Bibliografie tematiche / Cancer-On-Chip

Letteratura scientifica selezionata sul tema "Cancer-On-Chip"

Autore: Grafiati

Pubblicato: 8 giugno 2024

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Articoli di riviste sul tema "Cancer-On-Chip":

Torisawa, Yu-suke, Yuta Mishima e Shin Kaneko. "Developing thymus-on-a-chip and cancer-on-a-chip for cancer immunotherapy". Impact 2019, n. 2 (18 marzo 2019): 33–35. http://dx.doi.org/10.21820/23987073.2019.2.33.

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Zhang, Xiaojun, Mazharul Karim, Md Mahedi Hasan, Jacob Hooper, Riajul Wahab, Sourav Roy e Taslim A. Al-Hilal. "Cancer-on-a-Chip: Models for Studying Metastasis". Cancers 14, n. 3 (27 gennaio 2022): 648. http://dx.doi.org/10.3390/cancers14030648.

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The microfluidic-based cancer-on-a-chip models work as a powerful tool to study the tumor microenvironment and its role in metastasis. The models recapitulate and systematically simplify the in vitro tumor microenvironment. This enables the study of a metastatic process in unprecedented detail. This review examines the development of cancer-on-a-chip microfluidic platforms at the invasion/intravasation, extravasation, and angiogenesis steps over the last three years. The on-chip modeling of mechanical cues involved in the metastasis cascade are also discussed. Finally, the popular design of microfluidic chip models for each step are discussed along with the challenges and perspectives of cancer-on-a-chip models.

Lee, I.-Chi. "Cancer-on-a-chip for Drug Screening". Current Pharmaceutical Design 24, n. 45 (16 aprile 2019): 5407–18. http://dx.doi.org/10.2174/1381612825666190206235233.

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: The oncology pharmaceutical research spent a shocking amount of money on target validation and drug optimization in preclinical models because many oncology drugs fail during clinical trial phase III. One of the most important reasons for oncology drug failures in clinical trials may due to the poor predictive tool of existing preclinical models. Therefore, in cancer research and personalized medicine field, it is critical to improve the effectiveness of preclinical predictions of the drug response of patients to therapies and to reduce costly failures in clinical trials. Three dimensional (3D) tumor models combine micro-manufacturing technologies mimic critical physiologic parameters present in vivo, including complex multicellular architecture with multicellular arrangement and extracellular matrix deposition, packed 3D structures with cell–cell interactions, such as tight junctions, barriers to mass transport of drugs, nutrients and other factors, which are similar to in vivo tumor tissues. These systems provide a solution to mimic the physiological environment for improving predictive accuracy in oncology drug discovery. : his review gives an overview of the innovations, development and limitations of different types of tumor-like construction techniques such as self-assemble spheroid formation, spheroids formation by micro-manufacturing technologies, micro-dissected tumor tissues and tumor organoid. Combination of 3D tumor-like construction and microfluidic techniques to achieve tumor on a chip for in vitro tumor environment modeling and drug screening were all included. Eventually, developmental directions and technical challenges in the research field are also discussed. We believe tumor on chip models have provided better sufficient clinical predictive power and will bridge the gap between proof-of-concept studies and a wider implementation within the oncology drug development for pathophysiological applications.

Hao, Hsu-Chao, e Da-Jeng Yao. "Detection of Cancer Cells on a Chip". Current Topics in Medicinal Chemistry 15, n. 15 (22 maggio 2015): 1543–50. http://dx.doi.org/10.2174/1568026615666150414150950.

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Elmusrati, Mohammed, e Nureddin Ashammakhi. "Cancer-on-a-Chip and Artificial Intelligence". Journal of Craniofacial Surgery 29, n. 7 (ottobre 2018): 1682–83. http://dx.doi.org/10.1097/scs.0000000000004703.

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Komen, Job, Sanne M. van Neerven, Elsbeth G. B. M. Bossink, Nina E. de Groot, Lisanne E. Nijman, Albert van den Berg, Louis Vermeulen e Andries D. van der Meer. "The Effect of Dynamic, In Vivo-like Oxaliplatin on HCT116 Spheroids in a Cancer-on-Chip Model Is Representative of the Response in Xenografts". Micromachines 13, n. 5 (6 maggio 2022): 739. http://dx.doi.org/10.3390/mi13050739.

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The cancer xenograft model in which human cancer cells are implanted in a mouse is one of the most used preclinical models to test the efficacy of novel cancer drugs. However, the model is imperfect; animal models are ethically burdened, and the imperfect efficacy predictions contribute to high clinical attrition of novel drugs. If microfluidic cancer-on-chip models could recapitulate key elements of the xenograft model, then these models could substitute the xenograft model and subsequently surpass the xenograft model by reducing variation, increasing sensitivity and scale, and adding human factors. Here, we exposed HCT116 colorectal cancer spheroids to dynamic, in vivo-like, concentrations of oxaliplatin, including a 5 day drug-free period, on-chip. Growth inhibition on-chip was comparable to existing xenograft studies. Furthermore, immunohistochemistry showed a similar response in proliferation and apoptosis markers. While small volume changes in xenografts are hard to detect, in the chip-system, we could observe a temporary growth delay. Lastly, histopathology and a pharmacodynamic model showed that the cancer spheroid-on-chip was representative of the proliferating outer part of a HCT116 xenograft, thereby capturing the major driver of the drug response of the xenograft. Hence, the cancer-on-chip model recapitulated the response of HCT116 xenografts to oxaliplatin and provided additional drug efficacy information.

Zuchowska, Agnieszka, e Sandra Skorupska. "Multi-organ-on-chip approach in cancer research". Organs-on-a-Chip 4 (dicembre 2022): 100014. http://dx.doi.org/10.1016/j.ooc.2021.100014.

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Fey, M. F. "The impact of chip technology on cancer medicine". Annals of Oncology 13 (ottobre 2002): 109–13. http://dx.doi.org/10.1093/annonc/mdf647.

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Sabour, Andrew F., Seung-min Park, Jun Ho Son e Luke P. Lee. "An On-Chip Pcr Approach Enabling Cancer Diagnosis". Biophysical Journal 106, n. 2 (gennaio 2014): 618a. http://dx.doi.org/10.1016/j.bpj.2013.11.3420.

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MASUDA, Taisuke, Miyako NIIMI, Hayao NAKANISHI e Fumihito ARAI. "7B21 On-chip Cancer Diagnosis for Early Recognition of Gastric Cancer". Proceedings of the Bioengineering Conference Annual Meeting of BED/JSME 2012.24 (2012): _7B21–1_—_7B21–2_. http://dx.doi.org/10.1299/jsmebio.2012.24._7b21-1_.

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Più fonti

Tesi sul tema "Cancer-On-Chip":

Chatagnon, Amandine. "Spécificité de liaison et de répression de la " Methyl-CpG-Binding Domain protein 2 " (MBD2) : identification de gènes cibles impliqués dans les cancers". Phd thesis, Université Claude Bernard - Lyon I, 2009. http://tel.archives-ouvertes.fr/tel-00603777.

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De nombreux gènes suppresseurs de tumeurs sont inactivés par hyperméthylation dans les cancers. Cette inactivation serait en partie initiée par la protéine, MBD2 (Methyl-CpG-Binding Domain protein 2). Cette protéine recrute au niveau de séquences méthylées des complexes enzymatiques capables de modifier la structure chromatinienne et crée ainsi des régions fonctionnellement inactives. Dès lors, ce répresseur apparaît être une cible potentielle pour combattre le cancer. Dans cette perspective, rechercher les cibles de MBD2 et comprendre sa capacité à contrôler l'expression génique semblent cruciales. Au cours de deux études gènes candidats, nous avons pu démontrer (i) une réelle spécificité de cible du répresseur méthylationdépendant MBD2 pour les loci hTERT et pS2/TFF1 ; et (ii) un nouveau rôle de la protéine MBD2 en tant que modulateur de l'expression génique. De plus, les actions antagonistes entre le répresseur MBD2 et le trans-activateur naturel du gène pS2, le récepteur aux oestrogènes α, ont été explorées. Puis, l'analyse globale des profils de distribution de MBD2, de la méthylation de l'ADN, ainsi que de l'ARN polymérase II, sur puce promoteur a montré que MBD2 possède toutes les caractéristiques d'un répresseur trancriptionnel méthylation-dépendant. En effet, 74% des promoteurs fixés par MBD2 sont méthylés et cette liaison est associée dans 65% des cas à une répression transcriptionnelle.

Maassarani, Mahmoud El. "Identification de gènes cibles d'ErbB380kDa et caractérisation de leur implication au cours de la progression du cancer de la prostate". Thesis, Poitiers, 2014. http://www.theses.fr/2014POIT2275/document.

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Pour croître et proliférer, les cellules cancéreuses de la prostate activent des voies de signalisation dépendantes des androgènes. L'intervention thérapeutique en première ligne du cancer de la prostate (CaP) s'appuie donc d’abord sur le blocage de l'axe androgènes-récepteur aux androgènes (RA) mais rapidement, les patients développent des tumeurs résistantes (CRPC, Castration Resistant Prostate Cancer).Les récepteurs à activité tyrosine kinase de la famille ErbB semblent jouer un rôle dans cette résistance, en particulier le récepteur ErbB3. En effet, l'inactivation des voies en aval d'ErbB1 et ErbB2, en association avec les anti-androgéniques n'empêche pas la progression vers l'hormono-indépendance, et une accumulation nucléaire d'ErbB3 est observée dans les CRPC en même temps que la voie PI3K-Akt est réactivée.Dans ce contexte, nous avons validé l'expression d'une isoforme nucléaire ErbB380kDa chez les patients et dans des lignées hormono-sensible (LNCaP) et hormono-résistante (PC3). Par ChIP-on-chip, nous avons isolé 353 promoteurs cibles communs aux deux lignées, 245 spécifiques à la lignée LNCaP et 925 à la lignée PC3, et montré qu'ErbB380kDa est un co-régulateur transcriptionnel des gènes étudiés, parmi lesquels GATA2. L'analyse in silico de ces promoteurs révèle des sites de liaison pour les facteurs de transcription GATA2 et MZF1 au niveau des régions liant ErbB380kDa. Un complexe nucléaire GATA2-MZF1-ErbB380kDa est retrouvé dans les cellules LNCaP et PC3.Des travaux récents montrent que GATA2 s'associe au RA pour réguler l'expression de gènes et qu'il pourrait être participer à la dissémination métastatique dans le CaP.Nos résultats suggèrent qu'ErbB380kDa pourrait jouer un rôle régulateur, en amont de GATA2, dans les processus de résistance et l'apparition de métastases. Cette isoforme nucléaire insensible aux traitements actuels apparaît donc comme une cible privilégiée pour le ciblage thérapeutique
Prostate cancer (PCa) is dependent on androgens and functional androgen-receptor (AR) for growth and proliferation. Androgen-directed therapy is used at the first stages of the disease but cancer cells frequently become resistant (CRPC) by inappropriate reactivation of AR activity. As ErbB receptors are expressed in PCa cells, therapies aiming at inactivate the pathways downstream have been tested in advanced prostate cancers alongside hormone-based therapy. Still, a significant proportion of CRPC treated by ErbB1/2 inhibitors resist to treatment. ErbB3 could be responsible for this failure through both its unexpected nuclear localization and the reactivation of the PI3K-Akt pathway in those advanced tumors.We have described a nuclear ErbB380kDa isoform, expressed in hormone-sensitive (LNCaP) and hormone-resistant (PC3) PCa cell lines that accumulates in the nucleus of tumor cells during cancer progression. ChIP-on-chip experiments led us to characterize 353 target promoters binding ErbB380kDa in both cell lines; 245 promoters specific to LNCaP and 925 specific to PC3 cells, among which the promoter of GATA2. We show that ErbB380kDa functions as a transcriptional co-regulator for the studied genes, potentially through its interaction with transcription factors. In silico analysis revealed binding sites for GATA2 and MZF1 transcription factors on the target promoters, and a complex GATA2-MZF1-ErbB380kDa has been found in LNCaP and PC3 cells. Recent publications have reported a role for GATA2 in the regulation of RA responsive-genes and in metastatic spreading. We propose that ErbB380kDa could act, upstream of GATA2, to induce resistance mechanisms and facilitate cancer progression. Thus, ErbB380kDa emerges as a putative target for the development of new therapies in prostate cancer

Alexander, Frank. "RTEMIS: Real-Time Tumoroid and Environment Monitoring Using Impedance Spectroscopy and pH Sensing". Scholar Commons, 2014. https://scholarcommons.usf.edu/etd/5168.

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This research utilizes Electrical Impedance Spectroscopy, a technique classically used for electrochemical analysis and material characterization, as the basis for a non-destructive, label-free assay platform for three dimensional (3D) cellular spheroids. In this work, a linear array of microelectrodes is optimized to rapidly respond to changes located within a 3D multicellular model. In addition, this technique is coupled with an on chip micro-pH sensor for monitoring the environment around the cells. Finally, the responses of both impedance and pH are correlated with physical changes within the cellular model. The impedance analysis system realized through this work provides a foundation for the development of high-throughput drug screening systems that utilize multiple parallel sensing modalities including pH and impedance sensing in order to quickly assess the efficacy of specific drug candidates. The slow development of new drugs is mainly attributed to poor predictability of current chemosensitivity and resistivity assays, as well as genetic differences between the animal models used for tests and humans. In addition, monolayer cultures used in early experimentation are fundamentally different from the complex structure of organs in vivo. This requires the study of smaller 3D models (spheroids) that more efficiently replicate the conditions within the body. The main objective of this research was to develop a microfluidic system on a chip that is capable of deducing viability and morphology of 3D tumor spheroids by monitoring both the impedance of the cellular model and the pH of their local environment. This would provide a fast and reliable method for screening pharmaceutical compounds in a high-throughput system.

Han, Arum. "Microfabricated Multi-Analysis System for Electrophysiological Studies of Single Cells". Diss., Georgia Institute of Technology, 2005. http://hdl.handle.net/1853/11639.

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A micro-electrophysiological analysis system (-EPAS) using various microfabrication techniques for single cell study was developed. Conventional microfabrication techniques combined with plastic and polymer microfabrication techniques have been used to realize the system. The system is capable of performing patch clamp recording and whole cell electrical impedance spectroscopy (EIS) on a single cell. Methodologies for single cell manipulation were developed. The ion channel activities of primary cultured bovine chromaffin cells were measured in both the patch clamping mode and the whole cell EIS mode. Membrane capacitance of the chromaffin cell was calculated from these measurements. Increases in the capacitances were observed when certain ion channels were blocked using toxins. The dielectric properties of human breast cancer cell lines from different pathological stages were measured and compared to a normal human breast cell line in the whole cell EIS mode. The measured properties were correlated to the pathological stages of the breast cancer cell lines. Decreases in the membrane capacitances were observed for the more pathologically progressed cancer cell lines.

Veith, Irina. "Lung Cancer On-Chip for Immunotherapy Response Profiling Apoptosis Mapping in Space and Time of 3D Tumor Ecosystems Reveals Transmissibility of Cytotoxic Cancer Death". Thesis, université Paris-Saclay, 2020. http://www.theses.fr/2020UPASL036.

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Le cancer du poumon non à petites cellules (CPNPC) est l'une des rares maladies tumorales, avec mélanome et carcinome vésical, pour lesquelles les médicaments immuno-oncologiques ont conduit à une révolution thérapeutique. Seuls 20 à 30% des patients atteints de CPNPC bénéficient de la monothérapie avec inhibiteurs des points de contrôle immunitaires (ICP) avec des réponses durables, tandis que les combinaisons ont conduit à réponse longue dans jusqu'à 40% des patients. Notre étude vise à mieux caractériser la modulation du microenvironnement tumoral lors d'un traitement ICP, plus ou moins une chimiothérapie concomitante, afin de guider des stratégies d'immunothérapie plus convaincantes. Inspiré par la technologie d'organes sur puce, nous avons reconstitué ex vivo un microenvironnement de tumeur pulmonaire immunocompétent simplifié en réalisant des co-cultures 3D dans des dispositifs microfluidiques. Cette approche nous a permis de réaliser une imagerie en direct et une quantification des effets de l'ICP sur l'écosystème tumoral. L’architecture de la puce se compose de trois micro-chambres parallèles, séparées par des micro-piliers qui permettent le confinement d'un hydrogel biomimétique dans le canal central par capillarité. En co-cultivant des cellules CPNPC et des lymphocytes T cytotoxiques autologues (récoltés à partir des TIL du même patient et amplifiés ultérieurement in vitro), nous pourrions récapituler, visualiser et quantifier une activité cytotoxique efficace et spécifique des cellules T contre les cellules cancéreuses autologues. Pour cela, nous avons développé un nouvel algorithme qui pourrait localiser les cellules cancéreuses et, grâce à un rapporteur fluorescent de l'activité caspase, mesurer leur mort d'une manière spécifique au temps et à l'espace. Dans ces co-cultures 3D, l'activité cytotoxique des cellules T a été renforcée par le traitement avec l'inhibiteur PD-1 et l'inhibiteur PD-L1, reconstituant ainsi sur puce une réponse ICI. De plus, cette méthode nous a permis d'extraire un paramètre, le potentiel d'induction de la mort, qui estime mathématiquement la «contagiosité de la mort» en calculant la proximité dans l'espace et le temps des signaux de mort. Fait intéressant, cette analyse nous a révélé que la mort des cellules cancéreuses causée par la chimiothérapie ou par les cellules T cytotoxiques est contagieuse, alors que dans les conditions témoins, la mort des cellules cancéreuses est stochastique. Cette observation peut avoir des implications biologiques et cliniques, par exemple en ce qui concerne « l'effet spectateur », observé après un traitement de radiothérapie. De plus, afin d'avoir un aperçu moléculaire de l'impact de la co-culture sur les cellules T, en présence ou en l'absence d'ICI, nous avons analysé par cytométrie de flux l'expression de plusieurs marqueurs de cellules T. Après 3 jours de co-culture sur puce, les lymphocytes T ont montré une expression accrue des marqueurs d'activation, tels que CD69 et CD25, ainsi qu'une augmentation de l’expression des marqueurs d'épuisement, notamment PD-1, TIGIT, TIM-3, LAG- 3, CD137 et OX-40. Le couplage de l'analyse d'image et de l'étude de la plasticité des lymphocytes T, nous a permis d'associer pour la première fois l'activité cytotoxique finement quantifiée des lymphocytes T avec leur statut d'activation / épuisement et de décrire un phénotype réactif aux immunothérapies. Dans cette thèse, nous avons démontré que la tumeur-sur-puce peut être exploité pour évaluer l'efficacité des inhibiteurs de points de contrôle immunitaires, potentiellement pour déterminer l'effet de médicaments combinés et enfin pour étudier les mécanismes de résistance primaire des cellules cancéreuses
Non-small cell lung cancer (NSCLC) is one of the few tumor diseases, with melanoma and vesical carcinoma, for which immuno-oncology drugs led to a therapeutic revolution. Only 20 to 30% of the NSCLC patients benefit from immune checkpoint inhibitors (ICI) monotherapy with durable responses, while combinations led up to 40% of long responder patients. Our study aims to better characterize the modulation of the tumor microenvironment upon ICI treatment, plus or minus concurrent chemotherapy, in order to guide more compelling immunotherapy strategies. Inspired by the organ-on-a-chip technology, we implemented the reconstitution ex vivo of a simplified immunocompetent lung tumor microenvironment by performing 3D co-cultures in microfluidic devices. This approach allowed us to perform live-imaging and quantification of the effects of ICI on the tumor ecosystem.The design of the chip consists of three parallel micro-chambers, separated by micro-pillars that allow the confinement of a biomimetic hydrogel in the central channel by capillarity. By co-culturing autologous NSCLC cells and cytotoxic T lymphocytes (harvested from the TILs of the same patient and furtherly amplified in vitro) we could recapitulate, visualize and quantify an efficient and specific cytotoxic activity of the T cells against the autologous cancer cells. For this purpose, we developed a novel algorithm that could localize the cancer cells and, thanks to a fluorescent reporter of the caspase activity, measure their death in a time- and space-specific manner. In these 3D co-cultures the cytotoxic activity of T cells was enhanced by the treatment with PD-1 inhibitor and PD-L1 inhibitor, therefore reconstituting on-chip an ICI response. Furthermore, this method allowed us to extract a parameter, the potential of death induction, which mathematically estimates the “contagiousness of death” by computing the proximity in space and time of death signals. Interestingly, this analysis revealed us that the death of cancer cells caused by either chemotherapy or cytotoxic T cells is contagious, whereas in control conditions the cancer cells death is stochastic. This observation may have biological and clinical implications, for instance regarding the bystander effect, observed after radiotherapy treatment. Furthermore, in order to have a molecular insight on the impact of the co-culture on T cells, in presence or absence of ICI, we analyzed by flow cytometry the expression of several T cell markers. After 3 days of co-culture on chip, the T cells showed an increased expression of activation markers, such as CD69 and CD25, as well as an increased expression of exhaustion markers, notably PD-1, TIGIT, TIM-3, LAG-3, CD137 and OX-40. The coupling of image analysis and the study of T cell plasticity, allowed us to associate for the first time the finely quantified cytotoxic activity of the T cells and their activation/exhaustion status and describe a responsive phenotype to immunotherapies. In this thesis, we demonstrated that the tumor-on-chip is suitable to evaluate the efficacy of immune checkpoint inhibitors, to potentially assess the effect of combined drugs and to study the mechanisms of cancer cell primary resistance

Browne, Andrew W. "Translational Lab-on-a-Chips with the Development of a Novel Cancer Screening Method". University of Cincinnati / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1275659036.

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Salmanzadehdozdabi, Alireza. "Microfluidic differentiation of subpopulations of cells based on their bioelectrical signature". Diss., Virginia Tech, 2013. http://hdl.handle.net/10919/19370.

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Applications for lab-on-a-chip devices have been expanding rapidly in the last decade due to their lower required volume of sample, faster experiments, smaller tools, more control, and ease of parallelization compared to their macroscale counterparts. Moreover, lab-on-a-chip devices provide important capabilities, including isolating rare cells from body fluids, such as isolating circulating tumor cells from blood or peritoneal fluid, which are not feasible or at least extremely difficult with macroscale devices. Particles experience different forces (and/or torques) when they are suspended in a fluid in a microdevice. A dominant force is the drag force on the particle as it flows through the fluid. External forces such as dielectrophoresis, the motion of a particle due to its polarization in the presence of a non-uniform electric field, may also be applied. For instance, well-specified mixing or separation of particles can be achieved by using the combination of drag and dielectrophoretic forces. Two major mechanisms for manipulating particles in a microdevice include control of forces applied to the particles, such as those due to electric and velocity fields, and the geometry of the device that affects the nature of these fields. The coupling between the geometry of the microdevices and applied fields makes the prediction of associated forces inside the microdevice challenging and increasingly difficult when the applied field is time-dependent. Understanding the interaction of external forces and particles and fluid is critical for engineering novel microsystems. Determining this interaction is even more complicated when dealing with bioparticles, especially cells, due to their complex intrinsic biological properties which influence their electrical and mechanical properties. Particles with non-spherical geometries further increase the complexity, making drag and other shape-dependent forces, such as dielectrophoretic force, less predictable and more complicated. In order to introduce more complexity to the system and maintain precise control over particle movement and fluid flow, it is essential to have a comprehensive understanding about the mechanics of particles-fluid interaction and the dynamics of the particle movement. Although microfluidics has been investigated extensively, unanswered questions about the effect of forces on the particle remain. Answering these questions will facilitate designing novel and more practical microdevices for medical, biological, and chemical applications.
Microfluidics devices were engineered for differentiation of subpopulations of cells based on their bioelectrical properties. These microdevices were utilized for separating prostate, leukemia, and three different stages of breast cancer cells from hematologic cells with concentrations as low as 1:106 with efficiency of >95%. The microfluidic platform was also utilized to isolate prostate cancer stem cells (CSCs) from normal cancer cells based on their electrical signature. Isolating these cells is the first step towards the development of cancer specific therapies. The signal parameters required to selectively isolate ovarian cancer cells at different cancer stages were also compared with peritoneal cells as the first step in developing an early diagnostic clinical system centered on cell biophysical properties. Moreover, the effect of non-toxic concentrations of two metabolites, with known anti-tumor and pro-tumor properties, on the intrinsic electrical properties of early and late stages of ovarian cancer cells was investigated. This work is the first to show that treatment with non-toxic doses of these metabolites correlate with changes in cells electrical properties.
Ph. D.

Saint-Auret, Gaëlle. "Identification de la signature moléculaire de C/EBPβ dans la cellule d'hépatome humain Hep3B". Rouen, 2008. http://www.theses.fr/2008ROUES057.

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Le foie joue un rôle essentiel dans les régulations métaboliques complexes qui participent largement à l'homéostasie de l'organisme. De plus, cet organe orchestre les changements qualitatifs et quantitatifs intervenant dans la production de protéines de défense immédiatement nécessaires à la réponse à un syndrome inflammatoire aigü systémique et au retour progressif à l'homéostasie qui s'ensuit. Le facteur de transcription CCAAT enhancer-binding protein beta (C/EBPβ) enrichi dans le foie est très impliqué dans tous ces processus. Toutefois, il existe de nombreuses incohérences quant au rôle précisément joué par ce facteur de transcription. En effet, la traduction de son ARNm conduit à la formation de plusieurs isoformes de la protéine qui peuvent être activatrices (LAP) ou inhibitrices (LIP) et peu d'études, à notre connaissance, ont tenu véritablement compte de l'isoforme présente. Pour mieux comprendre le rôle de chacune de ces isoformes, nous avons mis en place, dans la lignée d'hépatome humain Hep3B, un modèle d'expression inductible de la forme activatrice (LAP) ou dominante-négative (LIP) de C/EBPβ. Le rôle antagoniste de ces 2 isoformes dans la transcription des gènes cibles de C/EBPβ a été utilisé comme stratégie pour mieux cerner les gènes régulés par ce facteur de transcription. L'identité et la transcription (directe ou indirecte) de ces ensembles de gènes-cibles de C/EBPβ ont ensuite été mises en évidence grâce à l'utilisation de deux méthodologies à grande échelle : l'analyse du transcriptome par puce à ADN et l'immunoprécipitation de chromatine sur puce (ChIP on chip). L'analyse du transcriptome nous a permis d'identifier 676 gènes inversement régulés par LAP et LIP dans la lignée d'hépatome Hep3B. L'analyse des fonctions biologiques régulées par ces gènes a mis en évidence une induction par la forme activatrice et une répression par la forme dominante-négative de C/EBPβ des voies du métabolisme hépatique (lipides, détoxication), de la transcription, de la traduction, de l'apoptose et des voies impliquées dans la régulation du processus de prolifération cellulaire. De plus, l'étude par ChIP on chip nous a permis d'identifier 38 nouvelles cibles directes de C/EBPβ. Compte tenu des résultats issus de l'analyse du transcriptome, plusieurs études fonctionnelles ont été réalisées. Ces études nous ont permis de démontrer pour la première fois que, non seulement LAP était capable de réprimer la prolifération en l'absence de RB et P53 mais que cette isoforme favorisait également l'apoptose des cellules induite par la staurosporine alors que LIP, à l'inverse, avait un effet protecteur. Par ailleurs, les cellules Hep3B permettant la surexpression contrôlée de LAP ou LIP ont été stimulées par du milieu conditionné riche en cytokines proinflammatoires afin de mimer la réponse hépatique à l'inflammation aigüe systémique. Dans ce contexte expérimental, et, toujours par analyse du transcriptome, nous avons mis en évidence un ensemble de 77 gènes régulés par LAP et LIP. Ces gènes semblent donc être de bons candidats susceptibles de participer activement à la réponse de l'organisme lors d'une inflammation aiguë. En conclusion, notre approche tout à fait originale, caractérisée par l'identification des gènes inversement régulés par les isoformes LAP et LIP de C/EBPβ, a permis de mieux comprendre comment ces deux isoformes régulent plusieurs processus physiologiques et pathologiques du foie
The liver plays an essential part in complex metabolic regulations which widely contribute to the body homeostasis. Moreover, this organ conducts the qualitative and quantitative changes in the production of specific proteins immediately induced during the acute phase response and allowing a progressive come back to homeostasis. The liver-enriched transcription factor CCAAT enhancer-binding protein beta (C/EBPβ) is widely involved in these processes, but its precise the role isnot still defined. Conflicting studies have described contradictory functions for this transcription factor which could be explained by the complex mechanisms regulating the C/EBPβ activity. Indeed, C/EBPβ encodes an intronless gene that generates a single mRNA that is alternatively translated into two major isoforms : an active LAP (liver-enriched activator protein) and a dominant negative LIP (liver-enriched inhibitory protein). Today, few studies have really taken into account the present isoform. In order to better understand the precise role of each isoform, we first engineered the Hep3B human hepatoma cell line with a Tet-off inducible LAP or LIP isoform. The antagonistic role of the both isoforms in C/EBPβ target-genes transcription has been used as a strategy to better define the C/EBPβ-regulated genes. Then, the identity and the transcription (direct or indirect) of all these target-genes were determined by two functional genomic approaches : the transcriptome analysis by cDNA arrays and the chromatine immunoprecipitation on chip (ChIP on chip). Using a cDNA microarray which provides a complete coverage of the liver transcriptome, we identified 676 genes inversely regulated by LAP and LIP in the Hep3B hepatoma line. The analysis of the biological functions regulated by these genes brought into the flore an induction by LAP and a repression by LIP of several pathways including hepatic metabolism (fat, detoxification), transcription, translation, apoptosis and regulation of the cell proliferation. Moreover, the ChIP on chip study allowed the identification of 38 C/EBPβ new direct targets. According to the data resulting from the transcriptome analysis, several functional studies have been carried out. They allowed us to prove, for the first time, that LAP was, not only able to suppress the cell proliferation in the absence of RB and P53, but that this isoform also increased the staurosporine-induced apoptosis in Hep3B cells while LIP had a protector effect. Furthermore, the Hep3B cells expressing LAP or LIP have been stimulated by a conditioned medium rich in proinflammatory cytokines in order to mimic the hepatic response to the acute phrase of inflammation. In this experimental context, and still by transcriptome analysis, we brought into the fore a group of 77 genes regulated by LAP and LIP which interestingly seem to be involved during the acute phrase response. To conclude, our original approach characterized by the identification of genes inversely regulated by LAP and LIP allowed us to better understand how these two isoforms of C/EBPβ manage several physiological and pathological liver processes

Ahmad-Cognart, Hamizah. "Study of the Metastatic Process of Circulating Tumour Cells by Organ-on-a-Chip In Vitro Models". Thesis, Sorbonne Paris Cité, 2018. http://www.theses.fr/2018USPCC139/document.

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90% de la mortalité par cancer provient de tumeurs disséminées, ou métastases. Ces métastases se forment à partir de cellules tumorales qui s'échappent d'une tumeur primaire, circulent dans le sang, puis quittent les vaisseaux sanguins pour enfin aller nicher dans des organes distants et former des tumeurs secondaires. Les processus par lesquels ces cellules circulantes envahissent les organes distants, remodèlent leur environnement pour créer une «niche micrométastatique», prolifèrent pour produire des métastases macroscopiques, sont mal connus, principalement en raison d'un manque de modèles expérimentaux. En effet ces événements sont rares, se produisent à une échelle microscopique et à des localisations à priori inconnues. La perte d'adhérence cellulaire des cellules tumorales se détachant des tissus tumoraux primaires est associée à un phénomène de transformation connu sous le nom de transition épithéliale-mésenchymateuse (EMT) conduisant à la perte des caractéristiques épithéliales. Dans ce travail, nous avons souhaité aborder la question du processus métastatiques par l'étude de l'influence de l'étape de circulation dans le flux sanguin sur différentes caractéristiques de cellules tumorales. Pour cela, des modèles microfluidiques contenant des constrictions mécaniques afin d'imiter la microcirculation sanguine ont été conçus et fabriqués. Nous avons soumis des cellules provenant de tumeurs primaires du sein dans des situations de confinement périodiques à l'intérieur de ces canaux microfluidiques en utilisant un système de contrôle de flux. Nous avons étudiés l'impact des déformations induites par les constrictions des canaux microfluidiques sur l'expression génétique des marqueurs EMT, la morphologie ainsi que la dynamique des changements morphologiques. Nous montrons que ces paramètres cellulaires sont touchés par la déformation mécanique imposée sous flux, suggérant que l'étape de circulation des cellules tumorales dans le sang a un rôle important dans la capacité de celles-ci à produire des métastases
90% of cancer mortality arises from metastases, due to cells that escape from a primary tumor, circulate in the blood as circulating tumor cells (CTCs), leave blood vessels and nest in distant organs. The processes by which CTCs invade distant organs, remodel their environment to create a “micrometastatic niche”, the eventual triggering of a proliferation leading to a macroscopic metastases, are poorly known, mostly because of a lack of experimental models. These events are rare; occur in the body at unknown places and on a microscopic scale. The loss of cell adhesion of tumor cells detaching from the primary tumor tissues will undergo a transformation phenomenon known as epithelial-to mesenchymal transition (EMT) leading to the loss of epithelial characteristics with different expression patterns of EMT markers (E-cadherin, N-cadherin, Vimentin, Snail1/2, Twist1/2, ZEB1/2). The changes in mechanical and physical properties of interacting cells during morphological and malignant transformation are investigated and their quantifications measured. Here, microfluidic models containing mechanical constrictions in order to mimic the blood microcirculation have been designed and fabricated. Metastatic breast cancer cells are subjected and confined to the microfluidic channels using a flow control system. These cells are circulated under optimal culture conditions, and monitored in the channels for the observance of biophysical occurrences from continuous mechanical cellular deformations. The biophysical effects of circulation and confinement on tumor cell morphogenesis will be investigated

Baka, Zakaria. "Élaboration de cancers sur puce pour des applications en thérapies anticancéreuses". Electronic Thesis or Diss., Université de Lorraine, 2023. http://www.theses.fr/2023LORR0175.

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Le cancer de l’ovaire constitue un véritable enjeu de santé public. Les nouveaux traitements se heurtent par ailleurs à des taux d’échec très élevés. Ceci s’explique notamment pour le manque de fiabilité des modèles précliniques classiques tels que la culture cellulaire en 2D. De nouveaux outils basés sur la culture cellulaire en 3D ont alors fait leur apparition tels que les sphéroïdes et les organoïdes. Or ces modèles ont leurs propres limites (coûts, difficultés d’application). La bio-impression 3D est une nouvelle approche permettant de créer des modèles tumoraux de manière contrôlée et reproductible. Néanmoins, elle a encore très peu été appliquée au cancer ovarien. En plus de la troisième dimension, il est important de prendre en compte les conditions dynamiques associées à l’environnement tumoral. Ceci est possible depuis quelques années grâce à la technologie des cancers sur puce basée sur la microfluidique. Cependant, cette technologie ne permet pas, à l’heure actuelle, de simuler le trajet vasculaire du médicament en amont de son interaction avec le tissu tumoral. Dans ce projet de thèse, nous avons souhaité créer un modèle tridimensionnel et dynamique du cancer ovarien en combinant les approches de bio-impression 3D et de microfluidique. Dans un premier temps, la bio-impression 3D a été utilisée pour créer la structure tumorale à proprement parlé. Pour y parvenir, nous avons formulé un hydrogel de gélatine et d’alginate de sodium dans lequel nous avons intégré des cellules cancéreuses ovariennes (SKOV-3) et des fibroblastes cancéreux (MeWo). Le tissu tumoral bio-imprimé a ensuite été caractérisé par différentes techniques pour démontrer sa viabilité et sa pertinence biologique. Sa réponse au cisplatine a également été évaluée. Dans un second temps, nous avons intégré le modèle tumoral bio-imprimé au sein d’un support microfluidique. Le rôle de ce support était de permettre la mise en culture du tissu bio-imprimé sous flux physiologique. Il devait également permettre de simuler le trajet vasculaire du médicament avant son interaction avec le tissu tumoral. Par la suite, nous avons fait appel à la simulation en mécanique des fluides pour concevoir une version améliorée du premier système. L’objectif étant de pouvoir tester, en même temps, plusieurs concentrations différentes de médicament sur un même dispositif microfluidique. Ce projet de thèse a démontré la capacité de la bio-impression 3D à créer des tissus tumoraux ovariens viables et fonctionnels. Il a par ailleurs ouvert des perspectives de recherche très intéressantes par rapport aux possibilités de combiner la bio-impression 3D et de la microfluidique en vue d’améliorer la modélisation préclinique des cancers ovariens
Ovarian cancer is a major public health issue. Moreover, new treatments still face very high failure rates. This is mainly due to the unreliability of conventional preclinical models such as 2D cell culture. Thus, new tools based on 3D cell culture have emerged such as spheroids and organoids. However, these models have their own limitations (cost, difficulty of application). 3D bioprinting is a new approach to create tunable and reproducible tumor models. However, very few bioprinted tumor models have been reported so far. Besides the “third dimension”, it is important to consider the dynamic conditions of the tumor environment. This has been possible for some years now thanks to microfluidics-based cancer-on-a-chip technology. However, this technology currently does not simulate the drug vascular transport before its interaction with the tumor cells. In this PhD project, we set out to create a dynamic, three-dimensional model of ovarian cancer by combining 3D bioprinting and microfluidics. First, 3D bioprinting was used to create the tumor structure itself. For that, we formulated a bio-ink comprising SKOV-3 ovarian cancer cells and MeWo cancer fibroblasts embedded in a gelatin – alginate hydrogel. The bioprinted tumor structures were then characterized by various techniques to demonstrate their viability and biological relevance. Their response to anticancer drug cisplatin was also assessed. In the second step, we integrated the bioprinted tumor model into a microfluidic support for culture under physiological flow. This support was also intended to simulate the drug's vascular transport prior to interaction with the tumor tissue. We then used computational fluid dynamics to design an improved version of the first system. The aim of this improved version was to simultaneously assess multiple drug concentrations. This PhD project demonstrated the ability of 3D bioprinting to create viable and functional ovarian tumor models. It has also brought interesting research prospects with regard to the possibilities of combining 3D bioprinting and microfluidics to improve preclinical modeling of ovarian tumors

Più fonti

Libri sul tema "Cancer-On-Chip":

Segal, Ester, e Pranjal Chandra. Nanobiosensors for Personalized and Onsite Biomedical Diagnosis. Institution of Engineering & Technology, 2016.

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Capitoli di libri sul tema "Cancer-On-Chip":

Tong, Ziqiu, Wing-Yin Tong, Bo Peng, Yingkai Wei, Arianna Oddo e Nicolas H. Voelcker. "Using Integrated Cancer-on-Chip Platforms to Emulate and Probe Various Cancer Models". In Nanotechnology Characterization Tools for Tissue Engineering and Medical Therapy, 151–204. Berlin, Heidelberg: Springer Berlin Heidelberg, 2019. http://dx.doi.org/10.1007/978-3-662-59596-1_4.

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Caballero, David, Rui L. Reis e Subhas C. Kundu. "Engineering Patient-on-a-Chip Models for Personalized Cancer Medicine". In Advances in Experimental Medicine and Biology, 43–64. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-36588-2_4.

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Ho-Pun-Cheung, Alexandre, Hafid Abaibou, Philippe Cleuziat e Evelyne Lopez-Crapez. "Detection of Single-Nucleotide Polymorphisms in Cancer-Related Genes by Minisequencing on a Microelectronic DNA Chip". In Microarrays, 267–78. Totowa, NJ: Humana Press, 2007. http://dx.doi.org/10.1007/978-1-59745-303-5_13.

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Yang, Yamin, e Hongjun Wang. "Microfluidic Technologies for Head and Neck Cancer: From Single-Cell Analysis to Tumor-on-a-Chip". In Early Detection and Treatment of Head & Neck Cancers, 43–62. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-69859-1_3.

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Parihar, Arpana, Nishant Kumar Choudhary, Dipesh Singh Parihar e Raju Khan. "Tumor-on-a-Chip: Microfluidic Models of Hypoxic Tumor Microenvironment". In Hypoxia in Cancer: Significance and Impact on Cancer Therapy, 297–328. Singapore: Springer Nature Singapore, 2023. http://dx.doi.org/10.1007/978-981-99-0313-9_14.

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Lopez-Muñoz, Gerardo A., Sheeza Mughal e Javier Ramón-Azcón. "Correction to: Sensors and Biosensors in Organs-on-a-Chip Platforms". In Microfluidics and Biosensors in Cancer Research, C1. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-04039-9_23.

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Li, Caiwei, Jiao Zhai e Yanwei Jia. "Digital Microfluidics with an On-Chip Drug Dispenser for Single or Combinational Drug Screening". In Microfluidic Systems for Cancer Diagnosis, 25–39. New York, NY: Springer US, 2023. http://dx.doi.org/10.1007/978-1-0716-3271-0_3.

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Mu, Xuan, e Yu Shrike Zhang. "Tumor-on-a-chip devices for cancer immunotherapy". In Engineering Technologies and Clinical Translation, 155–95. Elsevier, 2022. http://dx.doi.org/10.1016/b978-0-323-90949-5.00006-1.

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Anton Okhai, Timothy, Azeez O. Idris, Usisipho Feleni e Lukas W. Snyman. "Nanomaterial-Enhanced Receptor Technology for Silicon On-Chip Biosensing Application". In Biosensor - Current and Novel Strategies for Biosensing [Working Title]. IntechOpen, 2020. http://dx.doi.org/10.5772/intechopen.94249.

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Nanomaterials integration in biosensors designs are known to enhance sensing and signaling capabilities by exhibiting remarkably high surface area enhancement and intrinsic reactivity owing to their distinctive optical, chemical, electrical and catalytic properties. We present the synthesis and characterization of silver nanoparticles (AgNPs), and their immobilization on a silicon on-chip biosensor platform to enhance sensing capability for prostate specific antigen (PSA) - cancer biomarkers. Several techniques, including UV-Visible (UV-Vis) absorption spectrum, Fourier transforms infrared spectroscopy (FTIR), high resolution transmission electron microscopy (HRTEM), scanning electron microscopy (SEM) and field emission scanning electron microscopy (FESEM) were used for characterizing the AgNPs. The biochemical sensor consists of AgNPs immobilized on the receptor layer of a silicon avalanche mode light emitting device (Si AM LED) which enables on-chip optical detection biological analytes. A bio-interaction layer etched from the chip interacts with the evanescent field of a micro dimensioned waveguide. An array of detectors below the receptor cavity selectively monitor reflected light in the UV, visible, infrared and far infrared wavelength regions. AgNPs used as an immobilization layer in the receptor layer enhances selective absorption analytes, causing a change in detection signal as a function of propagation wavelength as light is dispersed. The analytes could range from gases to cancer biomarkers like prostate specific antigen.

Firoozbakhtian, Ali, Morteza Hosseini, Javad Gilnezhad e Mohammad Reza Ganjali. "Lab-on-a-chip systems for aptamer-based cancer biomarker screening". In Aptasensors for Point-of-Care Diagnostics of Cancer, 9–1. IOP Publishing, 2023. http://dx.doi.org/10.1088/978-0-7503-5012-9ch9.

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Atti di convegni sul tema "Cancer-On-Chip":

Liao, Han-Jung, Jean-An Chieh, Yu-Chen Chen, Kang-Yun Lee, Yao-Fei Chan, Shu-Chuan Ho, Wei-lun Sun et al. "Lung Cancer On Chip for Testing Immunotherapy". In 2021 21st International Conference on Solid-State Sensors, Actuators and Microsystems (Transducers). IEEE, 2021. http://dx.doi.org/10.1109/transducers50396.2021.9495530.

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Chang, Kuo-Wei, Tushar Harishchandra Punde, Gaurav Prashant Pendharkar, Po-Chen Shih, Yao-Fei Chan, Kang-Yun Lee, Ming-Yan Chen e Cheng-Hsien Liu. "Lung cancer model on chip for drug testing". In TRANSDUCERS 2015 - 2015 18th International Solid-State Sensors, Actuators and Microsystems Conference. IEEE, 2015. http://dx.doi.org/10.1109/transducers.2015.7181006.

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Darabi, Jeff, e Joseph Schober. "A Microfluidic Platform for On-Chip Analysis of Circulating Tumor Cells". In ASME 2021 Fluids Engineering Division Summer Meeting. American Society of Mechanical Engineers, 2021. http://dx.doi.org/10.1115/fedsm2021-65766.

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Abstract Studies have shown that primary tumor sites begin shedding cancerous cells into peripheral blood at early stages of cancer, and the presence and frequency of circulating tumor cells (CTCs) in blood is directly proportional to disease progression. The challenge is that the concentration of the CTCs in peripheral blood may be extremely low. In the past few years, several microfluidic-based concepts have been investigated to isolate CTCs from whole blood. However, these devices are generally hampered by complex fabrication processes and very low volumetric throughputs, which may not be practical for rapid clinical applications. This paper presents a high-performance yet simple magnetophoretic microfluidic chip for the enrichment and on-chip analysis of rare CTCs from blood. Microscopic and flow cytometric assays developed for selection of cancer cell lines, selection of monoclonal antibodies, and optimization of bead coupling are discussed. Additionally, on-chip characterization of rare cancer cells using high resolution immunofluorescence microscopy and modeling results for prediction of CTC capture length are presented. The device has the ability to interface directly with on-chip pre and post processing modules such as mixing, incubation, and automated image analysis systems. These features will enable us to isolate rare cancer cells from whole blood and detect them on the chip with subcellular resolution.

Pradhan, Shantanu, Ashley M. Smith, Charles J. Garson, Iman Hassani, Kapil Pant, Robert D. Arnold, Balabhaskar Prabhakarpandian e Elizabeth A. Lipke. "Abstract 620: Microfluidic cancer-on-a-chip platform for assessing anti-cancer drug efficacies". In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-620.

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Wan, Yuan, Young-tae Kim, Li Na, Andrew D. Ellington e Samir M. Iqbal. "Aptamer-Based Lab-on-Chip for Cancer Cell Isolation and Detection". In ASME 2010 First Global Congress on NanoEngineering for Medicine and Biology. ASMEDC, 2010. http://dx.doi.org/10.1115/nemb2010-13195.

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The isolation and detection of circulating tumor cells (CTCs), when these are few in number or small in mass, can enable early cancer detection [1]. Currently, most research endeavors to isolate circulating tumor cells rely on antibodies and immunohistochemistry [2,3]. Aptamer are alternative molecules that have affinities and specificities that are comparable to those of antibodies [4,5], but these can be more readily adapted to many applications [6–9], including lab-on-a-chip devices. Here, we report use of a novel epidermal growth factor receptor (EGFR) aptamer biochip to identify and isolate cancer cells that overexpress EGFR. These results provide a solid basis for the development of diagnostic devices that can readily identify and isolate CTCs.

Sala, Federico. "On-Chip high-throughput LSFM analysis of single cancer cells". In Virtual 12th Light Sheet Fluorescence Microscopy Conference 2020. Royal Microscopical Society, 2020. http://dx.doi.org/10.22443/rms.lsfm2020.27.

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Lee, Wonjun, Jiin Park, Dongil Kang e Seungbeum Suh. "Reconstituting Fundamentals of Bacteria Mediated Cancer Therapy On A Chip". In 2023 IEEE 36th International Conference on Micro Electro Mechanical Systems (MEMS). IEEE, 2023. http://dx.doi.org/10.1109/mems49605.2023.10052432.

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Picollet-D'hahan, N., B. Laperrousaz, S. Porte, P. Obeid, A. Tollance, F. Kermarrec, C. Belda-Marin et al. "Encapsulated organoids & organ-on-a-chip platform for cancer modeling". In 2017 IEEE International Electron Devices Meeting (IEDM). IEEE, 2017. http://dx.doi.org/10.1109/iedm.2017.8268366.

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Vieira, Dalila, Filipa Mata, Ana Moita e António Moreira. "Microfluidic Prototype of a Lab-on-Chip Device for Lung Cancer Diagnostics". In 10th International Conference on Biomedical Electronics and Devices. SCITEPRESS - Science and Technology Publications, 2017. http://dx.doi.org/10.5220/0006252700630068.

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Gopal, Ashwini, Zhiguo Wang, Kazunori Hoshino e Ziaozjing Zhang. "Multispectral analysis of cancer cells using quantum dot leds patterned on-chip". In TRANSDUCERS 2011 - 2011 16th International Solid-State Sensors, Actuators and Microsystems Conference. IEEE, 2011. http://dx.doi.org/10.1109/transducers.2011.5969745.

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