour. Various simulations are discussed in relation to the original experimental results. These results show the importance of cell movement in providing possible ways of assisting with drug delivery to the more therapeutically resistant regions of solid tumours. Finally the importance of necrosis formation is discussed by a simple extension to the model. Necrosis as a result of quiescent cell death leads to the commonly observed formation of a necrotic core in each case. However, using the model to consider the more recent hypothesis that apoptosis leads to the formation of necrotic regions provides interesting theoretical results.
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Evans, Charlotte L. "The biological and therapeutic significance of tumour necrosis. Identification and characterisation of viable cells from the necrotic core of multicellular tumour spheroids provides evidence of a new micro-environmental niche that has biological and therapeutic significance." Thesis, University of Bradford, 2014. http://hdl.handle.net/10454/13961.

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Tumour necrosis has long been associated with poor prognosis and reduced survival in cancer. Hypotheses to explain this include the idea that as aggressive tumours tend to grow rapidly, they outgrow their blood supply leading to areas of hypoxia and subsequently necrosis. However whilst this and similar hypotheses have been put forward to explain the association, the biological significance of the cells which make up necrotic tissue has been largely ignored. This stems from the belief that because a tumour is more aggressive and fast growing it develops areas of necrosis, rather than, the tumour is more aggressive because it contains areas of necrosis. Which came first like the egg and chicken is yet to be determined, however to date most research has only considered the possibility of the former. Viable cells were found in the necrotic core of Multicellular Tumour Spheroids. When examined these cells were found to be different to the original cell line in terms of proliferation, migration, and chemosensitivity. A proteomic analysis showed that these phenotypical changes were accompanied by changes in a large number of proteins within the cells, some of which could be potential therapeutic targets. Furthermore this has led to a new hypothesis for tumour necrosis and its association with poor prognosis. Necrotic tissue provides a microenvironemental niche for cells with increased survival capabilities. Protected from many chemotherapeutics by their non-proliferative status once conditions improve these cells can return to proliferation and repopulate the tumour with an increasingly aggressive population of cells.
Yorkshire Cancer Research
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Jamieson, Lauren Elizabeth. "Measuring redox potential in 3D breast cancer tumour models using SERS nanosensors." Thesis, University of Edinburgh, 2016. http://hdl.handle.net/1842/25964.

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Cellular redox potential is incredibly important for the control and regulation of a vast number of processes occurring in cells. Disruption of the fine redox balance within cells is has been associated with disease. Of particular interest to my research is the redox gradient that develops in cancer tumours, in which the internal regions are further from vascular blood supply and therefore become starved of oxygen and hypoxic. This makes treatment of these areas a lot more challenging, as radiotherapy approaches rely on the presence of oxygen and, with a poor vascular blood supply, drugs delivered through the blood stream will have poor access to these regions. Currently, there is limited knowledge regarding the quantitative nature of this redox gradient in cancerous tumours. To aid the development of drugs and therapies to overcome this problem, a system that enables quantitative mapping of redox potential through a tumour would be a vital tool. In this work redox sensitive molecules attached to gold nanoparticles (NPs) are delivered to cells and give signals using surface enhanced Raman scattering (SERS). Redox potential changes are monitored quantitatively by ratiometric changes in signal intensity of selected signals in the SER spectra acquired. Multicellular tumour spheroids (MTS) are used as a three dimensional (3D) in vitro tumour model, in which the 3D architecture and gradients observed in tumours in vivo develop. As redox potential is pH dependent and pH is another important physiological characteristic in its own right, a SERS pH sensor was developed and ultimately a system that multiplexes intracellular pH and redox measurement by SERS. Initially, simultaneous redox potential and pH measurements were performed in monolayer culture before extending this to MTS. Photothermal optical coherence tomography (OCT) was used to investigate overall 3D NP distribution in the MTS models. It was possible to control NP delivery to MTS to localise NPs to various regions. Redox potential and pH could then be measured using a fibre optic Raman probe, and spatial response to drug treatment monitored. Intracellular NP localisation was investigated using transmission electron microscopy (TEM), scanning electron microscopy (SEM), helium ion microscopy (HIM) and confocal fluorescence microscopy (CFM) and attempts were made to control NP delivery to particular intracellular compartments.
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Evans, Charlotte Louise. "The biological and therapeutic significance of tumour necrosis : identification and characterisation of viable cells from the necrotic core of multicellular tumour spheroids provides evidence of a new micro-environmental niche that has biological and therapeutic significance." Thesis, University of Bradford, 2014. http://hdl.handle.net/10454/13961.

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Tumour necrosis has long been associated with poor prognosis and reduced survival in cancer. Hypotheses to explain this include the idea that as aggressive tumours tend to grow rapidly, they outgrow their blood supply leading to areas of hypoxia and subsequently necrosis. However whilst this and similar hypotheses have been put forward to explain the association, the biological significance of the cells which make up necrotic tissue has been largely ignored. This stems from the belief that because a tumour is more aggressive and fast growing it develops areas of necrosis, rather than, the tumour is more aggressive because it contains areas of necrosis. Which came first like the egg and chicken is yet to be determined, however to date most research has only considered the possibility of the former. Viable cells were found in the necrotic core of Multicellular Tumour Spheroids. When examined these cells were found to be different to the original cell line in terms of proliferation, migration, and chemosensitivity. A proteomic analysis showed that these phenotypical changes were accompanied by changes in a large number of proteins within the cells, some of which could be potential therapeutic targets. Furthermore this has led to a new hypothesis for tumour necrosis and its association with poor prognosis. Necrotic tissue provides a microenvironemental niche for cells with increased survival capabilities. Protected from many chemotherapeutics by their non-proliferative status once conditions improve these cells can return to proliferation and repopulate the tumour with an increasingly aggressive population of cells.
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Stöhr, Daniela [Verfasser], and Peter [Akademischer Betreuer] Scheurich. "Characterising heterogeneous TRAIL responsiveness and overcoming TRAIL resistance in multicellular tumour spheroids / Daniela Stöhr ; Betreuer: Peter Scheurich." Stuttgart : Universitätsbibliothek der Universität Stuttgart, 2018. http://d-nb.info/1181099277/34.

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Kashtl, Ghasaq J. "Differential membrane-type matrix metalloproteinase expression in phenotypically defined breast cancer cell lines: Comparison of MT-MMP expression in environmentally-challenged 2D monolayer cultures and 3D multicellular tumour spheroids." Thesis, University of Bradford, 2018. http://hdl.handle.net/10454/17346.

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Matrix metalloproteinases (MMPs) are a family of zinc endopeptidases capable of digesting the extracellular matrix (ECM), which is essential for tissue structure and transmitting messages between cells. MMPs play an important role in cancer, controlling cell migration, proliferation, apoptosis, regulation of tumour expansion, angiogenesis and invasion. Previous research has indicated high expression of MT1-MMP in breast cancers suggesting a potential role in tumour progression. Our results confirm that 3D multicellular tumour spheroids (MCTS) using phenotype-specific breast cancer cell lines are a valuable experimental model of the tumour microenvironment. Optimisation of MCTS culture growth conditions using different breast cancer cell lines (MCF-7, T47D, MDA-MB-468 and MDA-MB-231) was performed. Unexpected detection of MT1-MMP in MCF-7 MCTS warranted further investigation. MT1-MMP expression in different micro-environmental conditions, including hypoxia and nutrient deprivation (serum-free induced autophagy) were measured in MCF-7 monolayer cultures and MCTS models using immunofluorescence (IF), immunohistochemistry (IHC) and western blot (WB). MT1-MMP expression was rapidly and irreversibly up-regulated in MCF-7 breast cancer cells under conditions of stress (hypoxia and autophagy) compared to normal conditions suggesting an important role of the culture environment on cells behaviour and protein expression. We employed isobaric tags for relative and absolute quantitation (iTRAQ) technology to correlate MT1-MMP increase with proteomic profiles in MCF-7 breast cancer cell grown under hypoxic, serum-free and 3D MCTS conditions. More than 3500 proteins were identified, which were clustered into groups based on response to unique or shared microenvironment changes. Hypoxic monolayer and spheroid cells exhibited changes in anaerobic metabolism and lipid synthesis, respectively, whereas autophagy resulted in up-regulation of cellular component disassembly. The result indicated multiple drivers of MT1-MMP expression in MCF-7 cells.
Al-Mstansiriya University, Iraq
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Kwok, T. T. "The influence of tumour geometry upon cellular response to cytotoxic agents : An in vitro study using multicellular spheroids." Thesis, University of Cambridge, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.372883.

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Alderden, Rebecca. "The Distribution of Platinum Complexes in Biological Systems." Thesis, The University of Sydney, 2006. http://hdl.handle.net/2123/1419.

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The toxicity of platinum anticancer drugs presents a major obstacle in the effective treatment of tumours. Much of the toxicity stems from a lack of specificity of the drugs for the sites at which they are able to exert maximum anticancer activity. An improved understanding of the behaviour of the drugs in the tumour environment may assist in the rational design of future platinum anticancer agents with enhanced specificity and reduced toxicity. In the work presented herein, the specificity of two classes of platinum anticancer agents was assessed (platinum(IV) cisplatin analogues and platinum(II) anthraquinone complexes). The interaction of the platinum(IV) agents with DNA, believed to be their main cellular target, was examined using XANES spectroscopy. This experiment was designed to assess the ability of the drugs to interact with DNA and thus exert their anticancer activity. It was shown that the platinum(IV) complexes were not reduced by DNA during 48 hr incubation. It was not possible to conclusively determine whether the interaction of the complexes with DNA was direct or platinum(II) catalysed, or whether interaction had occurred at all. The distribution of platinum(II) anthraquinone complexes and their corresponding anthraquinone ligands in tumour cells (A2780 ovarian and DLD-1 colon cancer cell lines) was investigated. The cytotoxicity of the compounds in DLD-1 cells was also assessed. It was found that the compounds were efficiently taken up into the cells and entered the lysosomal compartments almost exclusively. This suggested that the cytotoxicity of the drugs was caused by lysosomal disruption, or that the platinum complexes were degraded, leaving a platinum species to enter the cell nuclei and interact with DNA. Alternatively, the complexes may bind to proteins and transport into the nuclei of the cells, though with their fluorescence quenched by the protein. The penetration and distribution of platinum(IV) complexes was assessed in DLD-1 multicellular tumour spheroids (established models of solid tumours) using a number of synchrotron techniques, including micro-tomography, micro-SRIXE, and micro-XANES. The complexes were found to be capable of penetrating throughout the entire volume of the spheroids. Micro-XANES indicated that in central and peripheral spheroidal regions, bound platinum species were present largely as platinum(II).
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Alderden, Rebecca. "The Distribution of Platinum Complexes in Biological Systems." University of Sydney, 2006. http://hdl.handle.net/2123/1419.

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Doctor of Philosophy (PhD)
The toxicity of platinum anticancer drugs presents a major obstacle in the effective treatment of tumours. Much of the toxicity stems from a lack of specificity of the drugs for the sites at which they are able to exert maximum anticancer activity. An improved understanding of the behaviour of the drugs in the tumour environment may assist in the rational design of future platinum anticancer agents with enhanced specificity and reduced toxicity. In the work presented herein, the specificity of two classes of platinum anticancer agents was assessed (platinum(IV) cisplatin analogues and platinum(II) anthraquinone complexes). The interaction of the platinum(IV) agents with DNA, believed to be their main cellular target, was examined using XANES spectroscopy. This experiment was designed to assess the ability of the drugs to interact with DNA and thus exert their anticancer activity. It was shown that the platinum(IV) complexes were not reduced by DNA during 48 hr incubation. It was not possible to conclusively determine whether the interaction of the complexes with DNA was direct or platinum(II) catalysed, or whether interaction had occurred at all. The distribution of platinum(II) anthraquinone complexes and their corresponding anthraquinone ligands in tumour cells (A2780 ovarian and DLD-1 colon cancer cell lines) was investigated. The cytotoxicity of the compounds in DLD-1 cells was also assessed. It was found that the compounds were efficiently taken up into the cells and entered the lysosomal compartments almost exclusively. This suggested that the cytotoxicity of the drugs was caused by lysosomal disruption, or that the platinum complexes were degraded, leaving a platinum species to enter the cell nuclei and interact with DNA. Alternatively, the complexes may bind to proteins and transport into the nuclei of the cells, though with their fluorescence quenched by the protein. The penetration and distribution of platinum(IV) complexes was assessed in DLD-1 multicellular tumour spheroids (established models of solid tumours) using a number of synchrotron techniques, including micro-tomography, micro-SRIXE, and micro-XANES. The complexes were found to be capable of penetrating throughout the entire volume of the spheroids. Micro-XANES indicated that in central and peripheral spheroidal regions, bound platinum species were present largely as platinum(II).
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Book chapters on the topic "Multicellular tumour spheroids"

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Fasano, Antonio, and Alberto Gandolfi. "The Steady State of Multicellular Tumour Spheroids: A Modelling Challenge." In Lecture Notes on Mathematical Modelling in the Life Sciences, 179–202. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-4178-6_7.

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Goldstick, T. K., W. Mueller-Klieser, B. Bourrat, and L. A. Jurman. "Oxygen Consuming Regions in EMT60/Ro Multicellular Tumour Spheroids Determined by Nonlinear Regression Analysis of Experimental PO2 Profiles." In Oxygen Transport to Tissue IX, 381–88. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4684-7433-6_46.

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Mueller-Klieser, W., and P. Vaupel. "Tetrachlorodecaoxide Improves the Oxygenation Status of Multicellular Tumor Spheroids." In Oxygen Transport to Tissue VIII, 623–32. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-5188-7_75.

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Timmins, Nicholas E., and Lars K. Nielsen. "Generation of Multicellular Tumor Spheroids by the Hanging-Drop Method." In Methods in Molecular Medicine™, 141–51. Totowa, NJ: Humana Press, 2007. http://dx.doi.org/10.1007/978-1-59745-443-8_8.

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Walenta, Stefan, Jörg Dötsch, Beatrice Bourrat-Flöck, and Wolfgang Mueller-Klieser. "Size-Dependent Oxygenation and Energy Status in Multicellular Tumor Spheroids." In Advances in Experimental Medicine and Biology, 889–93. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4684-8181-5_102.

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Weber, F., M. Klinkhammer, B. Rasier, J. List, T. Höll, and M. Brock. "Interstitial Immunotherapy of Multicellular Tumor Spheroids Using Liposomes Containing Tumor Necrosis Factor-α." In Cerebellar Infarct. Midline Tumors. Minimally Invasive Endoscopic Neurosurgery (MIEN), 207–17. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-78801-7_34.

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Degner, F., H. Acker, and F. Pietruschka. "The Possible Linkage between Tumor Cell Metabolism and Tumor Cell Growth in Multicellular Spheroids." In Oxygen Transport to Tissue VIII, 555–64. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-5188-7_68.

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Freyer, James P. "Rates of Oxygen Consumption for Proliferating and Quiescent Cells Isolated from Multicellular Tumor Spheroids." In Advances in Experimental Medicine and Biology, 335–42. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2468-7_44.

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Görlach, A., and H. Acker. "The Relationship of Radiation Sensitivity and Microenvironment of Human Tumor Cells in Multicellular Spheroid Tissue Culture." In Advances in Experimental Medicine and Biology, 343–50. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2468-7_45.

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Khaitan, Divya, and Bilikere S. Dwarakanath. "Radiosensitization and Chemosensitization of Multicellular Tumor Spheroids by 2-Deoxy-d-Glucose is Stimulated by a Combination of TNFα and Glucose Deprivation-Induced Oxidative Stress." In Oxidative Stress in Cancer Biology and Therapy, 85–94. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-397-4_5.

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Conference papers on the topic "Multicellular tumour spheroids"

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LOBJOIS, Valérie, Odile MONDESERT, Céline FRONGIA, Annaick DESMAISON, Aurélie GOMES, Martine CAZALES, and Bernard Ducommun. "Abstract 327: 3D dynamics of the response to cell cycle checkpoint targeting drugs in multicellular tumour spheroids." 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.am2015-327.

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Phillips, Tom. "A versatile and highly customisable platform optimised for live high/super-resolution imaging of invading multicellular tumour spheroids in 3D collagen matrices." In European Light Microscopy Initiative 2021. Royal Microscopical Society, 2021. http://dx.doi.org/10.22443/rms.elmi2021.27.

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Valerio, Trisha I., Coline Furrer, Ashley R. Hoover, and Wei R. Chen. "Effects of photothermal therapy on multicellular tumor spheroids." In Biophotonics and Immune Responses XVII, edited by Wei R. Chen. SPIE, 2022. http://dx.doi.org/10.1117/12.2611599.

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Hye-Jin Jin, Taeyoon Kim, Young-Ho Cho, Jin-Mo Gu, Jhingook Kim, and Yong-Soo Oh. "A multicellular tumor spheroid formation and extraction chip." In 2010 IEEE 10th Conference on Nanotechnology (IEEE-NANO). IEEE, 2010. http://dx.doi.org/10.1109/nano.2010.5697838.

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Mokrani, N., O. Felfoul, Fatemeh Afkhami Zarreh, M. Mohammadi, R. Aloyz, G. Batist, and S. Martel. "Magnetotactic bacteria penetration into multicellular tumor spheroids for targeted therapy." In 2010 32nd Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC 2010). IEEE, 2010. http://dx.doi.org/10.1109/iembs.2010.5627105.

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Burattini, E. "Synchrotron Radiation μ-X Ray Fluorescence on Multicellular Tumor Spheroids." In X-RAY AND INNER-SHELL PROCESSES. AIP, 2003. http://dx.doi.org/10.1063/1.1536413.

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Shahid, Mohammed, Sunaina Arshad, Minru Hwang, Pratik K. Patel, Elaine Y. Yu, and Charles M. Roth. "Systematic nanoparticle diffusivity estimation using multicellular tumor spheroid model." In 2012 38th Annual Northeast Bioengineering Conference (NEBEC). IEEE, 2012. http://dx.doi.org/10.1109/nebc.2012.6207058.

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AlHasan, Layla, Aisha Qi, Aswan Al-Aboodi, Amged Rezk, Richie R. Shilton, Peggy P. Y. Chan, James Friend, and Leslie Yeo. "Surface acoustic streaming in microfluidic system for rapid multicellular tumor spheroids generation." In SPIE Micro+Nano Materials, Devices, and Applications, edited by James Friend and H. Hoe Tan. SPIE, 2013. http://dx.doi.org/10.1117/12.2034050.

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Desmaison, Annaïck, Katia Grenier, Celine Frongia, Corinne Lorenzo, Bernard Ducommun, and Valerie Lobjois. "Abstract 560: Mechanical stress activates a mitotic checkpoint in multicellular tumor spheroids." 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.am2013-560.

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Suh, S., E. J. Leaman, Ying Zhan, and B. Behkam. "Mathematical Modeling of Bacteria-Enabled Drug Delivery System Penetration into Multicellular Tumor Spheroids." In 2018 40th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2018. http://dx.doi.org/10.1109/embc.2018.8513596.

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Reports on the topic "Multicellular tumour spheroids"

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Furbert-Harris, Paulette M. Eosinophil Cell Lines in a Tri-Cell Multicellular Tumor Spheroid (MTS)/Endothelium Complex: Down Regulation of Adhesion and Integrin Molecules-Implications of Metastasis Inhibition. Fort Belvoir, VA: Defense Technical Information Center, October 2003. http://dx.doi.org/10.21236/ada442676.

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