Готові списки джерел за темами / Inhibiteur de la tyrosine kinase

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Добірка наукової літератури з теми "Inhibiteur de la tyrosine kinase"

Автор: Grafiati

Опубліковано: 17 травня 2025

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Статті в журналах з теми "Inhibiteur de la tyrosine kinase"

Faure, Sébastien. "Un nouvel inhibiteur de tyrosine kinase." Actualités Pharmaceutiques 47, no. 473 (April 2008): 8. http://dx.doi.org/10.1016/s0515-3700(08)70234-9.

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I*, Al-Ani, Ata T, Daoud E, and Hassan SF. "Pharmacokinetics of the Tyrosine Kinase Inhibitor, Alectinib." Bioequivalence & Bioavailability International Journal 8, no. 2 (August 13, 2024): 1–8. https://doi.org/10.23880/beba-16000241.

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In 2015, the FDA authorized the use of a new tyrosine kinase inhibitor, Alectinib (ALB), for the intracellular domain of anaplastic lymphoma kinase with exo-cranial pointed mutations. Alectinib became the first drug to be licensed in the first line in August 2017. Its pharmacological properties differ from those of its predecessors, and new research is needed to identify the potential pharmacological and clinical implications. This review presents a critical analysis of the pharmacokinetics of Alectinib and its impact on hepatobiliary metabolism. We present current clinical data and new knowledge that could be developed for further clinical research. With this study, we hope to identify perspectives that can further prolong the efficacy of the anaplastic lymphoma kinase (ALK) tyrosine kinase Alectinib. Tyrosine kinases with receptors for the ligands of platelet growth are a class of enzymes with a key position in the pathogenesis of various molecular alterations that drive idiopathic cancers. The different characteristics of these kinases make them currently a preferential target for the design of new cancer inhibitors. A clear example of their efficiency is the landmark obtained in patients bearing tumors with intronic rearrangements or ALK translocations. These tumors are mostly found in subjects suffering from non-small-cell lung cancer with adenocarcinoma histology and not of the non-smoking type. Moreover, the development of different resistance mechanisms designated allosteric through targeted second-line interventions has culminated in a marked increase in patient survival.

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Trojanek, Joanna B., Maria M. Klimecka, Anna Fraser, Grazyna Dobrowolska, and Grazyna Muszyńska. "Characterization of dual specificity protein kinase from maize seedlings." Acta Biochimica Polonica 51, no. 3 (September 30, 2004): 635–47. http://dx.doi.org/10.18388/abp.2004_3549.

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A protein kinase of 57 kDa, able to phosphorylate tyrosine in synthetic substrates pol(Glu4,Tyr1) and a fragment of Src tyrosine kinase, was isolated and partly purified from maize seedlings (Zea mays). The protein kinase was able to phosphorylate exogenous proteins: enolase, caseins, histones and myelin basic protein. Amino acid analysis of phosphorylated casein and enolase, as well as of phosphorylated endogenous proteins, showed that both Tyr and Ser residues were phosphorylated. Phosphotyrosine was also immunodetected in the 57 kDa protein fraction. In the protein fraction there are present 57 kDa protein kinase and enolase. This co-purification suggests that enolase can be an endogenous substrate of the kinase. The two proteins could be resolved by two-dimensional electrophoresis. Specific inhibitors of typical protein-tyrosine kinases had essentially no effect on the activity of the maize enzyme. Staurosporine, a nonspecific inhibitor of protein kinases, effectively inhibited the 57 kDa protein kinase. Also, poly L-lysine and heparin inhibited tyrosine phosphorylation by 57 kDa maize protein kinase. The substrate and inhibitor specificities of the 57 kDa maize protein kinase phosphorylating tyrosine indicate that it is a novel plant dual-specificity protein kinase.

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BISOTTO, Sandra, and Elizabeth D. FIXMAN. "Src-family tyrosine kinases, phosphoinositide 3-kinase and Gab1 regulate extracellular signal-regulated kinase 1 activation induced by the type A endothelin-1 G-protein-coupled receptor." Biochemical Journal 360, no. 1 (November 8, 2001): 77–85. http://dx.doi.org/10.1042/bj3600077.

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The multisubstrate docking protein, growth-factor-receptor-bound protein 2-associated binder 1 (Gab1), which is phosphorylated on tyrosine residues following activation of receptor tyrosine kinases and cytokine receptors, regulates cell proliferation, survival and epithelial morphogenesis. Gab1 is also tyrosine phosphorylated following activation of G-protein-coupled receptors (GPCRs) where its function is poorly understood. To elucidate the role of Gab1 in GPCR signalling, we investigated the mechanism by which the type A endothelin-1 (ET-1) GPCR induced tyrosine phosphorylation of Gab1. Tyrosine phosphorylation of Gab1 induced by endothelin-1 was inhibited by PP1, a pharmacological inhibitor of Src-family tyrosine kinases. ET-1-induced Gab1 tyrosine phosphorylation was also inhibited by LY294002, which inhibits phosphoinositide 3-kinase (PI 3-kinase) enzymes. Inhibition of Src-family tyrosine kinases or PI 3-kinase also inhibited ET-1-induced activation of the mitogen activated protein kinase family member, extracellular signal-regulated kinase (ERK) 1. Thus we determined whether Gab1 regulated ET-1-induced ERK1 activation. Overexpression of wild-type Gab1 potentiated ET-1-induced activation of ERK1. Structure–function analyses of Gab1 indicated that mutant forms of Gab1 that do not bind the Src homology (SH) 2 domains of the p85 adapter subunit of PI 3-kinase or the SH2-domain-containing protein tyrosine phosphatase 2 (SHP-2) were impaired in their ability to potentiate ET-1-induced ERK1 activation. Taken together, our data indicate that PI 3-kinase and Src-family tyrosine kinases regulate ET-1-induced Gab1 tyrosine phosphorylation, which, in turn, induces ERK1 activation via PI 3-kinase- and SHP-2-dependent pathways.

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Guilhot, F. "Inhibiteur de tyrosine-kinase de 1re génération: place des associations." Oncologie 14, no. 10-11 (October 2012): 583–88. http://dx.doi.org/10.1007/s10269-012-2222-1.

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Soodvilai, S., S. H. Wright, W. H. Dantzler, and V. Chatsudthipong. "Involvement of tyrosine kinase and PI3K in the regulation of OAT3-mediated estrone sulfate transport in isolated rabbit renal proximal tubules." American Journal of Physiology-Renal Physiology 289, no. 5 (November 2005): F1057—F1064. http://dx.doi.org/10.1152/ajprenal.00185.2005.

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It was shown previously that OAT3 activity was differentially regulated by protein kinases including MAPK, PKA, and PKC. The present study investigated the short-term effect of tyrosine kinase and phosphatidylinositol 3-kinase (PI3K) on OAT3-mediated organic anion transport in S2 segments of renal proximal tubules. Genistein, a tyrosine kinase inhibitor, and wortmannin, a PI3K inhibitor, inhibited transport of estrone sulfate, a prototypic substrate for OAT3, in a dose-dependent manner. Previously, we showed that epidermal growth factor (EGF) stimulated OAT3 activity via the MAPK pathway. In the present study, we investigated whether EGF-stimulated OAT3 activity was dependent on tyrosine kinase and PI3K. We showed that EGF stimulation of OAT3 was reduced by inhibition of tyrosine kinase or PI3K, suggesting that they play a role in the stimulatory process. Inhibitory effects also indicated that tyrosine kinase and PI3K are involved in the MAPK pathway for EGF stimulation of OAT3 in intact renal proximal tubules, with PI3K acting upstream and tyrosine kinase acting downstream of mitogen-activated/extracellular signal-regulated kinase kinase activation.

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ZHONG, Hongying, та Kenneth P. MINNEMAN. "Activation of tyrosine kinases by α1A-adrenergic and growth factor receptors in transfected PC12 cells". Biochemical Journal 344, № 3 (8 грудня 1999): 889–94. http://dx.doi.org/10.1042/bj3440889.

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We compared the role of tyrosine kinases in α1A-adrenergic receptor (AR) and growth factor receptor stimulation of mitogen-activated protein kinase pathways in PC12 cells. Norepinephrine (NE) (noradrenaline), epidermal growth factor (EGF) and nerve growth factor (NGF) caused different patterns of tyrosine phosphorylation in PC12 cells stably expressing α1A-ARs. NE increased tyrosine phosphorylation of focal adhesion-related kinase Pyk2 and a 70 kDa protein, probably paxillin, whereas EGF strongly stimulated tyrosine phosphorylation of the EGF receptor and cytokine-activated kinase Jak2. The EGF receptor inhibitor AG1478 inhibited activation of extracellular signal-regulated kinases (ERKs) by EGF but not by NE. EGF and NGF strongly activated tyrosine phosphorylation of Shc and caused association of Src-homology collagen (Shc) with growth-factor-receptor-bound protein 2 (Grb2); however, neither NE nor UTP caused substantial activation of the Shc/Grb2 pathway. NE, UTP, EGF and NGF all increased tyrosine phosphorylation of Src, and this was inhibited by the Src inhibitor PP2. However, PP2 inhibited ERK activation in response to NE and UTP, but not in response to EGF or NGF. PP2 also completely blocked NE-induced PC12 cell differentiation, but had no measurable effect on NGF-induced differentiation. These studies show that activation of mitogen-activated protein kinase pathways by G-protein-coupled receptors and tyrosine kinase receptors proceed through distinct molecular pathways in PC12 cells, and support an obligatory role for Src activation in mitogenic responses to α1A-ARs in these cells.

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Rane, M. J., S. L. Carrithers, J. M. Arthur, J. B. Klein, and K. R. McLeish. "Formyl peptide receptors are coupled to multiple mitogen-activated protein kinase cascades by distinct signal transduction pathways: role in activation of reduced nicotinamide adenine dinucleotide oxidase." Journal of Immunology 159, no. 10 (November 15, 1997): 5070–78. http://dx.doi.org/10.4049/jimmunol.159.10.5070.

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Abstract Formyl peptide receptor activation of three mitogen-activated protein kinase (MAPK) cascades, extracellular signal-regulated kinases (ERKs), N-terminal kinases (JNKs), and p38 MAPK was examined in differentiated HL-60 granulocytes. FMLP stimulated a concentration- and time-dependent increase in ERK, JNK, and p38 MAPK activities, all of which were dependent on a pertussis toxin-sensitive G protein. Pharmacologic inhibitors were used to examine the roles of tyrosine kinases, phosphatidylinositol 3-kinase, protein kinase C, and phospholipase C. FMLP-stimulated ERK activity was dependent on tyrosine kinases, phosphatidylinositol 3-kinase, protein kinase C, and phospholipase C; p38 MAPK activation was dependent on phosphatidylinositol 3-kinase and phospholipase C; while JNK activation was independent of all of these signaling components. The mitogen-activated protein kinase/ERK kinase inhibitor PD098059 reduced ERK activation by 90%, while an inhibitor of p38 MAPK, SB203580, inhibited p38 MAPK activation by 80%. Both PD098059 and SB203580 inhibited FMLP-stimulated superoxide release, as did inhibitors directed against protein kinase C, tyrosine kinases, and phosphatidylinositol 3-kinase. We conclude that formyl peptide receptors are coupled to three MAPK cascades by Gi proteins. ERKs, p38 MAPK, and JNKs are each activated by distinct proximal signal transduction pathways. Activation of p38 MAPK is necessary for FMLP stimulation of respiratory burst activity; however, a second signal that may involve ERK is also required for this activity.

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Jin, N., R. A. Siddiqui, D. English, and R. A. Rhoades. "Communication between tyrosine kinase pathway and myosin light chain kinase pathway in smooth muscle." American Journal of Physiology-Heart and Circulatory Physiology 271, no. 4 (October 1, 1996): H1348—H1355. http://dx.doi.org/10.1152/ajpheart.1996.271.4.h1348.

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Two separate signal transduction pathways exist in vascular smooth muscle: one for cell growth, proliferation, and differentiation and the other for contraction. Although activation of protein tyrosine kinases is intimately involved in the signaling pathway that induces cell growth, proliferation, and differentiation, activation of myosin light chain kinase (MLCK) is an important step in the pathway leading to smooth muscle contraction. Indirect evidence suggests that “cross talk” exists between these two signaling pathways, but the common intermediates are not well defined. The purpose of this study was to determine whether a vasoconstrictor and a mitogen initiate crossover signaling between the tyrosine kinase pathway and the MLCK pathway in vascular smooth muscle. Rat aorta and pulmonary arteries were isolated and stimulated with either fetal calf serum (FCS) or phenylephrine in the presence or absence of a tyrosine kinase inhibitor (genistein) or tyrosine phosphatase inhibitor [sodium o-vanadate (Na3 VO4)]. Isometric force was recorded as a function of time; myosin light chain phosphorylation, protein tyrosine phosphorylation, and mitogen-activated protein kinase (MAPK) mobility were determined by immunoblotting. The results demonstrate that FCS, which contains a variety of growth factors known to activate tyrosine kinases, induced myosin light chain phosphorylation and contraction in vascular smooth muscle. Phenylephrine, a vasoconstrictor known to activate MLCK, induced tyrosine phosphorylation of a 42-kDa protein identified as MAPK. Tyrosine phosphorylation of this protein was inhibited by genistein and enhanced by vanadate. Genistein significantly inhibited both serum- and phenylephrine-induced myosin light chain phosphorylation as well as the serum- and phenylephrine-induced force generation, whereas vanadate enhanced these responses. These data demonstrate interrelationship between activation of the tyrosine kinase pathway and the MLCK pathway in vascular smooth muscle. These interactions may influence smooth muscle contraction and be important in the regulation of smooth muscle cell proliferation.

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Berleur, M., B. Baroudjian, C. Pages, M. Battistella, I. Chami, N. Basset-Seguin, N. Madjlessi, et al. "Traitement des mélanomes mutés c-kit par inhibiteur de tyrosine kinase." Annales de Dermatologie et de Vénéréologie 142, no. 12 (December 2015): S498—S499. http://dx.doi.org/10.1016/j.annder.2015.10.147.

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Більше джерел

Дисертації з теми "Inhibiteur de la tyrosine kinase"

Chevot, Franciane. "Conception et synthèse d'inhibiteurs de la tyrosine kinase Tyro3." Thesis, Paris 11, 2012. http://www.theses.fr/2012PA112024.

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Le cancer est la plus grande cause de mortalité après les maladies cardiaques. Les cellules cancéreuses sont issues des cellules saines dont les systèmes de multiplications et de régulations ont été annihilés. Elles se multiplient anarchiquement et forment des tumeurs. Nous nous sommes donc intéressés au cancer de la vessie qui en termes d’incidences dans les pays industrialisés est le quatrième cancer chez l’homme et le neuvième chez la femme. Parmi les nombreux récepteurs surexprimés dans les cellules tumorales de vessie, la kinase Tyro3 s’est révélée indispensable à la survie de ces cellules tumorales. Le premier objectif de cette thèse est de synthétiser un inhibiteur sélectif de Tyro3 possédant un noyau purine. Une première stratégie est orienté vers la synthèse d’un inhibiteur de type I alors que la seconde stratégie est menée vers la synthèse d’un inhibiteur de type II. Deux composés montrent une activité intéressante à 1 µM sur Tyro3 et semblent adopter un profil d’inhibition de type II. Le second objectif de la thèse présente une approche méthodologique pour la substitution de la position 2 et 8 du noyau purine. Une première partie présente la double lithiation des positions 2 et 8 de la 6-chloro-9-(tétrahydro-2H-pyran-2-yl)-9H-purine suivie d’une substitution avec différents électrophiles. Le dérivé 2,8-diodé obtenu est engagé dans une réaction de Sonogashira conduisant à des dérivés 2-alcynyl-8-iodo ou 2,8-dialcynyle. Une seconde partie traite de l’amidation et amination pallado-catalysées de la 8-iodo-6-(phénylsulfanyl)-9-(tétrahydro-2H-pyran-2-yl)-9H-purine
After heart diseases, cancer is the most important cause of death. Cancerous cells are normal cells which multiplication and regulation system have been affected. They anarchically grow and give tumors. We have investigated in bladder cancer which is fourth cancer among men and ninth cancer among women in industrial countries. Amongst overexpressed receptors in bladder cancerous cells, Tyro3 seems to be essential for the survival of bladder cancerous cells. First goal of this thesis is to synthesize a potent and selective inhibitor of Tyro3 with a purine scaffold. Two approaches have done. The first approach is the synthesis of a type I inhibitor whereas the second approach is the synthesis of a type II inhibitor. Two compounds have shown an interesting activity against Tyro3 at 1 µM and they seem to be type II inhibitors. The second part of the thesis was the functionalization of position 2 and 8 of purine scaffold. We show first the double deprotonation by lithium species of 6-chloro-9-(tétrahydro-2H-pyran-2-yl)-9H-purine following by substitution with different electrophiles. Obtained 2,8-di-iodine compound is engaged in Sonogashira reaction which gives 2-alkyne or 2,8-di-alkyne compunds. And, we investigate in palladium catalyzed amidation and amination of 8-iodo-6-(phénylsulfanyl)-9-(tétrahydro-2H-pyran-2-yl)-9H-purine

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Komla-Ebri, Davide Selom Komi. "Nouvelles approches thérapeutiques pour l’achondroplasie." Thesis, Sorbonne Paris Cité, 2016. http://www.theses.fr/2016USPCB040/document.

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Des mutations faux-sens au niveau du récepteur à activité tyrosine kinase FGFR3 (Fibroblast Growth Factor Receptor 3) entrainent sa suractivation qui apporte des dysfonctions biologiques dans plusieurs maladies. L’achondroplasie, la forme la plus commune de chondrodysplasie liée à Fgfr3, est une maladie génétique rare, touchant 1 nouveau-né sur 20 000, caractérisée par des signes cliniques spécifiques : nanisme rhizomélique, membres courts, macrocéphalie, hypoplasie de l’étage moyen de la face, compression cervico-médullaire. L’activité anormale du récepteur induit des défauts de l’ossification endochondrale responsables du phénotype pathologique. Pendant longtemps le seul traitement pour cette maladie a été l’allongement chirurgical des membres, cependant au cours des dernières années de nombreux chercheurs ont développé des potentielles stratégies thérapeutiques basées sur des études moléculaires. L’objectif de ma thèse était d’évaluer une nouvelle approche thérapeutique pour l’achondroplasie. Une stratégie thérapeutique prometteuse prévoit l’utilisation de petits inhibiteurs chimiques, connus sous le nom d’inhibiteurs de tyrosine kinases, qui sont capables d’arrêter l’activité de FGFR3. J’ai estimé les effets d’un de ces composés, NVP-BGJ398, dans un modèle murin mimant le nanisme achondroplase (Fgfr3Y367C/+). Des expérimentations effectuées ont montré une amélioration des caractéristiques pathologiques dans les souris traitées avec NVP-BGJ398. Nous avons également examiné l’impact de la mutation activatrice de FGFR3 sur le développement mandibulaire. L’étude a reconnu un défaut dans la croissance mandibulaire chez l’homme et la souris atteints. En outre nous avons pu investiguer la croissance osseuse de la mandibule et corriger le défaut pathologique avec NVP-BGJ398. Enfin j’ai participé à des analyses moléculaires pour décrire comment trois mutations de FGFR3 localisées à la même position (Lys650) peuvent induire trois différents nanismes avec sévérité croissante. Les résultats ont fourni une meilleure compréhension des mécanismes moléculaires pathologiques et pourront mener à des nouvelles cibles pour des approches thérapeutiques
Missense mutations in the tyrosine kinase receptor FGFR3 (Fibroblast Growth Factor Receptor 3) lead to its overactivation causing biological dysfunctions in several diseases. Achondroplasia, the most common Fgfr3-related chondrodysplasia, is a rare genetic disorder, affecting 1 in 20000 live births, characterized by particular clinical features: rhizomelic dwarfism, short limbs, macrocephaly, midface hypoplasia, cervicomedullary compression. The abnormal activity of the receptor induces endochondral ossification defects that are responsible for the pathological phenotype. For a long time the only treatment for this disease was the limb lengthening surgery, however in recent years several researchers have developed potential therapeutic strategies based on molecular studies. The objective of my thesis was to evaluate a novel therapeutic approach for achondroplasia. A promising therapeutic strategy involved the use of small chemical inhibitors, known as tyrosine kinase inhibitors, that are able to arrest the FGFR3 activity. I have assessed the effects of one of these compounds, NVP-BGJ398, in a mouse model mimicking the acondroplastic dwarfism (Fgfr3Y367C/+). The experiments performed showed an improvement of all pathological hallmarks in NVP-BGJ398 treated mice. We have also inspected the impact of the activating FGFR3 mutation on the mandibular development. The study established a defect in mandibular growth in both affected patients and mice. Furthermore we could investigate the mandibular bone growth and correct the pathological defect with NVP-BGJ398. Finally I have participated in molecular analyses to describe how three FGFR3 mutations at the same position could lead to three different dwarfisms with increasing severity. The results provided a better understanding of FGFR3 pathological molecular mechanisms and could lead to new targets for therapeutic approaches

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Dang-Trung, Khoi͏̈-Nguyên. "Intérêt potentiel en chimiothérapie anticancéreuse des inhibiteurs de protéines à activité tyrosine kinase : exemple de la génistéine." Paris 5, 1995. http://www.theses.fr/1995PA05P119.

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Hammam, Kahina. "Nouveau concept de resensibilisation à la chimiothérapie en activant la nucléoside kinase dCK par le masitinib, un inhibiteur de protéines tyrosine kinases." Thesis, Aix-Marseille, 2014. http://www.theses.fr/2014AIXM5047.

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La résistance à la chimiothérapie constitue un frein majeur à son efficacité. Notre équipe a récemment pu montrer que le masitinib, un nouvel inhibiteur de protéines tyrosine kinases, possède une activité de resensibilisation des cellules tumorales résistantes à la chimiothérapie lorsqu'il est combiné à certaines chimio-drogues. L'objectif des travaux de cette thèse est de déterminer les voies de signalisation, modulées par l'action du masitinib, qui sont impliquées dans la resensibilisation aux chimiothérapies et amélioration de l'activité anti-tumorale.Dans la première partie de la thèse, nous avons pu identifier la nucléoside kinase dCK (désoxycytidine kinase), protéine activatrice d'un grand nombre de chimiothérapies, comme nouvelle cible du masitinib. Cette première étude nous a permis de mettre en évidence un nouveau concept thérapeutique: le masitinib, un composé chimique de type inhibiteur de protéines tyrosine kinases, peut jouer en même temps le rôle d'activateur de nucléoside kinase.Nous avons pu mettre en évidence dans la deuxième partie de la thèse que le traitement combiné entre l'épi-drogue décitabine et le masitinib peut être plus efficace pour la réexpression de certains gènes non ou peu induits par la décitabine seule.En conclusion, ces travaux nous ont permis de mettre en évidence l'interaction entre un inhibiteur de protéine tyrosine kinases et une nucléoside kinase, dans un concept d'activation enzymatique qui pourra certainement servir de base pour l'élaboration de nouvelles petites molécules chimiques spécifiques de l'activation de dCK ou d'autres nucléosides kinases nécessaires à l'activation des drogues de chimiothérapie
Resistance to chemotherapy is considered as one of the major blockers of its efficacy. Recently, our team demonstrated that masitinib, a new tyrosine kinases inhibitor, possesse a resensitization activity of cell lines resistant to chemotherapy when associated with chemodrugs.The aim of this work is to determine signaling pathways, modulated by masitinib action, that could explain the resensitization to chemotherapy and improvement of anti-tumoral activity.In the first part of this work, we identified the nucleoside kinase dCK (deoxycytidine kinase), a chemotherapy activating protein, as a new target of masitinib. In summary, this first part of the work allowed us to describe a new and never described concept: masitinib, a small molecule belonging to tyrosine kinases group, can also play a role as nucleoside kinase activator.We were able to demonstrate through the second part of the work that the combined treatment of the epidrug decitabine and masitinib can be more effective than decitabine treatment for the re-expression of some genes non or weakly induced by decitabine when used alone.In conclusion, These data allowed us to introduce an interaction between a tyrosine kinases inhibitor and a nucleoside kinase, as an enzymatic activation new concept. This could be used as a base for the design of new small chemical molecules specific for dCK or other nucleoside kinases essential for the activation of chemodrugs. This concept will obviously help to imagine and evaluate more potential therapeutic combinations of chemodrugs and small chemical molecules to overcome the resistance to chemotherapy dependent on nucleoside kinases

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Bencteux, Edith. "Conception et synthese d'inhibiteurs d'activite proteine tyrosine kinase potentiellement actifs dans le traitement du cancer." Lille 2, 1997. http://www.theses.fr/1997LIL2P264.

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Leroux, Florence. "Etude in vitro d'inhibiteurs de tyrosine kinases et de phosphodiesterases et d'un analogue du vasoactive intestinal peptide potentiellement actifs dans l'asthme." Lille 2, 1996. http://www.theses.fr/1996LIL2P253.

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Nguyen, Van tai. "Physiopathologie des toxicités hématologiques et vasculaires des inhibiteurs de récepteurs à activité tyrosine kinase anti-angiogénique dans le traitement du cancer." Electronic Thesis or Diss., Paris 13, 2025. http://www.theses.fr/2025PA131002.

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Les inhibiteurs de tyrosine kinase anti-angiogéniques (ITK) sont devenus des médicaments majeurs pour le traitement de divers types de cancer, mais leur utilisation est associée à une incidence élevée de toxicités sévères, notamment des toxicités hématologiques, telles que l'anémie sévère. Des différences considérables ont été observées entre les différents ITKs.Dans cette thèse, nous avons réalisé une méta-analyse afin d'évaluer plus efficacement la prévalence des toxicités des différents ITK anti-angiogéniques chez les patients atteints de cancer, ainsi que dans des sous-populations spécifiques, y compris les patients atteints de carcinome rénal. En utilisant des modèles murins précliniques, nous avons démontré que les ITK anti-angiogéniques induisaient une large gamme d'effets toxiques sur les tissus normaux par un effet cytotoxique sur les cellules endothéliales normales. Les toxicités hématologiques étaient particulièrement marquées avec le sunitinib. Nous avons montré que l'hypoxie induite par le sunitinib, à travers la destruction des vaisseaux normaux dans la moelle osseuse, affectait principalement les lignées érythrocytaires et myéloïdes, et cela était associé à un blocage dans la maturation des érythrocytes. Bien que l'anémie induite par le sunitinib soit associée à une réponse adaptative à l'hypoxie systémique, nous avons démontré que les concentrations d'érythropoïétine (EPO) dans la moelle osseuse totale des souris traitées par sunitinib étaient significativement plus faibles que chez les souris non traitées. Cela est cohérent avec la destruction des microvaisseaux dans la moelle osseuse sous traitement par sunitinib, empêchant l'EPO circulante d'atteindre la moelle osseuse à des concentrations adéquates. Nous avons également démontré un effet supplémentaire spécifique au sunitinib, qui inhibe le flux d'autophagie dans les progéniteurs érythroïdes, bloquant ainsi la maturation des érythrocytes et conduisant à une anémie plus sévère.Dans notre étude, nous avons décrypté la physiopathologie de l'anémie induite par les ITK anti-angiogéniques, que nous avons principalement liée à un effet direct sur les vaisseaux normaux de la moelle osseuse, ainsi qu'à l'inhibition du flux d'autophagie dans les progéniteurs érythroïdes sous sunitinib. Notre étude présente des applications translationnelles potentielles pour le choix des ITK anti-angiogéniques et la gestion de l'anémie induite par le traitement
Anti-angiogenic tyrosine kinase inhibitors (TKIs) have become major drugs for the treatment of various cancer types, but with an overall high incidence of severe toxicities, particularly haematological toxicities including severe anemia. Considerable differences have been observed across TKIs.In this thesis, we performed a meta-analysis to more efficiently assess the toxicity prevalence of the different anti-angiogenic TKIs among cancer patients, and in sub-populations of interest including patients with renal cell carcinoma. Using preclinical murine models, we demonstrated that anti-angiogenic TKIs induced a broad range of toxic effects on normal tissues through a cytotoxic effect on normal endothelial cells. Haematological toxicities were particulary marked with sunitinib. We showed that sunitinib-induced hypoxia through the destruction of normal vessels in the bone marrow mainly affected erythrocyte and myeloid lineages, and this was associated with a blockage in erythrocyte maturation. Althought sunitinib-induced anemia was associated with an adaptative response to systemic hypoxia, we demonstrated that erythropoietin (EPO) concentrations in the total bone marrow of sunitinib-treated mice were significantly lower than in untreated mice. This is coherent with the destruction of microvessels in the bone marrow under sunitinib treatment, preventing circulating EPO from reaching the bone marrow at relevant concentrations. We demonstrated an additional effect specific to sunitinib that induced autophagy flux inhibition in erythroid progenitors, with a blockage of erythrocyte maturation, leading to more severe anemia.In our study, we deciphered the pathophysiology of anti-angiogenic TKI-induced anemia, which we found to be mainly linked to a direct effect on bone-marrow normal vessels and also to autophagy flux inhibition in erythroid progenitors under sunitinib. Our study has potential translational applications for the choice of anti-angiogenic TKIs and the management of treatment-induced anemia

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Mésange, Paul. "Influence d’inhibiteurs tyrosine kinase sur la biologie et la survie de cellules de cancer colorectal." Thesis, Paris 5, 2014. http://www.theses.fr/2014PA05P635/document.

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Le but des travaux est de caractériser l’influence de la signalisation VEGF, en particulier la signalisation autocrine VEGF, sur la biologie et la sensibilité/résistance aux médicaments anticancéreux de cellules de cancer colorectal. Nous avons souhaité caractériser l’impact de la signalisation autocrine VEGF dans des modèles de CRC avec une résistance naturelle au bevacizumab, un anticorps anti-VEGF. Bien que ce composé soit actif dans le CRC, une sous population de patients ne répondent pas au traitement. Nos résultats montrent une sur régulation de la voie autocrine HIF-VEGF-VEGFR en réponse à une exposition prolongée au bevacizumab dans les cellules bevacizumab résistantes. Si la résistance à cet anticorps est bien établie, d’autres inhibiteur de la voie VEGF restent actifs (comme la petite molécule ciblée nintedanib) et peuvent inhiber la voie mTOR. La signalisation VEGF autocrine joue un rôle dans la survie de cellules de CRC. Chez les sujets résistants au bevacizumab, il serait intéressant d’introduire le nintedanib seul ou en combinaison pour accentuer l’inhibition angiogénique. Une autre combinaison d’agents (anti VEGF(R) et anti EGFR) a montré une efficacité dans des modèles de CRC en préclinique. La combinaison du bevacizumab et d’une petite molécule ciblant EGFR (erlotinib) a montré une plus grande efficacité que le bevacizumab seul dans des modèles de CRC indépendamment du statut KRAS. Le bevacizumab induit une activation de la voie de survie EGFR dans les cellules tumorales et dans les cellules endothéliales associées à la tumeur. Cette activation se trouve diminuée avec l’introduction de l’erlotinib. Les résultats indiquent que la combinaison du bevacizumab et de l’erlotinib sont plus actif en thérapie de maintenance que le bevacizumab seul, même pour les patients mutés KRAS. Ces résultats ont mené à l’étude clinique positive GERCOR phase III DREAM dans le cancer du côlon métastatique
The aim of the work is to characterize the influence of VEGF signaling , especially autocrine VEGF signaling , the biology and susceptibility / resistance to anticancer drugs of colorectal cancer cells. We wished to characterize the impact of the autocrine VEGF signaling in CRC models with natural resistance to bevacizumab , an anti -VEGF antibody. Although this compound is active in the CRC, a subpopulation of patients do not respond to treatment. Our results show an autocrine regulatory pathway HIF- VEGF- VEGFR in response to prolonged exposure to bevacizumab in bevacizumab resistant cells. If the resistance to the antibody is established, other inhibitos of VEGF pathway remain active (such as small molecule nintedanib ) and can inhibit the mTOR pathway. Autocrine VEGF signaling plays a role in CRC cell survival. In subjects resistant to bevacizumab, it would be interesting to introduce the nintedanib alone or in combination to enhance the angiogenic inhibition. Another combination of targeted agents ( anti-VEGF (R) and anti EGFR) has shown efficacy in preclinical models of CRC. The combination of bevacizumab and a small molecule targeting EGFR (erlotinib) showed greater efficacy than bevacizumab alone in CRC models regardless of KRAS status. Bevacizumab induces activation of the EGFR survival pathway in tumor cells and in endothelial cells associated with the tumor. This activation is decreased with the introduction of erlotinib. The results indicate that the combination of bevacizumab and erlotinib are more active in maintenance therapy than bevacizumab alone, even for patients mutated KRAS . These findings led to the positive Phase III clinical study GERCOR DREAM in metastatic colon cancer

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Losson, Hélène. "Combinaisons de nouveaux inhibiteurs de désacétylase d’histones 6 avec des inhibiteurs de tyrosine kinase pour le traitement de la leucémie myéloïde chronique." Thesis, Université de Lorraine, 2020. http://www.theses.fr/2020LORR0003.

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Les patients atteints de leucémie myéloïde chronique (LMC) breakpoint cluster region-Abelson (BCR-ABL)+ sont traités avec des inhibiteurs de tyrosine kinase (ITK), comme l’imatinib, cependant certains développent des résistances et des effets secondaires sévères. Des traitements combinés à base d’inhibiteurs d’histone désacétylase (HDAC)6 (HDAC6i), pouvant potentiellement réduire l’expression de BCR-ABL, apparaît être une approche intéressante pour prévenir l’apparition de résistances aux ITK. De plus, l’implication d’HDAC6 dans les voies de dégradation des protéines rend son inhibition couplée à celle du protéasome susceptible de sensibiliser les cellules aux ITK. Notre hypothèse est que la combinaison ITK-HDAC6i pourrait être efficace pour le traitement de la LMC. Dans un premier temps, les effets anti-cancéreux d’un HDAC6i identifié dans notre laboratoire, le composé 7b, à celui de référence, la tubacine, en combinaison avec l’imatinib ont été comparés. La combinaison imatinib-7b a généré des effets anti- cancéreux plus importants que la combinaison imatinib-tubacine et a provoqué une mort synergique apoptotique dépendante des caspases dans les cellules K-562 et réduit la proportion de cellules souches leucémiques alors qu’elle n’a eu qu’un effet modéré sur des cellules saines. Enfin, la combinaison a diminué plus fortement la capacité de formation de colonies et la masse tumorale des cellules de LMC respectivement en milieu semi-solide et dans des poissons zèbres xénogreffés, par rapport aux composés seuls. D’un point de vue mécanistique, la combinaison induit l’ubiquitination et la dégradation de BCR-ABL, et la dérégulation de protéines de ses voies de signalisation impliquées dans la prolifération et la survie cellulaire. La protéine HDAC6 possédant deux sites catalytiques, nos résultats tendent à montrer que le composé 7b cible le deuxième. Dans un second temps, une étude a été initiée sur un nouvel HDAC6i de type hydroxamate, le MAKV-15, qui diminue l’expression de BCR-ABL, et qui en pré-traitement avec le bortezomib, sensibilise les cellules à l’imatinib, entrainant une augmentation de la mort apoptotique dépendante des caspases dans les cellules sensibles et résistantes à l’imatinib. Enfin, nos résultats suggèrent que l’inhibition d’HDAC6 potentialise l’effet de l’imatinib, pourrait prévenir l’apparition de résistances et que de telles combinaisons pourraient représenter une approche thérapeutique prometteuse pour les patients atteints de LMC
Breakpoint cluster region-Abelson (BCR-ABL)+ chronic myeloid leukemia (CML) patients receive tyrosine kinase inhibitors (TKIs) such as imatinib as the first-line treatment; however, some patients develop resistances and severe adverse effects. Combination treatments, especially with histone deacetylase (HDAC)6 inhibitors (HDAC6i), appear as an attractive option to prevent TKI resistances considering the capacity of HDAC6i to downregulate BCR-ABL. Moreover, HDAC6 is implicated in protein degradation pathways, so that its inhibition combined with that of the proteasome could sensitize cells to TKIs. Thus, we hypothesized that HDAC6i combined to TKIs could be effective for CML treatment. In the first part, we compared the anti-CML effects of a HDAC6i identified in our laboratory, compound 7b, to the reference HDAC6i tubacin, in combination with imatinib. Results showed that the imatinib-7b combination generated stronger anti- CML effects than imatinib-tubacin. Especially, the imatinib-7b combination elicited a potent synergistic caspase- dependent apoptotic cell death and drastically reduced the proportion of cancer stem cells in K562 CML cells, whereas it only moderately impacted various healthy cell models. Ultimately, the imatinib-7b combination decreased more potently the colony forming capacities and tumor mass formation of CML cells in a semisolid methylcellulose medium and in xenografted zebrafishes, respectively, compared to each compound alone. Mechanistically, the combination induced BCR-ABL ubiquitination and downregulation leading to a dysregulation of multiple key proteins of its downstream pathways involved in CML proliferation and survival. Results tend to demonstrate that 7b could target the second site. In the second part, we initiated a study of a novel hydroxamate-based HDAC6i, MAKV-15, and preliminary results demonstrated it triggered BCR-ABL downregulation. Accordingly, in pre-treatment with bortezomib it sensitizes CML cells to imatinib leading to enhanced caspase-dependent apoptotic death in imatinib-sensitive and imatinib-resistant CML cells. Considering that HDAC6 is reported to possess two functional catalytic sites, we finally attempted to determine which catalytic site is targeted by these HDAC6i. Taken together, our results suggest that HDAC6i potentiate the effect of imatinib and could overcome TKI resistance in CML cells and therefore such combination may represent a promising therapeutic approach for CML patients

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Peyressatre, Marion. "Développement de biosenseurs fluorescents et d’inhibiteurs pour suivre et cibler CDK5/p25 dans le glioblastome." Thesis, Montpellier, 2016. http://www.theses.fr/2016MONT3513/document.

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CDK5 est une protéine kinase exprimée de façon ubiquitaire et activée principalement dans le système nerveux central, ou elle joue un rôle important dans la transmission synaptique, la guidance axonale et la migration cellulaire, la plasticité synaptique et le développement neuronal. CDK5 est associée à la protéine p35 au niveau de la membrane cellulaire, et activée par clivage calpaine-dépendant de cette dernière en p25, ce qui conduit à la relocalisation de CDK5/p25 dans le cytoplasme cellulaire. CDK5/p25 phosphoryle de nombreux substrats dont la protéine Tau, contribuant ainsi à l’apparition de plaques neurofibrillaires responsable des pathologies neurodégénératives comme Alzheimer et Parkinson, lorsqu’elle est hyperactivée. Plus récemment, l’expression et l’hyperactivation de CDK5 a été décrite comme impliquée dans le développement de cancers et en particulier de tumeurs cérébrales. Toutefois aucune approche ne permet actuellement de détecter et de mesurer l’activité de CDK5/p25 directement dans des cellules vivantes, au sein des tissus et des tumeurs concernées, dû à un manque d’outils fiables et sensibles pour quantifier les changements dynamiques de son activité kinase. Par ailleurs, peu d’inhibiteurs sont actuellement disponibles pour inhiber CDK5/p25, de manière spécifique, la plupart ciblant la poche de fixation de l’ATP.Le premier objectif de ma thèse a consisté à développer un biosenseur d’activité fluorescent de nature peptidique appelé CDKACT5 qui rapporte l’activité kinase de CDK5/p25 recombinante et dans des extraits cellulaires de manière dynamique et réversible suivant stimulation ou inhibition de cette kinase. Une fois caractérisé et validé in vitro, le biosenseur a été appliqué à la détection d’altérations de CDK5/p25 dans différentes lignées cellulaires de glioblastome dans des essais fluorescents d’activité kinase. Enfin CDKACT5 a été introduit dans des cellules neuronales vivantes afin de suivre les changements dynamiques d’activité de CDK5/p25 par microscopie de fluorescence et vidéo microscopie.Le deuxième objectif de ma thèse a consisté à développer un biosenseur fluorescent conformationnel dans le but d’identifier des inhibiteurs non compétitifs de l’ATP ciblant la boucle d’activation de CDK5. Le biosenseur CDKCONF5 a été exploité pour réaliser un criblage haut débit de trois chimiothèques de petites molécules. Les touches identifiées ont été validées et caractérisées in vitro, pour déterminer leur potentiel inhibiteur dans des tests d’activité kinase et de prolifération cellulaire, ainsi que leur mécanisme d’action. Ces molécules constituent des candidats prometteurs pour une chimiothérapie sélective du glioblastome
CDK5 is a protein kinase ubiquitously expressed but mainly activated in the central nervous system, where it plays an important role in neuronal functions such as synaptic transmission, axonal guidance and migration, synaptic plasticity and neuronal development. CDK5 is associated with p35 protein at the cell membrane, then activated by calpain-mediated cleavage of p35 into p25, which promotes relocalization of CDK5/p25 into the cytoplasm. CDK5/p25 phosphorylates a wide variety of substrates including Tau, thereby contributing to appearance of neurofibrillary plaques responsable for neurodegenerative pathologies such as comme Alzheimer’s et Parkinson’s, when hyperactivated. More recent studies suggest that CDK5 expression and hyperactivation are involved in glioblastoma during cell invasion and CDK5 expression has been reported to be correlated with the pathological grade of gliomas. However there are currently no tools available to monitor CDK5/p25 activity in its native cellular environment, in tissues or in tumours, due to an overall lack of reliable tools to quantify dynamic changes in its kinase activity in a sensitive and continuous fashion. Furthermore, few inhibitors are currently available to target CDK5/p25 in a specific fashion and most of them are ATP competitive inhibitors.The first goal of my thesis was to develop a fluorescent peptide biosensor named CDKACT5, that specifically reports on recombinant CDK5/p25 and on endogenous CDK5 activity in cell extracts in a dynamic and reversible fashion following stimulation or inhibition of this kinase. Once validated in vitro, this biosensor was applied to detect alterations in CDK5/p25 activity in different glioblastoma cell lines in fluorescent kinase activity assays. Finally CDKACT5 was introduced into cultured neuronal cells to monitor dynamic changes in CDK5/p25 activity by fluorescence imaging and time-lapse microscopy.The second goal of my thesis project consisted in developing a conformational fluorescent biosensor to identify non-ATP competitive inhibitors targeting the activation loop of CDK5. CDKCONF5 was implemented to perform a high throughput screen of three small molecule libraries. The hits identified were validated and characterized to determine their inhibitory potential in kinase activity and proliferation assays, as well as their mechanism of action. These compounds constitute promising for selective chemotherapy in glioblastoma

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Книги з теми "Inhibiteur de la tyrosine kinase"

Focosi, Daniele, ed. Resistance to Tyrosine Kinase Inhibitors. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-46091-8.

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Mustelin, Tomas. Src family tyrosine kinases in leukocytes. Austin: R.G. Landes, 1994.

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Heilmeyer, L. M. G. 1937- and NATO Advanced Study Institute on Tyrosine Phosphorylation/Dephosphorylation and Downstream Signalling (1992 : Acquafredda di Maratea, Italy), eds. Tyrosine phosphorylation/dephosphorylation and downstream signalling. Berlin: Springer-Verlag, 1993.

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D, Fabbro, and McCormick Frank 1950-, eds. Protein tyrosine kinases: From inhibitors to useful drugs. Totowa, N.J: Humana Press, 2006.

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Germano, Serena. Receptor tyrosine kinases: Methods and protocols. New York: Humana Press, 2015.

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Shulman, Johanna. Biochemical analysis of activating mutations of the Kit receptor tyrosine kinase. Ottawa: National Library of Canada, 1998.

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Gibson, Spencer Bruce. Role of the TEC family tyrosine kinase EMT in T cell activation. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1997.

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Easterfield, Howard James. Analogues of phosphotyrosine: New components of ligands for protein tyrosine kinase enzymes. Birmingham: University of Birmingham, 1999.

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Cudmore, Stephen Bruce. The effect of postnatal development on synaptic tyrosine kinase of rat forebrain. Ottawa: National Library of Canada, 1991.

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Ho, Jacqueline. A requirement for the receptor tyrosine kinase, Flk1, in hematopoiesis and vasculogenesis. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1999.

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Частини книг з теми "Inhibiteur de la tyrosine kinase"

Moses, Marsha A. "Tyrosine Kinase Inhibitor." In Encyclopedia of Systems Biology, 2307–8. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-9863-7_1558.

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Bozec, A., and G. Milano. "Monoclonaux contre inhibiteurs de tyrosine kinase." In Les thérapies ciblées, 81–97. Paris: Springer Paris, 2008. http://dx.doi.org/10.1007/978-2-287-36008-4_6.

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Bhaskar, L. V. K. S., and L. Saikrishna. "Drug Resistance Against Tyrosine Kinase Inhibitor in Gastrointestinal Malignancies." In Role of Tyrosine Kinases in Gastrointestinal Malignancies, 191–224. Singapore: Springer Singapore, 2018. http://dx.doi.org/10.1007/978-981-13-1486-5_14.

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Kariya, Yoshiaki, Masashi Honma, and Hiroshi Suzuki. "Systems Pharmacology of Tyrosine Kinase Inhibitor-Associated Toxicities." In Systems Pharmacology and Pharmacodynamics, 353–70. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-44534-2_16.

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Kriegsmann, Katharina, Mark Kriegsmann, and Mathias Witzens-Harig. "Acalabrutinib, A Second-Generation Bruton’s Tyrosine Kinase Inhibitor." In Small Molecules in Hematology, 285–94. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-91439-8_14.

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Isfort, Susanne, Martina Crysandt, Deniz Gezer, Steffen Koschmieder, Tim H. Brümmendorf, and Dominik Wolf. "Bosutinib: A Potent Second-Generation Tyrosine Kinase Inhibitor." In Small Molecules in Hematology, 87–108. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-91439-8_4.

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Isfort, Susanne, Gunhild Keller-v. Amsberg, Philippe Schafhausen, Steffen Koschmieder, and Tim H. Brümmendorf. "Bosutinib: A Novel Second-Generation Tyrosine Kinase Inhibitor." In Recent Results in Cancer Research, 81–97. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-54490-3_4.

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Motyckova, Gabriela, and Richard M. Stone. "Development of Midostaurin as a Tyrosine Kinase Inhibitor." In Targeted Therapy of Acute Myeloid Leukemia, 201–14. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1393-0_10.

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Grüllich, Carsten. "Cabozantinib: A MET, RET, and VEGFR2 Tyrosine Kinase Inhibitor." In Recent Results in Cancer Research, 207–14. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-54490-3_12.

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Zhang, Ji, and Jie Jack Li. "Pazopanib (Votrient): A VEGFR Tyrosine Kinase Inhibitor for Cancer." In Modern Drug Synthesis, 111–22. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2010. http://dx.doi.org/10.1002/9780470768594.ch9.

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Тези доповідей конференцій з теми "Inhibiteur de la tyrosine kinase"

Abid, H., N. Siddiqui, and V. Thirukonda. "Tyrosine Kinase Inhibitor Induced Interstitial Lung Disease." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a3137.

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Henzler, Tanja, Stefanie Pohl, Nicole Schneiderhan-Mara, Stefanie Rimmele, April Livengood, Robert Kovelman, and Thomas Herget. "Abstract LB-227: Receptor tyrosine kinase phosphorylation: Simultaneous detection of 10 kinases upon inhibitor treatment." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-lb-227.

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Fuhrmann, T., M. Krumbholz, U. Steffen, S. Sembill, and M. Metzler. "Effects of the allosteric tyrosine kinase inhibitor asciminib on bone metabolism." In 35. Jahrestagung der Kind-Philipp-Stiftung für pädiatrisch onkologische Forschung. Georg Thieme Verlag KG, 2024. http://dx.doi.org/10.1055/s-0044-1786576.

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Suzuki, Toshihiro, Risa Ito, Toshimitsu Yamaoka, Tohru Ohmori, Kazuto Nishio, and Yuki Ogasawara. "Abstract 4098: Tyrosine kinase inhibitor resistance were decreased in spheroid culture platform." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-4098.

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Eiring, Anna M., Rebecca Ellwood, Carme Ripoll Fiol, Robert K. Hills, Georgios Nteliopoulos, Alistair Reid, Dragana Milojkovic, Jane Apperley, and Jamshid Sorouri-Khorashad. "Abstract 3018: Mechanisms of tyrosine kinase inhibitor resistance in chronic myeloid leukemia." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-3018.

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Xin, Y., M. Cereda, K. T. Martin, S. Humayun, I. Duncan, H. Profka, S. Kadlecek, and R. R. Rizi. "Tyrosine Kinase Inhibitor Imatinib Alleviates the Progression of Ventilator-Induced Lung Injury." In American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a1301.

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Iyer, Sudarshan R., Igor Odintsov, Adam J. Schoenfeld, Hiroki Sato, Evan Siau, Alexander Drilon, Gregory J. Riely, Romel Somwar, Marc Ladanyi, and Monika A. Davare. "Abstract 1111: MYC promotes tyrosine kinase inhibitor resistance inROS1fusion positive lung cancers." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-1111.

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Perez, Michael, Andrew Morrison, and Kelly Sloane. "Bruton Tyrosine Kinase Inhibitor Associated Cryptococcal Meningitis Manifesting as Stroke (P1-10.002)." In 2023 Annual Meeting Abstracts. Lippincott Williams & Wilkins, 2023. http://dx.doi.org/10.1212/wnl.0000000000202063.

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Wang, Lei G., Antonio Montaño, Allison Solanki, Nathan McMahon, Kenneth M. Tichauer, Kimberley S. Samkoe, and Summer L. Gibbs. "Quantitative imaging of tyrosine kinase inhibitor distribution in live cells and tissues." In Frontiers in Biological Detection: From Nanosensors to Systems XIV, edited by Benjamin L. Miller, Sharon M. Weiss, Amos Danielli, Ramesh Raghavachari, and Mikhail Y. Berezin. SPIE, 2022. http://dx.doi.org/10.1117/12.2612233.

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Звіти організацій з теми "Inhibiteur de la tyrosine kinase"

Sawada, Takashi, and Mamoru Narukawa. A systematic review of treatment-related adverse events for combination therapy of multiple tyrosine kinase inhibitor and immune checkpoint inhibitor. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, September 2023. http://dx.doi.org/10.37766/inplasy2023.9.0011.

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Kim, Dong W. Molecular Profiling of Prostate Cancer to Determine Predictive Markers of Response to Radiation and Receptor Tyrosine Kinase Inhibitor Therapy. Fort Belvoir, VA: Defense Technical Information Center, September 2006. http://dx.doi.org/10.21236/ada468523.

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Guo, Wenpei, Jianwei Diao, Zhenyuan Jiang та Zhankui Wang. Comparative efﬁcacy and safety of tyrosine kinase inhibitor for systemic sclerosis - associated interstitial lung diseases A Bayesian network meta-analysis protocol. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, грудень 2020. http://dx.doi.org/10.37766/inplasy2020.12.0150.

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Zheng, Jiaxi, and Haihua Yang. Clinical Benefits of Immune Checkpoint Inhibitors and Predictive Value of Tumor Mutation Burden in Hepatocellular Carcinoma: A Systematic Review and Meta-Analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, January 2022. http://dx.doi.org/10.37766/inplasy2022.1.0008.

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Анотація:

Review question / Objective: Is immunotherapy associated with beneficial clinical outcomes for hepatocellular carcinoma (HCC) and how can combination immunotherapy be deployed to produce the best benefit? Is tumor mutation burden (TMB) a predictive biomarker for immune‐checkpoint inhibitors? Condition being studied: To this date, about 50 single-arm clinical trials and several randomized control trials (RCTs) presented final or interim results of investigations on the efficacy of PD-1/PD-L1 inhibitors for advanced HCC. In the CheckMate 459, IMbrave 050, and ORIENT-32, immunotherapies were found to significantly improve progression-free survival (PFS) and overall survival (OS) compared with sorafenib (a tyrosine-kinase inhibitor, as standard systemic treatment) in patients with advanced hepatocellular carcinoma. However, these clinical trials were different on clinical phases, sample size, and response evaluation criteria, and inconsistent clinical outcomes were shown in several trials.

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Kim, Beong Ki, Ye Seul Seong, Eunyoung Kim, Sehyun Kwak, Sanghoon Lee, Eunhye Lee, Yoonsoo Jang, and Chi Young Kim. Optimizing Epidermal Growth Factor Receptor-Tyrosine Kinase Inhibitor Treatment in Lung Cancer: The Influence of Gastric Acid Suppressants – An Updated Systematic Review and Meta-Analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, May 2024. http://dx.doi.org/10.37766/inplasy2024.5.0108.

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Wang, Zexian, Yaru Guo, Xiaojin Wu, Xiaohan Qin, Zhiling Wan, and Chen Liu. Bevacizumab plus Epidermal Growth Factor Receptor (EGFR)-Tyrosine Kinase Inhibitor versus EGFR-TKI alone for advanced EGFR-mutant non-small cell lung cancer: a meta-analysis of randomized clinical trials. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, December 2023. http://dx.doi.org/10.37766/inplasy2023.12.0059.

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Qin, Xiaohan, Yaru Guo, Xiaojin Wu, Zexian Wang, Zhiling Wan, and Chen Liu. Chemotherapy plus Epidermal Growth Factor Receptor (EGFR)-Tyrosine Kinase Inhibitor versus EGFR-TKI alone for advanced EGFR-mutant non-small cell lung cancer: a meta-analysis of randomized clinical trials. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, January 2024. http://dx.doi.org/10.37766/inplasy2024.1.0128.

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Weier, Heinz-Ulrich. Expression Profiling of Tyrosine Kinase Genes. Fort Belvoir, VA: Defense Technical Information Center, August 2003. http://dx.doi.org/10.21236/ada423672.

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Weier, Heinz U. Expression Profiling of Tyrosine Kinase Genes. Fort Belvoir, VA: Defense Technical Information Center, August 2000. http://dx.doi.org/10.21236/ada391061.

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Miller, Tod. Peptide-Bassed Inhibitors of Neu Tyrosine Kinase. Fort Belvoir, VA: Defense Technical Information Center, June 1999. http://dx.doi.org/10.21236/ada375133.

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