Auswahl der wissenschaftlichen Literatur zum Thema „Elr+cxcl“
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Zeitschriftenartikel zum Thema "Elr+cxcl"
Penco-Campillo, Manon, Clément Molina, Patricia Piris, Nouha Soufi, Manon Carré, Marina Pagnuzzi-Boncompagni, Vincent Picco et al. „Targeting of the ELR+CXCL/CXCR1/2 Pathway Is a Relevant Strategy for the Treatment of Paediatric Medulloblastomas“. Cells 11, Nr. 23 (05.12.2022): 3933. http://dx.doi.org/10.3390/cells11233933.
Der volle Inhalt der QuelleGiuliano, Sandy, Mélanie Guyot, Renaud Grépin und Gilles Pagès. „The ELR+CXCL chemokines and their receptors CXCR1/CXCR2“. OncoImmunology 3, Nr. 4 (April 2014): e28399. http://dx.doi.org/10.4161/onci.28399.
Der volle Inhalt der QuelleKomolafe, Kayode, und Maricica Pacurari. „CXC Chemokines in the Pathogenesis of Pulmonary Disease and Pharmacological Relevance“. International Journal of Inflammation 2022 (17.09.2022): 1–16. http://dx.doi.org/10.1155/2022/4558159.
Der volle Inhalt der QuelleBoshagh, Mohammad Amin, Poorya Foroutan, Mohammad Raman Moloudi, Shohreh Fakhari, Parisa Malakouti, Bahram Nikkhoo und Ali Jalili. „ELR positive CXCL chemokines are highly expressed in an animal model of ulcerative colitis“. Journal of Inflammation Research Volume 12 (Juni 2019): 167–74. http://dx.doi.org/10.2147/jir.s203714.
Der volle Inhalt der QuelleMontemagno, Christopher, Arnaud Jacquel, Charlotte Pandiani, Olivia Rastoin, Rosie Dawaliby, Thomas Schmitt, Maxence Bourgoin et al. „Unveiling CXCR2 as a promising therapeutic target in renal cell carcinoma: exploring the immunotherapeutic paradigm shift through its inhibition by RCT001“. Journal of Experimental & Clinical Cancer Research 43, Nr. 1 (19.03.2024). http://dx.doi.org/10.1186/s13046-024-02984-2.
Der volle Inhalt der QuelleGrytsai, Oleksandr, Maeva Dufies, Julie Le Du, Olivia Rastoin, Leticia Christina Pires Gonçalves, Lou Mateo, Sandra Lacas-Gervais et al. „A Potent Solution for Tumor Growth and Angiogenesis Suppression via an ELR+CXCL-CXCR1/2 Pathway Inhibitor“. ACS Medicinal Chemistry Letters, 03.04.2024. http://dx.doi.org/10.1021/acsmedchemlett.4c00053.
Der volle Inhalt der QuelleKoduri, Madhuri Amulya, Deeksha Prasad, Shriya Upadhyaya, Jilu Jaffet, Swapna S. Shanbhag, Sayan Basu und Vivek Singh. „Differential expression of tear film cytokines in Stevens–Johnson syndrome patients and comparative review of literature“. Scientific Reports 11, Nr. 1 (16.09.2021). http://dx.doi.org/10.1038/s41598-021-97575-y.
Der volle Inhalt der QuelleSchisler, Jonathan C., Robert Schuck, Xuming Dai, Kaitlin Lenhart, Craig R. Lee, George A. Stouffer und Cam Patterson. „Clinical Evidence of a Protective Role for CXCL5 in Coronary Artery Disease Progression in the Elderly“. FASEB Journal 30, S1 (April 2016). http://dx.doi.org/10.1096/fasebj.30.1_supplement.1177.17.
Der volle Inhalt der QuelleDissertationen zum Thema "Elr+cxcl"
Mateo, Lou. „Synthèse et évaluation de nouveaux antagonistes des récepteurs CXCR1-2 pour cibler conjointement l’angiogenèse et l’inflammation dans les pathologies cancéreuses“. Thesis, Université Côte d'Azur, 2021. http://www.theses.fr/2021COAZ4006.
Der volle Inhalt der QuelleCancer is one of the main causes of death in the world. Angiogenesis and inflammation represent two essential hallmarks in the development and progression of tumors and are essential for the survival of the cancer cells. Better knowledge of cellular mechanisms has enabled the development of targeted anti-angiogenic therapies. However, the emergence of resistance constitutes the main limitation of these current anti-angiogenics targeted therapies, as you may know the anti-VEGF therapies. But in parallel to the VEGF pathway, another crucial pro-angiogenic and pro-inflammatory axis in cancers is required: the CXCL-ELR+/CXCR pathway, particularly in metastatic kidney cancer. The aim of this work was to develop original small organic molecules able to inhibit the ligand/receptor interaction (CXCL-ELR+ / CXCR1-2) in order to have both anti-inflammatory and anti-angiogenic activities. The 2-aminobenzothiazinone pattern was chosen for the preparation of 3 new classes of inhibitors. Divergent synthesis strategies were used to obtain the members of families 1 & 2, although the conditions have been adapted according to the reactivity of each substrate. The last family of molecules was prepared according to a linear synthesis. However, this latter strategy displayed some limitations during the cyclisation step. Thereafter, biological evaluations revealed a promising compound exhibiting an IC50 of 0.6 μM on the 786-O cell line compared with our reference molecule (IC50 = 2 μM). Other result highlighted that this compound also exerted an inhibition of the chemotaxis of cells expressing CXCR1-2 receptors. Further studies on zebrafish are planned with this compound in order to study its ability to interfere with the angiogenesis phenomenon in vivo
Penco-Campillo, Manon. „Le VEGFC et les récepteurs CXCR1/2 : des cibles pertinentes pour le traitement des médulloblastomes pédiatriques“. Electronic Thesis or Diss., Université Côte d'Azur, 2022. http://www.theses.fr/2022COAZ6025.
Der volle Inhalt der QuelleMedulloblastoma (MB) is the most common and aggressive pediatric brain tumor. Despite aggressive multimodal treatment, resulting in significant side effects, 30% of patients develop resistance and relapse following the appearance of metastases within 5 years. Recurrences cannot be controlled by conventional (radio- and chemotherapy) or targeted (anti-angiogenic, anti-inflammatory, anti-immune checkpoint) treatments. The objective of my thesis is therefore to discover new targets and relevant therapeutic strategies for these patients at diagnosis or after a relapse.MBs are highly vascularized tumors. The phenomenon of resistance is, in part, linked to the development of blood (angiogenesis) and lymphatic (lymphangiogenesis) vessels in the tumor, which constitute the main routes of metastatic dissemination. The lymphatic growth factor, VEGFC, and its receptors/co-receptors are the major players in lymphangiogenesis. In the first part of my thesis, I showed that VEGFC is inversely correlated to MB cell growth and aggressiveness. Indeed, VEGFC decreases the proliferation and migration of MB cells, as well as their ability to form pseudo-vessels in vitro, by an autocrine signalization. Cells resistant to radiotherapy show elevated levels of VEGFC and lose their ability to migrate and form pseudo-vessels. Irradiation reduces the aggressiveness of MB cells by a VEGFC-dependent process. VEGFC-overexpressing cells and radiation-resistant cells form smaller experimental tumors in nude mice. Thus, VEGC appears to be a negative regulator of MB growth. These results pave the way for the development of pro-VEGFC therapies in these cancers.In the second part of my thesis, I correlated the expression of the ELR+CXCL/CXCR1-2 pro-angiogenic and pro-inflammatory signaling pathway to shorter survival in patients with MB. I showed that a novel pharmacological inhibitor (C29) of CXCR1-2 receptors inhibits proliferation, CXCL8/CXCR1-2-dependent migration, invasion and pseudo-vessel formation by susceptible or resistant MB cells to radiotherapy. C29 reduces the growth of experimental MBs in an ex vivo organotypic mouse model and crosses the blood-brain barrier. Thus, targeting CXCR1-2 represents a promising strategy for the treatment of pediatric MB, at first line or at relapse.Key words: pediatric medulloblastoma, VEGFC/VEGFR, CXCR1-2, ELR+CXCL cytokines, targeted therapy, lymphangiogenesis, angiogenesis