Academic literature on the topic 'Targeting tumorale'
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Journal articles on the topic "Targeting tumorale"
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Dhani, Neesha, and Michael Milosevic. "Targeting tumoral hypoxia: finding opportunity in complexity." Future Oncology 8, no. 9 (September 2012): 1065–68. http://dx.doi.org/10.2217/fon.12.100.
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Raavé, René, Toin H. van Kuppevelt, and Willeke F. Daamen. "Chemotherapeutic drug delivery by tumoral extracellular matrix targeting." Journal of Controlled Release 274 (March 2018): 1–8. http://dx.doi.org/10.1016/j.jconrel.2018.01.029.
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He, Z., Z. Meng, P. Liang, L. Xing, X. Zheng, and G. Wang. "P13.15 Pre-clinical trial of T601 oncolytic virus for high grade glima via intra-tumoral injection." Neuro-Oncology 23, Supplement_2 (September 1, 2021): ii35—ii36. http://dx.doi.org/10.1093/neuonc/noab180.122.
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Abstract BACKGROUND An effective therapeutic method still hasn’t been devised for lethal high grade glioma. Thus, a method with high anti-tumoral efficiency, tumoral targeting, and acceptable side effect needs to be designed. Oncolytic virotherapy which can specifically lyse tumor cells via mass replication and deleting nucleotide metabolism related gene, like TK, required in viral replication and overexpressed in tumor cells, provides hope for patients. However, the virus only contained TK deletion is unable to show sufficient specificity of anti-tumoral response in tumor cells. Here, the adapted strain of vaccinia virus with high tumoral specificity due to TK and RR deletion and FUC1 insertion, named T601, is chosen in this project. In clinical application, intra-tumoral injection showed improved anti-tumoral efficiency and acceptable side effect. However, intra-tumoral viral injection in orthotropic glioma model is rare. In this project, various biosafety and antitumoral efficiency parameter would be tested for confirming the biosafety and reliability of intra-tumoral T601 viral injection for future clinical trials. MATERIAL AND METHODS For measuring the IC50 of T601, 10 different amounts of virus was tested in vitro via calculating cell viability with CCK-8(cell counting kit-8). For measuring the further antitumoral response of FCU1, different concentration of the 5-FC was added into the medium with IC50 viral amount. To ensure the biosafety of T601, MTD (maximum tolerance dose) was measured. Based on the MTD result, for evaluating the anti-tumoral efficiency, 106 pfu,105 pfu,104 pfu of virus was intra-tumoral injected in orthotopic GBM bearing mice. Tumor size was measured once a week through in vivo bioimaging system. RESULTS 0.022 MOI, the IC50 of T601, showed high cytotoxicity of T601. Moreover, the significantly decreased cell viability under the combined treatment of 5-FC and 0.22MOI T601 showed intact anti-tumoral function. In MTD assay, except for 107 group, no significant weight loss was found. However, in 107 pfu group, mean body weight decreased around 10% and animal fatality happened on day 9. According to the MTD result, certain amount of virus was intra-tumorally injected. In all treatment group, the tumor size was significantly shrined. At the same time, the survival rate of mice under viral treatment was significantly extended. CONCLUSION In summary, T601 exhibited efficient anti-tumoral function and acceptable side effect. T601 treatment prolonged the survival period of GBM mice with acceptable neurotoxicity, demonstrating that T601 contains necessary criterial for intra-tumoral injection. Ultimately, this project provided basic reference information of dose for future clinical trial.
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Halin, Cornelia, Luciano Zardi, and Dario Neri. "Antibody-Based Targeting of Angiogenesis." Physiology 16, no. 4 (August 2001): 191–94. http://dx.doi.org/10.1152/physiologyonline.2001.16.4.191.
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The selective targeting of neovasculature opens new avenues for the diagnosis and therapy of angiogenesis-related diseases such as cancer, blinding ocular disorders, and rheumatoid arthritis. Here we review recent advances in the identification of markers of angiogenesis as well as in the isolation and use of antibodies (and their derivatives) for the in vivo targeting of both tumoral and nontumoral neovasculature.
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Do, Manh-Hung, Phuong To, Young-Suk Cho, Se-Young Kwon, Eu Hwang, Chan Choi, Sang-Hee Cho, Sang-Jin Lee, Silvio Hemmi, and Chaeyong Jung. "Targeting CD46 Enhances Anti-Tumoral Activity of Adenovirus Type 5 for Bladder Cancer." International Journal of Molecular Sciences 19, no. 9 (September 10, 2018): 2694. http://dx.doi.org/10.3390/ijms19092694.
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CD46 is generally overexpressed in many human cancers, representing a prime target for CD46-binding adenoviruses (Ads). This could help to overcome low anti-tumoral activity by coxsackie-adenoviral receptor (CAR)-targeting cancer gene therapy viruses. However, because of scarce side-by-side information about CAR and CD46 expression levels in cancer cells, mixed observations of cancer therapeutic efficacy have been observed. This study evaluated Ad-mediated therapeutic efficacy using either CAR-targeting Ad5 or CD46-targeting Ad5/35 fiber chimera in bladder cancer cell lines. Compared with normal urothelia, bladder cancer tissue generally overexpressed both CAR and CD46. While CAR expression was not correlated with disease progression, CD46 expression was inversely correlated with tumor grade, stage, and risk grade. In bladder cancer cell lines, expression levels of CD46 and CAR were highly correlated with Ad5/35- and Ad5-mediated gene transduction and cytotoxicity, respectively. In a human EJ bladder cancer xenograft mouse model, with either overexpressed or suppressed CD46 expression levels, Ad5/35-tk followed by ganciclovir (GCV) treatment significantly affected tumor growth, whereas Ad5-tk/GCV had only minimal effects. Overall, our findings suggest that bladder cancer cells overexpress both CAR and CD46, and that adenoviral cancer gene therapy targeting CD46 represents a more suitable therapy option than a CAR-targeting therapy, especially in patients with low risk bladder cancers.
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Koltai, Tomas, Stephan Joel Reshkin, Tiago M. A. Carvalho, and Rosa A. Cardone. "Targeting the Stromal Pro-Tumoral Hyaluronan-CD44 Pathway in Pancreatic Cancer." International Journal of Molecular Sciences 22, no. 8 (April 12, 2021): 3953. http://dx.doi.org/10.3390/ijms22083953.
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Pancreatic ductal adenocarcinoma (PDAC) is one of the deadliest malignancies. Present-day treatments have not shown real improvements in reducing the high mortality rate and the short survival of the disease. The average survival is less than 5% after 5 years. New innovative treatments are necessary to curtail the situation. The very dense pancreatic cancer stroma is a barrier that impedes the access of chemotherapeutic drugs and at the same time establishes a pro-proliferative symbiosis with the tumor, thus targeting the stroma has been suggested by many authors. No ideal drug or drug combination for this targeting has been found as yet. With this goal in mind, here we have explored a different complementary treatment based on abundant previous publications on repurposed drugs. The cell surface protein CD44 is the main receptor for hyaluronan binding. Many malignant tumors show over-expression/over-activity of both. This is particularly significant in pancreatic cancer. The independent inhibition of hyaluronan-producing cells, hyaluronan synthesis, and/or CD44 expression, has been found to decrease the tumor cell’s proliferation, motility, invasion, and metastatic abilities. Targeting the hyaluronan-CD44 pathway seems to have been bypassed by conventional mainstream oncological practice. There are existing drugs that decrease the activity/expression of hyaluronan and CD44: 4-methylumbelliferone and bromelain respectively. Some drugs inhibit hyaluronan-producing cells such as pirfenidone. The association of these three drugs has never been tested either in the laboratory or in the clinical setting. We present a hypothesis, sustained by hard experimental evidence, suggesting that the simultaneous use of these nontoxic drugs can achieve synergistic or added effects in reducing invasion and metastatic potential, in PDAC. A non-toxic, low-cost scheme for inhibiting this pathway may offer an additional weapon for treating pancreatic cancer.
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Muller, Alexander J., and Peggy A. Scherle. "Targeting the mechanisms of tumoral immune tolerance with small-molecule inhibitors." Nature Reviews Cancer 6, no. 8 (August 1, 2006): 613–25. http://dx.doi.org/10.1038/nrc1929.
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Muller, Alexander J., and Peggy A. Scherle. "Erratum: Targeting the mechanisms of tumoral immune tolerance with small-molecule inhibitors." Nature Reviews Cancer 6, no. 9 (August 17, 2006): 742. http://dx.doi.org/10.1038/nrc1979.
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Wu, Deyang, Xiaowei Liu, Jingtian Mu, Jin Yang, Fanglong Wu, and Hongmei Zhou. "Therapeutic Approaches Targeting Proteins in Tumor-Associated Macrophages and Their Applications in Cancers." Biomolecules 12, no. 3 (March 2, 2022): 392. http://dx.doi.org/10.3390/biom12030392.
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Tumor-associated macrophages (TAMs) promote tumor proliferation, invasion, angiogenesis, stemness, therapeutic resistance, and immune tolerance in a protein-dependent manner. Therefore, the traditional target paradigms are often insufficient to exterminate tumor cells. These pro-tumoral functions are mediated by the subsets of macrophages that exhibit canonical protein markers, while simultaneously having unique transcriptional features, which makes the proteins expressed on TAMs promising targets during anti-tumor therapy. Herein, TAM-associated protein-dependent target strategies were developed with the aim of either reducing the numbers of TAMs or inhibiting the pro-tumoral functions of TAMs. Furthermore, the recent advances in TAMs associated with tumor metabolism and immunity were extensively exploited to repolarize these TAMs to become anti-tumor elements and reverse the immunosuppressive tumor microenvironment. In this review, we systematically summarize these current studies to fully illustrate the TAM-associated protein targets and their inhibitors, and we highlight the potential clinical applications of targeting the crosstalk among TAMs, tumor cells, and immune cells in anti-tumor therapy.
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Gisbert-Garzarán, Miguel, Daniel Lozano, and María Vallet-Regí. "Mesoporous Silica Nanoparticles for Targeting Subcellular Organelles." International Journal of Molecular Sciences 21, no. 24 (December 18, 2020): 9696. http://dx.doi.org/10.3390/ijms21249696.
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Current chemotherapy treatments lack great selectivity towards tumoral cells, which leads to nonspecific drug distribution and subsequent side effects. In this regard, the use of nanoparticles able to encapsulate and release therapeutic agents has attracted growing attention. In this sense, mesoporous silica nanoparticles (MSNs) have been widely employed as drug carriers owing to their exquisite physico-chemical properties. Because MSNs present a surface full of silanol groups, they can be easily functionalized to endow the nanoparticles with many different functionalities, including the introduction of moieties with affinity for the cell membrane or relevant compartments within the cell, thus increasing the efficacy of the treatments. This review manuscript will provide the state-of-the-art on MSNs functionalized for targeting subcellular compartments, focusing on the cytoplasm, the mitochondria, and the nucleus.
Dissertations / Theses on the topic "Targeting tumorale"
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Gava, Fabien. "Etude des mécanismes d'agrégation cellulaire tumorale." Thesis, Toulouse 3, 2018. http://www.theses.fr/2018TOU30372.
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Les métastases sont responsables de 90% des décès attribués au cancer justifiant qu'une large part des recherches actuelles en cancérologie soit consacrée à l'étude des mécanismes responsables de leur formation. Il a récemment été démontré que des clusters ou agrégats de cellules tumorales circulantes (CTCs) détectés dans la circulation sanguine des patients présentent un potentiel métastatique largement plus important que des cellules tumorales circulantes isolées. Il a également été montré que leur présence est corrélée avec un pronostic péjoratif pour les patients atteints de plusieurs types de cancers d'origine épithéliale. Ces observations ouvrent des perspectives diagnostiques et thérapeutiques prometteuses mais qui nécessitent de mieux comprendre comment se forment et se maintiennent ces clusters. Dans ce contexte notre laboratoire a développé un essai semi-automatisé in vitro basé sur la vidéo-microscopie permettant d'étudier les mécanismes impliqués dans l'agrégation de cellules tumorales dans des conditions ancrage indépendantes. Cet essai a permis de démontrer l'implication de la protéine de jonction adhérente E-cadhérine et des protéines de jonctions desmosomales DSG2 et DSC2 dans l'agrégation de cellules tumorales. L'objectif de mes travaux de thèse a été de poursuivre l'exploration de l'implication des protéines de jonctions intercellulaires de type épithélial dans l'agrégation des cellules tumorales en conditions ancrage-indépendantes et de chercher à identifier de nouveaux régulateurs. Dans un premier temps j'ai pu démontrer et explorer le rôle des jonctions communicantes (ou jonctions gap), ainsi que de la P-cadhérine dans l'agrégation des cellules tumorales mammaires et colorectales. Au cours de la seconde partie de mes travaux, j'ai développé une stratégie basée sur la classification de lignées tumorales selon leur comportement au cours du processus d'agrégation. Afin d'établir les paramètres de cette classification, nous avons exploré les capacités agrégatives de 28 lignées cellulaires tumorales d'origine épithéliale. Cette étude nous a permis de mettre en évidence une forte diversité de comportement au cours de ce processus et de définir des classes de lignées intégrant les aspects dynamiques du processus d'agrégation ainsi que la structure des agrégats obtenus. La combinaison de cette classification avec les données d'expression aujourd'hui disponibles pourrait permettre l'identification de nouveaux régulateurs originaux de l'agrégation. Nos résultats ont mis en évidence de nouveaux régulateurs de l'agrégation cellulaire tumorale ancrage-indépendante ainsi qu'une large diversité de comportement de différentes lignées cellulaires tumorales. Nos travaux ouvrent ainsi des perspectives vers une meilleure compréhension des mécanismes impliqués, vers l'application à l'étude des cellules tumorales circulantes provenant de patients et également au ciblage thérapeutique de ces clustersMetastases are responsible for 90% of cancer-related deaths justifying the current cancer research's substantial part dedicated to study their formation's mechanisms. It has been recently demonstrated that clusters (or aggregates) of circulating tumor cells (CTCs) identified in patient's blood samples have a far higher metastatic potential than isolated circulating tumor cells. It also has been shown that their detection is correlated with a poor prognosis for patients suffering from epithelial cancers. These observations open up promising diagnostic and therapeutic perspectives but that still requires further investigation on the mechanisms of clusters formation. In this context our laboratory developed an in vitro semi-automated assay based on video microscopy enabling the study of mechanisms involved in tumor cell anchorage-independent clustering. This assay allowed to demonstrate the involvement of adherent junction protein E-cadherin and desmosomal junction proteins DSG2 and DSC2 during tumor cell clustering. The aim of my work was to investigate epithelial intercellular junction's proteins involvement in tumor cell aggregation in anchorage-independent conditions and to search for new regulators. In the first instance I explored and demonstrated the role of communicating junctions (or gap junctions) and P-cadherin in tumor cell aggregation of breast and colorectal cancer cell lines. In the second part, I developed a strategy based on tumor cell lines classification depending on their characteristics of the aggregation process. With the aim of determining the parameters of this classification, I examined aggregation abilities of 28 tumor cell lines derived from epithelial cancers. This study provides evidence for a high variability during this process and allows defining cell lines categories integrating both aggregation process dynamic aspects and aggregates structure. The combination of this classification with current available expression data could lead to the identification of original new aggregation regulators. Together, these results have underscored new anchorage-independent tumor cell aggregation regulators and a wide range of behaviors of different tumor cell lines observed. Our work provides opportunities into a better understanding of involved mechanisms, towards an application to study circulating tumor cells from patients and also a therapeutic targeting of these clusters
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Murarasu, Thomas. "The Shiga Toxin B-Subunit : a Promising Scaffold for the Targeting of Tumor Specific Glycosphingolipids." Thesis, Université Paris-Saclay (ComUE), 2017. http://www.theses.fr/2017SACLS512.
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Le cancer représente la second cause de décès au monde. Le développement de traitements innovants contre le cancer repose aujourd’hui sur l’identification de biomarqueurs des tumeurs et le développement de produits thérapeutiques capables de reconnaitre ces marqueurs de façon spécifique. Ces produits thérapeutiques de nouvelles générations ont le potentiel d’éliminer spécifiquement les cellules tumorales et donc de réduire les effets secondaires des traitements ainsi que les risques de rechute. Malheureusement, un certain nombre de patients ne peuvent bénéficier de ces traitements, du fait de l’absence de biomarqueurs connus à la surface de leur tumeur. Ce projet a ainsi pour ambition de développer de nouvelles thérapies ciblées en exploitant une nouvelle classe de biomarqueurs et ainsi de venir enrichir l’arsenal thérapeutique disponible pour le traitement des cancersCancer is the second cause of death worldwide. Recent advance in cancer treatments involved the identification of cancer biomarkers and the development of efficient therapeutic products able to specifically recognize them. This new class of products has the ability to specifically target tumor cells, with the major advantages to decrease or abolish treatments side effects and relapses of the disease. Unfortunately, a certain number of patients do not respond to those treatments lacking the expression of those biomarkers on their tumor. This project aims at developing new targeted therapies by exploiting a new class of cancer biomarkers, which would potentially extend the therapeutics options against cancer
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Collet, Guillaume. "Thérapie génique de l'angiogenèse tumorale ciblée par des cellules endothéliales immatures." Phd thesis, Université d'Orléans, 2012. http://tel.archives-ouvertes.fr/tel-00843646.
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Les facteurs de croissance endothéliaux (VEGFs) sont produits par les tumeurs qui sont hypoxiques. Principaux responsables de la néo-vascularisation pathologique, ils régulent le stroma tumoral. Les nouvelles stratégies qui ciblent et inhibent le VEGF ouvrent vers la thérapie anti-cancéreuse moderne. Elles ont pour but de contrôler l'angiogenèse tumorale plutôt que la détruire. Le défi est donc de piéger sélectivement le VEGF produit en excès, dans le microenvironnement tumoral, sous l'effet de l'hypoxie. La thèse présentée dans ce manuscrit est consacrée à la réalisation d'une nouvelle stratégie ciblante par l'intermédiaire de cellules, aussi appelée " Cheval de Troie ". Elle combine dans la même entité, une unité de ciblage et un système de délivrance spécifique d'un gène/molécule thérapeutique. Dans le but d'adresser la thérapie aux cellules cancéreuses sans affecter les cellules saines, un modèle de cellules endothéliales de type précurseur (CEPs) a été utilisé comme cellules ciblantes capables d'atteindre spécifiquement le site tumoral. Les CEPs ont été " armées " pour exprimer un gène thérapeutique chargé d'inhiber le VEGF. La neutralisation a été obtenue par la production d'une forme soluble du récepteur-2 du VEGF (VEGFR2 soluble), agissant comme inhibiteur. Caractéristique des tumeurs solides se développant, l'hypoxie a été choisie pour déclencher/éteindre l'expression et la sécrétion du VEGFR2 soluble, en introduisant, en amont du gène thérapeutique, une séquence régulatrice : HRE. Adressé au site tumoral par les CEPs, le régulateur de l'angiogenèse qu'est la forme soluble du VEGFR2, est exprimé de manière conditionnée et réversible, à l'hypoxie. Ceci ouvre à de nouvelles stratégies de normalisation contrôlée et stable des vaisseaux tumoraux en vue de l'utilisation de thérapies combinées.
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Calì, Bianca. "Cellular communication and cancer therapy: targeting Ca2+and NO signalling within the tumour microenvironment." Doctoral thesis, Università degli studi di Padova, 2014. http://hdl.handle.net/11577/3423745.
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Cell death and bystander effect are crucial for both the efficacy of cancer therapy and the modulation of anti-tumour immune response. The ‘bystander effect’ refers to a process whereby untreated cells exhibit either the deleterious or beneficial indirect effects as a result of signals received from nearby targeted cells. Various molecular players and pathways have been suggested to mediate the bystander effects, nevertheless to date it is not known which are the key molecules and cellular mechanisms underpinning cell death signal propagation. Several reports suggest the involvement of both nitric oxide (NO) and reactive nitrogen species (RNS) in mediating the bystander effect. Nevertheless their role in the process has not been totally defined since these molecules can either inhibit or sustain tumour progression. Additionally, the methods conventionally applied for NO tracking do neither necessarily reflect real-time NO production nor allow studies into intact three-dimensional tumour mass.
The primary aim of this study was to investigate and characterize cell signals responsible for the bystander effect within the tumour microenvironment, paying particular attention to NO. To this purpose, we exploited intravital microscopy by taking advantage of the novel fluorecent probe for NO (CuFL) and the dorsal skinfold chamber model on living tumour-bearing mice subjected to photodynamic therapy (PDT).
Notably, the PDT-triggered bystander effect was associated to the generation of very fast NO and Ca2+ waves within the whole tumour mass, supported the hypothesis that constitutive NOS activity might be crucial for the beneficial spread of bystander response and death signals propagation. Additionally, we demonstrated that PDT triggered apoptosis in bystander cells, through gap junction intercellular communication.
Finally, our results, provide the first direct evidence of NO involvement in bystander responses within a three-dimensional tumour mass, and strikingly corroborate the notion that connexin gap junction are instrumental for mediating bystander death signals propagation.La morte cellulare e l’effetto bystander rappresentano degli elementi decisivi per l’efficacia della terapia antitumorale nonchè per la modulazione della risposta immunitaria contro il cancro. Per “effetto bystander” si intende il processo per il quale le cellule non soggette a determinati trattamenti farmacologici subiscono indirettamente gli effetti terapeutici, siano essi positivi o negativi, risultanti dal trattamento esclusivo delle cellule vicine. Nonostante siano state proposte diverse molecole e vie di segnalazione coinvolte nell’effetto bystander, i messaggeri molecolari essenziali ed i meccanismi che sottendono alla propagazione dei segnali di morte non sono ancora noti. Diversi studi suggeriscono un coinvolgimento dell’ossido nitrico (NO) e delle specie reattive dell’azoto (RNS) nell’effetto bystander tuttavia, il loro ruolo nel processo non è tuttora totalmente chiaro, considerato che essi possono sia inibire che sostenere la progressione del tumore. Inoltre, i metodi tradizionalmente usati per lo studio dell’ossido nitrico non riflettono necessariamente la produzione di NO in tempo reale nè consentono studi su complesse masse tumorali tridimensionali. L’obiettivo principale di questo studio è stato quello di individuare e caratterizzare i segnali cellulari responsabili dell’effetto bystander all’interno del microambiente tumorale, rivolgendo particolare attenzione all’NO. A questo scopo, abbiamo utilizzato delle tecniche di microscopia intravitale, avvalendoci di una nuova sonda fluorescente per l’NO (CuFL) e del modello sperimentale delle camerette dorsali impiantate su topi affetti da tumore e sottoposti a terapia fotodinamica (PDT). Da questo studio è emerso che l’effetto bystander indotto dalla terapia fotodinamica è associato alla generazione all’interno della massa neoplastica di onde molto rapide di segnali di NO e di Ca2+. Questi eventi avallano l’ipotesi che l’attività delle isoforme costitutive dell’enzima NOS possa esercitare un ruolo cruciale nella diffusione delle risposte bystander e nella trasmissione dei segnali di morte. Questo lavoro inoltre ci ha consentito di dimostrare che la terapia fotodinamica è in grado di indurre l’apoptosi delle cellule vicine non trattate (bystander) attraverso i meccanismi di comunicazione intercellulare mediati dalle giunzioni comunicanti. Infine, i risultati ottenuti hanno fornito la prima evidenza diretta della partecipazione dell’NO all’effetto bystander all’interno di una massa tumorale tridimensionale e corroborano efficacemente l’ipotesi che le giunzioni comunicanti formate da connesine siano essenziali per garantire la propagazione dei segnali di morte osservati nell’effetto bystander.
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Coulibaly, Tata Safiatou. "Double approche à la thérapie anti-tumorale à l'aide de vecteurs lentiviraux." Thesis, Strasbourg, 2017. http://www.theses.fr/2017STRAJ087/document.
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Le traitement du cancer par thérapie génique nécessite d’une part des gènes suicides efficaces et, d’autre part, l’adressage spécifique de ces gènes aux cellules cancéreuses. J'ai d'abord caractérisé un nouveau gène suicide dérivé de la désoxycytidine kinase humaine (dCK) : le M36. Comparé à la dCK, le M36 permet une meilleure sensibilisation des certaines cellules cancéreuses aux traitements avec différents chimiothérapeutiques comme la gemcitabine et la cytarabine. Ces résultats sont particulièrement encourageants pour l'élimination des cellules cancéreuses résistantes à ces traitements du fait d’un défaut de la dCK. Dans une deuxième partie, je me suis intéressée à l'adressage spécifique des transgènes aux cellules cancéreuses par les vecteurs lentiviraux. J'ai travaillé à la preuve de concept qu’une enveloppe (Env) VIH modifiée peut permettre un tel ciblage. J'ai généré une Env qui a fortement diminué son tropisme naturel et qui comporte un motif liant le marqueur tumoral modèle HER2Cancer gene therapy requires the use of an effective suicide gene and the specific targeting of cancer cells. In my PhD work, I have first characterized a new potential suicide gene derived from human deoxycytidine kinase (dCK): M36. Compared to dCK, M36 improves sensitization of certain cancer cells to treatment with chemotherapeutic compounds as gemcitabine and AraC. These results are particularly encouraging for the elimination of cancer cells resistant to the treatment because of a defect with dCK. In a second part, I have worked at the proof of concept that a modified HIV envelope can allow specific targeting of cancer cells by lentiviral vectors. During this work, I have generated a CD4i envelope with a strongly diminished natural tropism and that carries a motif known to bind the model cell surface cancer marker HER2. This envelope constitutes a good starting material to be improved by evolution in cell culture to obtain specific targeting of HER2+ cells
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Poupard, Nicolas. "Conception de polysaccharides sulfatés inhibiteurs de l’héparanase pour le traitement de l’angiogénèse tumorale." Thesis, La Rochelle, 2017. http://www.theses.fr/2017LAROS011/document.
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L’angiogénèse tumorale correspond à la formation de nouveaux vaisseaux sanguins afin d’alimenter la tumeur et d’amplifier son développement. Cette étape constitue un facteur pronostique défavorable pour les patients et son inhibition représente un fort intérêt thérapeutique. Parmi les acteurs participant à l’angiogénèse tumorale, on retrouve l’enzyme de dégradation héparanase au sein du microenvironnement tumoral de nombreux cancers. Ces travaux de thèse ont pour objectif de développer des inhibiteurs spécifiques de l’héparanase à partir de polysaccharides sulfatés pour le traitement de l’angiogénèse tumorale. La première partie de ces travaux a été consacrée à l’élaboration de polysaccharides sulfatés de bas poids moléculaires issus de sources animales (Héparine, Chrondroïtine sulfate), algales (Fucoïdanes, Carraghénane-λ-ι-κ) ou bactérienne (Dextran sulfate). Nous avons utilisé pour cela un procédé de dépolymérisation radicalaire assisté par ultrasons, développé en 2013 au laboratoire, que nous avons associé à un procédé de modification chimique appelé glycol-split. Les composés produits ont été évalués pour leurs activités d’inhibition de l’héparanase et de la coagulation sanguine. Ce criblage a notamment permis l’identification d’un dérivé de bas poids moléculaire issu de Carraghénane-λ possédant une forte inhibition de l’héparanase pour une faible inhibition de la coagulation. La deuxième partie de ces travaux s’est ensuite concentrée sur l’évaluation du potentiel anti-angiogénique des inhibiteurs de l’héparanase. Dans ce but, nous avons dans un premier temps évalué le rôle de l’hypoxie et/ou le manque de nutriments sur la production d’héparanase par des cellules de cancers mammaires. Dans ces conditions de stress, nous avons observé que la lignée MCF-7 excrétait une forte quantité d’héparanase. L’analyse en Matrigel 3D du réseau angiogénique formé par des cellules microvasculaires HskMEC, en présence du surnageant de MCF-7 riche en héparanase, a montré une forte stimulation de l’angiogénèse. Les mêmes tests réalisés en présence des inhibiteurs de l’héparanase ont montré une inhibition de l’angiogénèse qui semblait corrélée avec l’inhibition de l’héparanaseTumor angiogenesis is defined by the spouting of new blood vessels from preexisting ones in order to sustain and amplify the tumor development. This crucial step is associated with poor prognosis for patients and it’s inhibition is therefore considered as a primising way to treat cancer. Among several actors participating in the angiogenesis process, the degradative enzyme heparanase is active in the tumor microenvironment of many cancers. The work presented in this thesis aim to develop specific heparanase inhibitors using sulfated polysaccharides for the treatment of tumor angiogenesis. The first part of this work is dedicated to the conception of low molecular weights sulfated polysaccharides obtainable from animal source (Héparine, Chondroïtine sulfate), algal source (Fucoidan, Carrageenan-λ-ι-κ) and bacterial source (dextran sulfate). To do so, we used a depolymeriation process based on free radicals associated to ultrasonic waves developed in 2013 in the laboratory. This depolymerization method was then coupled with a chemical process called glycol-split. The produced compounds were evaluated for their capacity to inhibit heparanase and blood coagulation. This screening phase lead to the identification of a low molecular weight compound produced from λ-carrageenan endowed with a strong heparanase inhibition power and a low impact on the blood coagulation. The second part of this work was then focused on the evaluation of the anti-angiogenic properties of our best heparanase inhibitors. To do so, we first evaluated the role of hypoxia and lack of nutrients on the heparanase production from breast cancer cell lines. In these higly stressful conditions, we observed that the MCF-7 cell line secreted a huge amount of heparanase. 3D Matrigel angiogenesis network formation using Hsk-MEC microvascular cells in the presence of MCF-7 heparanase rich supernatant showed a strong angiogenesis stimulation. Same tests realized in the presence of heparanase inhibitors showed an angiogenesis inhibition power that seemed correlated with heparanase inhibition
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Ehret, Christophe. "Synthèse de nouveaux ligands du récepteur CD1d : applications à la vaccination anti-tumorale." Phd thesis, Université de Strasbourg, 2012. http://tel.archives-ouvertes.fr/tel-00767140.
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L'objectif de cette thèse a été d'optimiser la réponse immunitaire anti-tumorale induite par les cellules dendritiques (DC) et les cellules iNKTs, en réponse à la prise en charge du KRN7000 (a-galactosyl-céramide) par la molécule CD1d située sur les DCs. Le premier axe de travail visait à synthétiser de nouveaux analogues du KRN7000, en fonctionnalisant la position C6 du sucre et en greffant un groupement phényl sur l'une des chaînes grasses. Les études in vitro ont montré que les modifications apportées par rapport au KRN7000 n'ont pas altéré la prise en charge des molécules obtenues par les DCs. Dans tous les cas, une sécrétion de cytokines a pu être observée. Des études complémentaires visant à décrire le profil cytokinique in vivo sont en cours. Le second axe a consisté en la mise au point d'une stratégie de vectorisation du KRN7000 afin de favoriser sa présentation aux DCs, en l'associant à des molécules d'intérêt comme un peptide spécifique d'une tumeur, une molécule de ciblage des DCs ou des ligands des TLRs. Dans les conditions utilisées, le phénomène d'anergie induit classiquement par l'administration répétée du KRN7000 n'a pas pu être levé. Cependant, nous avons montré d'une part que le KRN7000 vectorisé dans les liposomes est toujours pris en charge par les cellules dendritiques, et d'autre part qu'une réponse immunitaire se traduisant par la production de cytokines par les cellules iNKTs est induite.
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Pautu, Vincent. "Steath and pH-sensitive lipid nanocapsules : targeting the tumor microenvironment of melanoma." Thesis, Angers, 2018. http://www.theses.fr/2018ANGE0042.
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Il a été démontré que l’acidité de l’environnement tumoral jouait un rôle dans la résistance aux chimiothérapies. L’utilisation de nanovecteurs, tels que les nanocapsules lipidiques (LNC), permet non seulement d’améliorer le temps de biodistribution de substances actives, mais aussi de cibler l’environnement tumoral tout en protégeant les actifs de cet environnement acide. L’objectif de cette thèse porte ainsi sur l’optimisation et l’évaluation de LNC furtives et pH-sensibles dans le contexte du mélanome.Dans un premier temps, ces travaux ont consisté à caractériser la vascularisation de mélanomes humain et murin. Ces études ont permis de comparer différentes tumeurs (densité, taille et structure) et de déterminer si l’usage de nanomédecines est approprié dans ce contexte.La seconde partie s’est orientée sur l’élaboration de polymères combinant furtivité et pH-sensibilité. Ces copolymères composés de N-vinylpyrrolidone (NVP)et de vinylimidazole ont été synthétisés par polymérisation RAFT et post-insérés à la surface des LNC. Ces modifications ont donné lieu à des LNC présentant des charges de surface pH-dépendantes,entrainant une augmentation de leur internalisation à pH acide dans des cellules de mélanome. Finalement, des études de biodistribution ont mis en évidence l’intérêt de la NVP dans le développement de nanovecteurs furtifs. En conclusion, les copolymères développés ont permis de prolonger le temps de circulation, mais aussi d’apporter des propriétés pH-sensibles qui pourraient améliorer l’internalisation tumorale des LNC in vivo et donc de potentialiser l’effet d’une thérapie anticancéreuseTumor acidity has been shown to play a major role in resistance to chemotherapy. The use of nanomedicines, as lipid nanocapsules (LNC), allows to protect drugs from this acidic environment. They can also improve the biodistribution of therapeutics and to target the tumor environment. The aim of this thesis concerns the evaluation and characterization of stealth and pH-sensitive LNC in the context of melanoma. Firstly, these works consisted in characterizing the vascularization of human and mice melanoma. These studies allowed to compare different tumors (density, size and structure), and determine if the used of nanocarrier is suitable in the context of melanoma.The second part of this thesis described the development and the characterization of new copolymers, combining stealth and pH-sensitive properties. These copolymers, composed of Nvinylpyrrolidone(NVP) and vinylimidazole, were synthesized by RAFT polymerization and were post in sertedonto LNC surface. These modifications allowed to obtain charge reversal nanocarriers, leading to increase their melanoma cell uptake underacid pH. Finally, biodistribution of these modified nanoparticles was studied in vivo and highlighted the interest of NVP in the development of stealth nanocarriers. To conclude, the developed copolymers able to extend nanocarrier circulation time and to provide pH-responsive properties which should increase the tumor internalization of LNC invivo and potentiate the effect of anticancer drugs
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Destouches, Damien. "Ciblage de la nucléoline de surface par les pseudopeptides NucAnts dans l’inhibition de la croissance tumorale et de l’angiogenèse associée." Thesis, Paris Est, 2009. http://www.theses.fr/2009PEST0045.
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La recherche contre le cancer est aujourd’hui tournée vers les thérapies ciblées. Dans ce contexte, la nucléoline et la nucléophosmine sont fortement impliquées dans la croissance tumorale et l’angiogenèse associée et surexprimées dans les cellules tumorales et endothéliales activées. Elles apparaissent donc comme des cibles de choix. Le pseudopeptide HB-19 lie la nucléoline de surface, inhibe la croissance cellulaire de nombreuses lignées de cellules tumorales et induit la mort de ces cellules tumorales par apoptose. D’autre part, il inhibe, in vitro et in vivo, plusieurs étapes de l’angiogenèse tumorale. Ces deux activités mènent, in vivo, à l’inhibition de la croissance tumorale dans de nombreux modèles de croissance tumorale chez la souris. Dans le but d’améliorer les activités observées avec HB- 19, des pseudopeptides dérivés de ce dernier ont été synthétisés. Ainsi le NucAnt 6L (N6L) montre une activité 5 à 10 fois supérieure à celle de HB-19 selon les modèles. Son activité anti-métastatique a également été démontrée. L’étude du mécanisme d’action des pseudopeptides a permis d’identifier deux nouveaux récepteurs: les héparanes sulfates et la nucléophosmine. L’importance du TIMP-3 dans son activité anti-métastatique a également été soulignée. Enfin, aucune toxicité n’a été observée chez les souris aux doses employées et la synthèse de N6L peut être effectuée à l’échelle industrielle. N6L apparaît donc comme un composé prometteur pour une thérapie anti-cancéreuseThe cancer research is nowadays interested in targeting therapies. In this context, nucleolin and nucleophosmin are proteins highly involved in tumor growth and angiogenesis and over-expressed in activated endothelial and tumor cells. So, they appear as very promising targets. The pseudopeptide HB-19 binds to cell surface-expressed nucleolin, inhibits different tumor cell growth and induces cell death by apoptosis. Furthermore, it inhibits, in vitro and in vivo, several steps of angiogenesis. These two activities lead, in vivo, to the suppression of tumor growth and angiogenesis in several mice models. In order to improve the activities observed with HB-19, new compounds derived from HB-19 were synthesized. So, NucAnt 6L (N6L) show 5 to 10 fold stronger anti-tumoral activity than HB- 19 depending of the model. Study of their action mechanism allowed us to identify two new receptors: nucleophosmin and heparan sulfates. The importance of TIMP-3 in anti-metastatic activity has also been highlighted. Finally, no toxicity has been observed in mice treated with N6L which can easily industrially be synthesized. N6L appears to be a promising compound for anti-cancer therapies
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TULLIO, CHIARA. "Development of an effective tumor-targeted contrast agent for magnetic resonance imaging based on Mn/H-ferritin nanocomplexes." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2021. http://hdl.handle.net/10281/307662.
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La risonanza magnetica per immagini è una delle tecniche diagnostiche più sofisticate attualmente utilizzate in clinica. I mezzi di contrasto di contrasto (MC) possono essere somministrati per ottenere una migliore risoluzione delle immagini dei tessuti detectabili, nonché per ridurre il rischio di diagnosi errate causate dalla limitata sensitività di questa tecnica. Attualmente, soltanto alcuni MC a base di gadolinio sono approvati per un utilizzo in ambito clinico. Tuttavia, a causa di alcune problematiche legate alla loro tossicità, la loro somministrazione è consentita soltanto in particolari pazienti e con il minimo dosaggio. In questa tesi è riportata la sintesi e la validazione di un nuovo tipo di MC a base di manganese: Mn@HFn-RT. Il manganese è un metallo endogeno paramagnetico in grado di produrre un contrasto positivo simile al gadolinio e con una inferiore tossicità per l’uomo. Ioni di manganese sono stati caricati efficacemente all’interno del guscio di una proteina ricombinante chiamata H-ferritina, che si è dimostrato essere riconosciuta dalle cellule che overesprimono il recettore TfR1, come accade nella maggior parte delle cellule tumorali. Mn@HFn-RT è stato caratterizzato, dimostrando un’eccellente stabilità colloidale, un’ottima relassività ed un buon profilo di sicurezza. Da esperimenti condotti in vitro è stato possibile confermare la capacità di Mn@HFn-RT di raggiungere efficacemente le cellule tumorali, e si è inoltre dimostrata la sua abilità di favorire il riconoscimento di masse tumorali in vivo: infatti, Mn@HFn-RT somministrato con un basso dosaggio di metallo, ha dimostrato una ottima clearance ed è stato in grado di far risaltare una massa di tumore al seno impiantato in topo. Per tali motivi, Mn@HFn-RT può essere considerato un promettente MC per la risonanza magnetica.Magnetic resonance imaging is one of the most sophisticated diagnostic tools in clinic. Contrast agents (CAs) may be exploited to afford much clearer images of detectable organs and to reduce the risk of misdiagnosis, due to the limited sensitivity of the technique. Actually, only a few gadolinium-based CAs are approved for clinical use. Nevertheless, concerns over their toxicity remain and their administration is approved only under strict control. In the present study it is reported the synthesis and validation of a novel manganese-based CA, Mn@HFn-RT. Manganese is an endogenous paramagnetic metal able to produce a positive contrast like gadolinium, however it is estimated to cause lower toxicity for human body. MN ions have been efficiently loaded inside the shell of a recombinant human protein called H-ferritin that is recognized by cells overexpressing TfR1, including the majority of cancer cell. Mn@HFn-RT was characterized, showing excellent colloidal stability, superior relaxivity and good safety profile. From in vitro experiments it was possible to confirm the ability of Mn@HFn-RT to efficiently target cancer cells and thus favor the detection of the tumor region in a breast cancer in vivo model with very low metal dosages and showing rapid clearance. Mn@HFn-RT looks a promising CA candidate to be developed for MRI.
Books on the topic "Targeting tumorale"
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Reader, Jocelyn, Sarah Lynam, Amy Harper, Gautam Rao, Maya Matheny, and Dana M. Roque. Ovarian Tumor Microenvironment and Innate Immune Recognition. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190248208.003.0004.
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Ovarian adenocarcinoma is typified by detection at late stages with dissemination of cancer cells into the peritoneal cavity and frequent acquisition of chemoresistance. A number of studies show the importance of the tumor microenvironment and innate immune recognition in tumor progression. Ovarian cancer cells can regulate the composition of their stroma to promote the formation of ascitic fluid rich in cytokines and bioactive lipids such as PGE2, and to stimulate the differentiation of stromal cells into a pro-tumoral phenotype. In response, cancer-associated fibroblasts, cancer-associated mesenchymal stem cells, tumor-associated macrophages, and other peritoneal cells can act through direct and indirect mechanisms to regulate tumor growth, chemoresistance via alteration of class III β tubulin, angiogenesis and dissemination. This chapter deciphers the current knowledge about the role of stromal cells, associated secreted factors, and the immune system on tumor progression. This suggests that targeting the microenvironment holds great potential to improve the prognosis of patients with ovarian adenocarcinoma.
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Mouldy, Sioud, ed. Target discovery and validation: Reviews and protocols. Totowa, N.J: Humana Press, 2007.
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Sioud, Mouldy. Target Discovery and Validation Reviews and Protocols: Emerging Strategies for Targets and Biomarker Discovery, Volume 1. Humana Press, 2010.
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Target Discovery and Validation Reviews and Protocols: Emerging Molecular Targets and Treatment Options,Volume 2 (Methods in Molecular Biology). Humana Press, 2007.
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Sioud, Mouldy. Target Discovery and Validation Reviews and Protocols: Emerging Molecular Targets and Treatment Options,Volume 2. Humana Press, 2010.
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Sioud, Mouldy. Target Discovery and Validation Reviews and Protocols: Emerging Strategies for Targets and Biomarker Discovery, Volume 1 (Methods in Molecular Biology). Humana Press, 2006.
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Target Discovery and Validation Reviews and Protocols: Emerging Strategies for Targets and Biomarker Discovery. Humana P.,U.S., 2006.
Find full textBook chapters on the topic "Targeting tumorale"
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Nanni, Cristina, and Stefano Fanti. "Molecular Imaging and Tumoral Antigen Targeting." In Radiological Imaging of the Kidney, 863–70. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-54047-9_35.
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Villegas, Maria Rocio, Victoria Lopez, Verónica Rodríguez-García, Alejandro Baeza, and María Vallet-Regí. "Janus-Type Mesoporous for Sequential Tumoral Cell and Targeting." In Methods in Molecular Biology, 341–61. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1262-0_22.
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Juhl, H., F. Czubayko, and D. Henne-Bruns. "Ribozym-targeting als gentherapeutisches Verfahren zur Behandlung maligner Tumore." In Vielfalt und Einheit der Chirurgie Humanität und Wissenschaft, 1474–77. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-642-45774-6_361.
Full textConference papers on the topic "Targeting tumorale"
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Andreu, David, Beatriz G. de la Torre, and Gandhi Rádis-Baptista. "NrTP, a cell penetrating peptide exquisitely targeting the nucleolus of tumoral cells." In XIth Conference Biologically Active Peptides. Prague: Institute of Organic Chemistry and Biochemistry, Academy of Sciences of the Czech Republic, 2009. http://dx.doi.org/10.1135/css200911001.
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Ucar, Deniz A., Giulia Monticone, Fokhrul Hossain, Samarpan Majumder, Dorota Wyczechowska, Matthew J. Dean, Luis Del Valle, et al. "Abstract 6691: Delivering intra-tumoral immune modulators and targeting cancer stem cells using recombinant- AAVs." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-6691.
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MITOU, Géraldine, Julie FRENTZEL, Laurence LAMANT, Fabienne MEGGETTO, Estelle ESPINOS, Patrice CODOGNO, Pierre BROUSSET, and Sylvie GIURIATO. "Abstract 663: Targeting autophagy potentiates the anti-tumoral action of crizotinib in ALK-positive anaplastic large cell lymphoma." 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.am2015-663.
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Casciaro, Sergio, Giulia Soloperto, Francesco Conversano, Ernesto Casciaro, Antonio Greco, Stefano Leporatti, Aime Lay-Ekuakille, and Giuseppe Gigli. "Automatic image detection of Halloysite clay Nanotubes as a future ultrasound theranostic agent for tumoral cell targeting and treatment." In 2014 IEEE International Instrumentation and Measurement Technology Conference (I2MTC). IEEE, 2014. http://dx.doi.org/10.1109/i2mtc.2014.6860878.
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Paez, Alejandra V., Carla Pallavicini, Federico Schuster, Jimena Giudice, Pia Valacco, Estefania Labanca, Nicolas Anselmino, et al. "Abstract 5058: Hitting the brakes on the migratory capacity of tumoral cells: Targeting key regulators of actin dynamics in prostate cancer." 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.am2016-5058.
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Mössner, Ekkehard, Gerald Tuffin, Sara Colombetti, Olivier Freytag, Samuel Moser, Claire Dunn, Marina Bacac, et al. "Abstract LB-236: M4-3-ML2, a novel glycoengineered humanized IgG1 antibody, targeting a membrane-proximal epitope of MCSP/CSPG4 exhibits potent ADCC inductionin vitroandin vivoanti-tumoral efficacy in disseminated melanoma models." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-lb-236.
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