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DTSTART;TZID=Europe/Madrid:20170303T100000
DTEND;TZID=Europe/Madrid:20170303T110000
DTSTAMP:20260422T020908
CREATED:20170213T103423Z
LAST-MODIFIED:20170215T152756Z
UID:27594-1488535200-1488538800@ibecbarcelona.eu
SUMMARY:IBEC Seminar: Maria Virumbrales
DESCRIPTION:“Development of microfluidic tools to reproduce and characterize the tumor microenvironment”\nMaria Virumbrales\, University of Zaragoza\nCompelling evidence over the years has demonstrated that the tumor microenvironment (TME) shapes tumor initiation\, development and response to therapy. This results in a high heterogeneity within the same cancer type\, and hinders the process of finding effective treatments.[1\,2] \nIn this context\, microfluidics has proven a worthy sum of techniques to create comprehensive and personalized cancer in vitro 3D models reproducing the TME in a more relevant fashion than traditional in vitro setups. \nMicrofluidics also permits a high degree of control over the setup\, combining different cell types in an orderly manner\, as well as different physical and biochemical cues. [3] Furthermore\, microfluidics facilitates optical inspection and diminishes sample sizes and reagent volumes needed for each experiment. Microfluidic devices are also compatible with high-throughput approaches\, which make them an interesting option for drug testing\, research and development.[4] \nHence\, we developed two microfluidic tumor models\, which we used to model and characterize different aspects of the TME. TME was characterized in terms of hypoxia\, proliferation rates\, reactive oxygen species concentration\, apoptosis rate and glucose uptake.[5] Moreover\, the influence of tumor cells on an endothelium was investigated. Furthermore\, we carried out pharmacodynamic and drug efficiency studies in these newly-established models. Thereafter\, we developed a simple enzymatic protocol to extract cells seeded in 3D from the microfluidic devices. Cells could be sorted by flow cytometry according to the expression of specific surface markers or by using different fluorescent stains. RNA was extracted for downstream quantification and gene profiling was carried out for the mentioned aspects of the tumor microenvironment. \nAll in all\, we developed two easy-to-use microfluidic models for personalized medicine capable of comprehensive reproduction of the TME\, which allows characterization of tumor signatures by means of microscopy and traditional benchtop methods. \n\nBalkwill FR\, Capasso M\, Hagemann T (2012) The tumor microenvironment at a glance. J Cell Sci 125: 5591-5596.\nKlemm F\, Joyce JA (2015) Microenvironmental regulation of therapeutic response in cancer. Trends Cell Biol 25: 198-213.\nSackmann EK\, Fulton AL\, Beebe DJ (2014) The present and future role of microfluidics in biomedical research. Nature 507: 181-189.\nDu G\, Fang Q\, den Toonder JMJ (2016) Microfluidics for cell-based high throughput screening platforms—A review. Analytica Chimica Acta 903: 36-50.\nAyuso JM\, Virumbrales-Munoz M\, Lacueva A\, Lanuza PM\, Checa-Chavarria E\, et al. (2016) Development and characterization of a microfluidic model of the tumour microenvironment. Sci Rep 6: 36086.\n\n 
URL:https://ibecbarcelona.eu/event/ibec-seminar-maria-virumbrales/
CATEGORIES:IBEC Seminar
END:VEVENT
BEGIN:VEVENT
DTSTART;TZID=Europe/Madrid:20170303T100000
DTEND;TZID=Europe/Madrid:20170303T110000
DTSTAMP:20260422T020908
CREATED:20170213T103423Z
LAST-MODIFIED:20170213T103423Z
UID:95988-1488535200-1488538800@ibecbarcelona.eu
SUMMARY:IBEC Seminar: Maria Virumbrales
DESCRIPTION:“Development of microfluidic tools to reproduce and characterize the tumor microenvironment”\nMaria Virumbrales\, University of Zaragoza\nCompelling evidence over the years has demonstrated that the tumor microenvironment (TME) shapes tumor initiation\, development and response to therapy. This results in a high heterogeneity within the same cancer type\, and hinders the process of finding effective treatments.[1\,2] \nIn this context\, microfluidics has proven a worthy sum of techniques to create comprehensive and personalized cancer in vitro 3D models reproducing the TME in a more relevant fashion than traditional in vitro setups. \nMicrofluidics also permits a high degree of control over the setup\, combining different cell types in an orderly manner\, as well as different physical and biochemical cues. [3] Furthermore\, microfluidics facilitates optical inspection and diminishes sample sizes and reagent volumes needed for each experiment. Microfluidic devices are also compatible with high-throughput approaches\, which make them an interesting option for drug testing\, research and development.[4] \nHence\, we developed two microfluidic tumor models\, which we used to model and characterize different aspects of the TME. TME was characterized in terms of hypoxia\, proliferation rates\, reactive oxygen species concentration\, apoptosis rate and glucose uptake.[5] Moreover\, the influence of tumor cells on an endothelium was investigated. Furthermore\, we carried out pharmacodynamic and drug efficiency studies in these newly-established models. Thereafter\, we developed a simple enzymatic protocol to extract cells seeded in 3D from the microfluidic devices. Cells could be sorted by flow cytometry according to the expression of specific surface markers or by using different fluorescent stains. RNA was extracted for downstream quantification and gene profiling was carried out for the mentioned aspects of the tumor microenvironment. \nAll in all\, we developed two easy-to-use microfluidic models for personalized medicine capable of comprehensive reproduction of the TME\, which allows characterization of tumor signatures by means of microscopy and traditional benchtop methods. \n\nBalkwill FR\, Capasso M\, Hagemann T (2012) The tumor microenvironment at a glance. J Cell Sci 125: 5591-5596.\nKlemm F\, Joyce JA (2015) Microenvironmental regulation of therapeutic response in cancer. Trends Cell Biol 25: 198-213.\nSackmann EK\, Fulton AL\, Beebe DJ (2014) The present and future role of microfluidics in biomedical research. Nature 507: 181-189.\nDu G\, Fang Q\, den Toonder JMJ (2016) Microfluidics for cell-based high throughput screening platforms—A review. Analytica Chimica Acta 903: 36-50.\nAyuso JM\, Virumbrales-Munoz M\, Lacueva A\, Lanuza PM\, Checa-Chavarria E\, et al. (2016) Development and characterization of a microfluidic model of the tumour microenvironment. Sci Rep 6: 36086.\n\n 
URL:https://ibecbarcelona.eu/event/ibec-seminar-maria-virumbrales-2/
CATEGORIES:IBEC Seminar
END:VEVENT
BEGIN:VEVENT
DTSTART;TZID=Europe/Madrid:20170306T120000
DTEND;TZID=Europe/Madrid:20170306T130000
DTSTAMP:20260422T020908
CREATED:20170222T083846Z
LAST-MODIFIED:20170222T083846Z
UID:96001-1488801600-1488805200@ibecbarcelona.eu
SUMMARY:IBEC Seminar: David Cahen
DESCRIPTION:Electron Transport across Peptides and Proteins\nProf. David Cahen\, Weizmann Institute of Science\nElectron transport (ETp)\, i.e.\, electronic conduction across peptides and proteins in a solid state–like configuration is surprisingly efficient\, and comparable to\, or at times even more efficient than via completely conjugated molecules of comparable length. Working with modified proteins and with homopeptides we find both cofactors and secondary structure to matter for ETp efficiency. An open question is if contact to the external world is the dominant factor\, or intra-protein transport. This is important\, also for electron transfer\, ET: nature regulates ET via redox chemistry\, i.e.\, injection and extraction of electrons; this is where ET and ETp are related\, because the analog in the latter is the coupling to the electrodes. In ET control over the process is achieved at the free energy price of a redox event\, but no redox process is required for ETp. This allows studying ETp via non-redox proteins\, such as rhodopsins or albumins (“dopable” proteins)\, pointing to peptides as efficient transport media; studying transport via\, including coupling to them\, can help to learn about protein ETp.
URL:https://ibecbarcelona.eu/event/ibec-seminar-david-cahen-2/
CATEGORIES:IBEC Seminar
END:VEVENT
BEGIN:VEVENT
DTSTART;TZID=Europe/Madrid:20170306T120000
DTEND;TZID=Europe/Madrid:20170306T130000
DTSTAMP:20260422T020908
CREATED:20170222T083846Z
LAST-MODIFIED:20170303T081702Z
UID:27719-1488801600-1488805200@ibecbarcelona.eu
SUMMARY:IBEC Seminar: David Cahen
DESCRIPTION:Electron Transport across Peptides and Proteins\nProf. David Cahen\, Weizmann Institute of Science\nElectron transport (ETp)\, i.e.\, electronic conduction across peptides and proteins in a solid state–like configuration is surprisingly efficient\, and comparable to\, or at times even more efficient than via completely conjugated molecules of comparable length. Working with modified proteins and with homopeptides we find both cofactors and secondary structure to matter for ETp efficiency. An open question is if contact to the external world is the dominant factor\, or intra-protein transport. This is important\, also for electron transfer\, ET: nature regulates ET via redox chemistry\, i.e.\, injection and extraction of electrons; this is where ET and ETp are related\, because the analog in the latter is the coupling to the electrodes. In ET control over the process is achieved at the free energy price of a redox event\, but no redox process is required for ETp. This allows studying ETp via non-redox proteins\, such as rhodopsins or albumins (“dopable” proteins)\, pointing to peptides as efficient transport media; studying transport via\, including coupling to them\, can help to learn about protein ETp.
URL:https://ibecbarcelona.eu/event/ibec-seminar-david-cahen/
CATEGORIES:IBEC Seminar
END:VEVENT
BEGIN:VEVENT
DTSTART;TZID=Europe/Madrid:20170329T120000
DTEND;TZID=Europe/Madrid:20170329T130000
DTSTAMP:20260422T020908
CREATED:20170308T135727Z
LAST-MODIFIED:20170308T135727Z
UID:96007-1490788800-1490792400@ibecbarcelona.eu
SUMMARY:IBEC Seminar: Aranzazu Villasante
DESCRIPTION:Cancer Engineering: Strategies to Engineer Predictable Tumor Models\nDr. Aranzazu Villasante\, Department of Biomedical Engineering\, Columbia University\, New York\nAlthough many drugs show promise in monolayer or in animal models systems\, most fail to translate in humans and this is because they lack of ability to replicate the human microenvironment in patients. In response to these limitations\, I have generated a set of predictable tissue-engineered (TE) models of cancer by using different strategies. Today\, I am going to focus on some of these approaches to engineer pediatric tumors in vitro. Firstly\, I will show a TE model of Ewing’s sarcoma (ES) within its bone niche. This particular strategy is based on engineered human bone by introducing osteoclasts in co-culture with osteoblasts in the 3-dimensional bone niche. This model mimics bone remodeling and recapitulates some of the features observed in the osteolytic process in cancer and also\, the effects of the therapeutic reagent Zoledronic acid observed in patients. The second strategy consists in designing biomaterials with the same tumor composition to mimic the biological and mechanical properties of tumors from patients. I have developed 3D porous collagen 1-hyaluronic acid scaffolds (Col1-HA scaffolds) for studies of tumor derivedexosomes\, which are known to be initiators of pre-metastatic niche formation in certain sites. Interestingly\, I found high levels of a critical mediator of ES growth and metastasis (EZH2) in exosomes isolated from both patients and TE model of ES. Alternatively\, we cultured TE models based on Col1-HA scaffolds into a mechanical loading bioreactor for better mimicking biomechanical forces in ES. We found that biomechanical stimuli modulate osteolytic-related proteins (i.e. RUNX2) and sensitivity to anticancer drugs\, such as Sorafenib. I will also explain the use of perfusion bioreactors and cell sheet engineering to develop a novel model of Neuroblastoma (NB) to study the effect of consolidative drugs\, such as Isotretinoin\, on tumor vasculature and stem-like cells. Here\, I will show the existence of sub-populations of NB cells with different levels of stemness properties; these levels are related to the capacity of stem-like cells to transdifferentiate and also\, to chemoresistance and relapse. Finally\, the take-home message of my talk will be that TE models can bridge the gap between 2D in vitro cultures and in vivo animal models in a predictive\, inexpensive and low timeconsuming fashion for successfully understand cancer biology and improve cancer treatments.
URL:https://ibecbarcelona.eu/event/ibec-seminar-aranzazu-villasante-2/
CATEGORIES:IBEC Seminar
END:VEVENT
BEGIN:VEVENT
DTSTART;TZID=Europe/Madrid:20170329T120000
DTEND;TZID=Europe/Madrid:20170329T130000
DTSTAMP:20260422T020908
CREATED:20170308T135727Z
LAST-MODIFIED:20170308T135727Z
UID:28031-1490788800-1490792400@ibecbarcelona.eu
SUMMARY:IBEC Seminar: Aranzazu Villasante
DESCRIPTION:Cancer Engineering: Strategies to Engineer Predictable Tumor Models\nDr. Aranzazu Villasante\, Department of Biomedical Engineering\, Columbia University\, New York\nAlthough many drugs show promise in monolayer or in animal models systems\, most fail to translate in humans and this is because they lack of ability to replicate the human microenvironment in patients. In response to these limitations\, I have generated a set of predictable tissue-engineered (TE) models of cancer by using different strategies. Today\, I am going to focus on some of these approaches to engineer pediatric tumors in vitro. Firstly\, I will show a TE model of Ewing’s sarcoma (ES) within its bone niche. This particular strategy is based on engineered human bone by introducing osteoclasts in co-culture with osteoblasts in the 3-dimensional bone niche. This model mimics bone remodeling and recapitulates some of the features observed in the osteolytic process in cancer and also\, the effects of the therapeutic reagent Zoledronic acid observed in patients. The second strategy consists in designing biomaterials with the same tumor composition to mimic the biological and mechanical properties of tumors from patients. I have developed 3D porous collagen 1-hyaluronic acid scaffolds (Col1-HA scaffolds) for studies of tumor derivedexosomes\, which are known to be initiators of pre-metastatic niche formation in certain sites. Interestingly\, I found high levels of a critical mediator of ES growth and metastasis (EZH2) in exosomes isolated from both patients and TE model of ES. Alternatively\, we cultured TE models based on Col1-HA scaffolds into a mechanical loading bioreactor for better mimicking biomechanical forces in ES. We found that biomechanical stimuli modulate osteolytic-related proteins (i.e. RUNX2) and sensitivity to anticancer drugs\, such as Sorafenib. I will also explain the use of perfusion bioreactors and cell sheet engineering to develop a novel model of Neuroblastoma (NB) to study the effect of consolidative drugs\, such as Isotretinoin\, on tumor vasculature and stem-like cells. Here\, I will show the existence of sub-populations of NB cells with different levels of stemness properties; these levels are related to the capacity of stem-like cells to transdifferentiate and also\, to chemoresistance and relapse. Finally\, the take-home message of my talk will be that TE models can bridge the gap between 2D in vitro cultures and in vivo animal models in a predictive\, inexpensive and low timeconsuming fashion for successfully understand cancer biology and improve cancer treatments.
URL:https://ibecbarcelona.eu/event/ibec-seminar-aranzazu-villasante/
CATEGORIES:IBEC Seminar
END:VEVENT
END:VCALENDAR