Littérature scientifique sur le sujet « PI3K TARGET »
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Articles de revues sur le sujet "PI3K TARGET"
Diacovo, Thomas, Dosh Whye, Evgeni Efimenko, Jianchung Chen, Valeria Tosello, Kim De Keersmaecker, Adam Kashishian et al. « Therapeutic Utility of PI3Kγ Inhibition in Leukemogenesis and Tumor Cell Survival ». Blood 120, no 21 (16 novembre 2012) : 1492. http://dx.doi.org/10.1182/blood.v120.21.1492.1492.
Texte intégralBorsari, Chiara, et Matthias P. Wymann. « Targeting Phosphoinositide 3-Kinase – Five Decades of Chemical Space Exploration ». CHIMIA 75, no 12 (9 décembre 2021) : 1037. http://dx.doi.org/10.2533/chimia.2021.1037.
Texte intégralBarberis, Laura, et Emilio Hirsch. « Targeting phosphoinositide 3-kinase γ to fight inflammation and more ». Thrombosis and Haemostasis 99, no 02 (2008) : 279–85. http://dx.doi.org/10.1160/th07-10-0632.
Texte intégralMiller, Michelle, Philip Thompson et Sandra Gabelli. « Structural Determinants of Isoform Selectivity in PI3K Inhibitors ». Biomolecules 9, no 3 (26 février 2019) : 82. http://dx.doi.org/10.3390/biom9030082.
Texte intégralMercurio, Laura, Martina Morelli, Claudia Scarponi, Giovanni Luca Scaglione, Sabatino Pallotta, Cristina Albanesi et Stefania Madonna. « PI3Kδ Sustains Keratinocyte Hyperproliferation and Epithelial Inflammation : Implications for a Topically Druggable Target in Psoriasis ». Cells 10, no 10 (2 octobre 2021) : 2636. http://dx.doi.org/10.3390/cells10102636.
Texte intégralLaurent, Pierre-Alexandre, Cédric Garcia, Marie-Pierre Gratacap, Bart Vanhaesebroeck, Pierre Sié, Bernard Payrastre et Anne-Dominique Terrisse. « The class I phosphoinositide 3-kinases α and β control antiphospholipid antibodies-induced platelet activation ». Thrombosis and Haemostasis 115, no 06 (2016) : 1138–46. http://dx.doi.org/10.1160/th15-08-0661.
Texte intégralKuracha, Murali R., Venkatesh Govindarajan, Brian W. Loggie, Martin Tobi et Benita L. McVicker. « Pictilisib-Induced Resistance Is Mediated through FOXO1-Dependent Activation of Receptor Tyrosine Kinases in Mucinous Colorectal Adenocarcinoma Cells ». International Journal of Molecular Sciences 24, no 15 (2 août 2023) : 12331. http://dx.doi.org/10.3390/ijms241512331.
Texte intégralXenou, Lydia, et Evangelia A. Papakonstanti. « p110δ PI3K as a therapeutic target of solid tumours ». Clinical Science 134, no 12 (juin 2020) : 1377–97. http://dx.doi.org/10.1042/cs20190772.
Texte intégralMaffei, Angelo, Giuseppe Lembo et Daniela Carnevale. « PI3Kinases in Diabetes Mellitus and Its Related Complications ». International Journal of Molecular Sciences 19, no 12 (18 décembre 2018) : 4098. http://dx.doi.org/10.3390/ijms19124098.
Texte intégralChen, Shiyi, Wenkang Huang, Xiaoyu Li, Lijuan Gao et Yiping Ye. « Identifying Active Compounds and Mechanisms of Citrus changshan-Huyou Y. B. Chang against URTIs-Associated Inflammation by Network Pharmacology in Combination with Molecular Docking ». Evidence-Based Complementary and Alternative Medicine 2022 (13 juillet 2022) : 1–10. http://dx.doi.org/10.1155/2022/2156157.
Texte intégralThèses sur le sujet "PI3K TARGET"
Stamatkin, Christopher W. « PHOSPHATIDYLINOSITOL 3-KINASE (PI3K) AS A THERAPEUTIC TARGET IN NSCLC ». UKnowledge, 2014. http://uknowledge.uky.edu/pharmacy_etds/58.
Texte intégralMcCarragher, Leeza Sarah Marie. « PI3K signalling blockade : a target for chemotherapeutic enhancement in breast cancer ». Thesis, University of Sheffield, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.401117.
Texte intégralCerovac, Vesna. « Studies on the PI3K/mTOR pathway as cytostatic treatment target in pituitary adenomas ». Diss., lmu, 2010. http://nbn-resolving.de/urn:nbn:de:bvb:19-119322.
Texte intégralULTIMO, Simona. « Inhibition of the PI3K/Akt/mTOR signaling pathway as a therapeutic target for Acute Lymphoblastic Leukemia ». Doctoral thesis, Università degli studi di Ferrara, 2018. http://hdl.handle.net/11392/2487845.
Texte intégralLa Leucemia Linfoblastica Acuta (LLA) è un tumore maligno ematologico caratterizzato da una proliferazione clonale incontrollata di progenitori della linea cellulare di tipo B (LLA-B) o timociti allo stadio immaturo (LLA-T). L’attivazione della via di trasduzione del segnale di PI3K/Akt/mTOR è una caratteristica comune della LLA-B e T ed influisce sulla crescita e sopravvivenza cellulare. Gli inibitori della via di PI3K/Akt/mTOR sono attualmente in fase di studio per uso clinico, sia come singoli agenti che in combinazione con la convenzionale chemioterapia utilizzata nel trattamento dei pazienti affetti da LLA-T. In questo studio sono stati analizzati gli effetti di un pannello di inibitori della via di PI3K/Akt/mTOR su linfociti T-CD4+ di individui sani e confrontati con linee cellulari tumorali umane di LLA-T. Successivamente è stato verificato se il trattamento di inibizione multipla della proteina Akt potesse aumentare l’efficacia dei farmaci somministrati singolarmente e superare la resistenza al farmaco ottenendo la riduzione della concentrazione del singolo agente. Pertanto, sono stati studiati e testati gli effetti di tre inibitori su linee cellulari umane di LLA-T diretti contro Akt ma con differenti modi di azione: GSK690693, MK-2206 e Perifosina. Questa combinata somministrazione di farmaci ha mostrato un significativo effetto sinergico ed ha influito sulla via di PI3K/Akt/mTOR ad una concentrazione molto più bassa rispetto a quella del singolo farmaco. Il più elevato effetto sinergico per una totale inibizione di Akt è stato associato alla tempistica adottata per ciascuna somministrazione. I risultati ottenuti hanno suggerito che, mirare Akt come bersaglio chiave nella via del segnale di PI3K/Akt/mTOR con la somministrazione multipla di farmaci, potrebbe rappresentare una nuova e promettente strategia per il trattamento dei pazienti affetti da LLA-T. E’ stato inoltre studiata l’azione dei microRNA (miRNA), una classe di piccoli RNA non codificanti che giocano un ruolo in vari processi biologici, quali la proliferazione, la morte cellulare e la genesi del cancro. La regolazione incontrollata dei miRNA è implicata nell’invasione di diversi tumori umani e la leucemia non è esclusa. Usando modelli in vitro è stata eseguita un’analisi degli effetti degli inibitori della via del segnale di PI3K sui livelli di espressione dei miRNA coinvolti nella LLA e nell’attivazione di PI3K. I risultati emersi hanno mostrato che questi farmaci potrebbero modulare l’espressione dei miRNA, pertanto, la regolazione dei loro profili di espressione nella LLA, utilizzando gli inibitori diretti contro la via di PI3K, potrebbe costituire un nuovo terapeutico approccio per il prossimo futuro. Infine, è stata valutata l’efficacia degli inibitori della via del segnale di PI3K nelle linee cellulari di LLA-B e T caratterizzate dalla proteina di fusione Abl1 che causa una proliferazione cellulare incontrollata. Sono stati studiati gli effetti di farmaci contro il gene Bcr-Abl1 come Imatinib, Nilotinib e GZD824 utilizzati in combinazione con i farmaci diretti contro la via di PI3K. La combinazione di questi farmaci ha mostrato una ridotta vitalità cellulare, innescando il processo di morte e autofagia cellulare in maniera sinergica. Questi dati hanno suggerito che la selezione di inibitori diretti contro la via di PI3K/Akt/mTOR somministrati in combinazione con farmaci contro il gene di fusione Bcr-Abl1, potrebbe rappresentare un allettante nuovo intervento terapeutico da prendere in considerazione nel trattamento della LLA-B e T portatrice del cromosoma Philadelphia (Ph+).
DARICI, SALIHA NUR. « LEUCEMIA MIELOIDE ACUTA CON MUTAZIONE FLT3-ITD : razionale per l'uso combinato di inibitori di fosfoinositide 3-chinasi e recettori tirosin chinasici ». Doctoral thesis, Università degli studi di Modena e Reggio Emilia, 2022. http://hdl.handle.net/11380/1278342.
Texte intégralAcute myeloid leukemia (AML) has a very poor 5-year survival of ~20% in Europe. The internal tandem duplication (ITD) mutation of the Fms-like receptor tyrosine kinase 3 (FLT3) (FLT3-ITD) is the most frequent mutation (~25%) in normal karyotype AML. In recent clinical studies, few patients display prolonged remissions with receptor tyrosine kinase (RTK) inhibitors, such as FLT3 inhibitors (FLT3i) therapy, highlighting a substantial unmet need for novel effective treatment. Persistence of leukemia stem cells (LSC) drive AML leukemogenesis, responsible for drug resistance and disease relapse following conventional chemotherapy. Growing evidence recognizes that FLT3-ITD mutation leads to the constitutive activation of FLT3 kinase and its downstream pathways, including PI3K/AKT/mTOR signaling, strongly associated with LSC survival and crosstalk between LSC and stromal cells associated bone marrow (BM) tumor environment (TME). The TME provides protection of FLT3-ITD AML cells against FLT3 inhibitors. Thus, the PI3K/AKT/mTOR pathway may represent as a putative target for FLT3-ITD AML. This study aims to test the hypothesis that PI3K/AKT/mTOR inhibition could sensitize FLT3-ITD AML cells to RTKi-lead targeted therapy using human AML cell lines and primary patient blasts. First, I uncover the phenotypic profile of FLT3-ITD versus FLT3 wildtype cell lines following treatment with selected FLT3i or PI3K/AKT/mTORi that have failed treatment of AML as monotherapy in clinical studies. More specifically, I determine the drug efficacy by means of cell growth measurement and assessment of cell cycle status and apoptosis. I was able to demonstrate that BAY-806946 (pan PI3Ki) and PF-04691502 (dual PI3K/mTORi) exerted growth inhibitory activity caused by G1 cell cycle arrest and apoptosis, and this effect was irrespective of FLT3 status. Quizartinib (FLT3i) selectively inhibited cell growth in FLT3-ITD AML and this effect was mainly caused by apoptosis. The observed drug-induced apoptotic effect was however not as efficient as chemotherapy. Next, I provide proof-of-concept for the combination of quizartinib and BAY-806946 using both FLT3-ITD AML cell lines and primary patient blasts. When evaluating on primary patient blasts, I take into consideration the protective role of mesenchymal stromal cells and physiological growth factors to mimic the BM microenvironment. Hereby, I co-cultured FLT3-ITD AML blasts with stromal cell line MS-5 and added growth factors essential for AML survival and differentiation such as IL-3, TPO and G-CSF at physiological concentration. As expected, treatment with BAY-806946 enhanced both cytostatic and cytotoxic effect of quizartinib in FLT3-ITD AML cell line MOLM-13 as well as primary patient blasts in co-culture. More importantly, enhanced apoptosis was measured in the stem cell like CD34+CD38- population. Lastly, I elucidate the cytokine profile and persistent phosphoproteins as putative targets following combination treatment. Ultimately, this study demonstrates the potential of PI3K/AKT/mTORi to enhance the efficacy of RTKi quizartinib for the treatment of FLT3-ITD AML.
Lonetti, Annalisa <1982>. « Study of PI3K/Akt signaling pathway as potential molecular target for T-cell acute lymphoblastic leukemia (T-ALL) treatment : pan-inhibition of PI3K catalitic isoforms as better therapeutic approach ». Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2015. http://amsdottorato.unibo.it/6763/1/Annalisa_Lonetti_tesi.pdf.
Texte intégralLonetti, Annalisa <1982>. « Study of PI3K/Akt signaling pathway as potential molecular target for T-cell acute lymphoblastic leukemia (T-ALL) treatment : pan-inhibition of PI3K catalitic isoforms as better therapeutic approach ». Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2015. http://amsdottorato.unibo.it/6763/.
Texte intégralVenugopal, Smrruthi Vaidegi. « Differential Roles of Mammalian Target of Rapamycin Complexes 1 and 2 in Migration of Prostate Cancer Cells ». DigitalCommons@Robert W. Woodruff Library, Atlanta University Center, 2019. http://digitalcommons.auctr.edu/cauetds/189.
Texte intégralStellwagen, Florian [Verfasser], Jürgen E. [Akademischer Betreuer] Gschwend, Angela [Akademischer Betreuer] Krackhardt et Margitta [Akademischer Betreuer] Retz. « Bedeutung des PI3K/mTOR Signalweges als Ziel einer Target- Therapie im Harnblasenkarzinom / Florian Stellwagen. Gutachter : Jürgen E. Gschwend ; Angela Krackhardt ; Margitta Retz. Betreuer : Jürgen E. Gschwend ». München : Universitätsbibliothek der TU München, 2013. http://d-nb.info/104718530X/34.
Texte intégralGeng, Xinyan. « Investigations into how best to target FGFR2 mutant endometrial cancer ». Thesis, Queensland University of Technology, 2017. https://eprints.qut.edu.au/123437/1/Xinyan%20Geng%20Thesis.pdf.
Texte intégralLivres sur le sujet "PI3K TARGET"
How consumers pick a hotel : Strategic segmentation and target marketing. New York : Haworth Press, 1997.
Trouver le texte intégralHow consumers pick a hotel : Strategic segmentation and target marketing. New York : Routledge/Taylor & Francis Group, 2010.
Trouver le texte intégralFaithful - Target Club Pick. Simon & Schuster, 2017.
Trouver le texte intégralLacy Eye - Target Club Pick. Grand Central Pub, 2016.
Trouver le texte intégralChiarella, Jessica. And Again : Target Club Pick. Touchstone Books, 2016.
Trouver le texte intégralHouse of Thieves - Target Club Pick. Sourcebooks Landmark, 2016.
Trouver le texte intégralFifield, Richard. The Flood Girls - Target Club Pick. Gallery Books, 2016.
Trouver le texte intégralJewell, Lisa. The Girls in the Garden : Target Club Pick. Atria Books, 2017.
Trouver le texte intégralZevin, Gabrielle. The Storied Life of Aj Fikry-target Club Pick. Algonquin Books, 2014.
Trouver le texte intégralReading Planet : Rocket Phonics - Target Practice - Ants ! - Pink A. Taylor & Francis Group, 2021.
Trouver le texte intégralChapitres de livres sur le sujet "PI3K TARGET"
Khwaja, Asim. « PI3K as a Target for Therapy in Haematological Malignancies ». Dans Current Topics in Microbiology and Immunology, 169–88. Berlin, Heidelberg : Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/82_2010_71.
Texte intégralMargolin, Kim A. « Targeting the mTOR, PI3K, and AKT Pathways in Melanoma ». Dans Targeted Therapeutics in Melanoma, 107–23. New York, NY : Springer New York, 2011. http://dx.doi.org/10.1007/978-1-61779-407-0_8.
Texte intégralBeagle, Brandon, et David A. Fruman. « The PI3K-AKT-mTOR Signaling Network in AML ». Dans Targeted Therapy of Acute Myeloid Leukemia, 335–62. New York, NY : Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1393-0_17.
Texte intégralCastel, Pau, et Maurizio Scaltriti. « Mechanisms of Resistance to PI3K and AKT Inhibitors ». Dans Resistance to Targeted Anti-Cancer Therapeutics, 117–46. Cham : Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67932-7_6.
Texte intégralFernandes, Maria Sofia, João Miguel Sanches et Raquel Seruca. « Targeting the PI3K Signalling as a Therapeutic Strategy in Colorectal Cancer ». Dans Targeted Therapy of Colorectal Cancer Subtypes, 35–53. Cham : Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-030-02771-1_4.
Texte intégralWymann, Matthias. « PI3Ks—Drug Targets in Inflammation and Cancer ». Dans Subcellular Biochemistry, 111–81. Dordrecht : Springer Netherlands, 2012. http://dx.doi.org/10.1007/978-94-007-3012-0_5.
Texte intégralRoden, Dylan F., Jennifer M. Johnson, Petr Szturz, Paolo Bossi et Athanassios Argiris. « New and Promising Targeted Therapies in First and Second-Line Settings ». Dans Critical Issues in Head and Neck Oncology, 277–96. Cham : Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-63234-2_18.
Texte intégralCarroll, Martin. « Targeting the PI3 Kinase-mTOR Signaling Pathway in AML ». Dans Targeted Therapy of Acute Myeloid Leukemia, 363–70. New York, NY : Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1393-0_18.
Texte intégralHarvey, R. Donald, Jeannine Silberman et Sagar Lonial. « The PI3 Kinase/Akt Pathway as a Therapeutic Target in Multiple Myeloma ». Dans Myeloma Therapy, 309–22. Totowa, NJ : Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-564-0_20.
Texte intégralBonavida, Benjamin. « Sensitization of Immune-Resistant Tumor Cells to CTL-Mediated Apoptosis via Interference at the Dysregulated NF-κB/Snail/YY1/PI3K/RKIP/PTEN Resistant Loop ». Dans Resistance to Targeted Anti-Cancer Therapeutics, 177–208. Cham : Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-17807-3_9.
Texte intégralActes de conférences sur le sujet "PI3K TARGET"
Herzog, Lee-or, Bianca J. Lee, Thanh-Trang Vo, Honyin Chiu, Sharmila Mallya, Amos Fung, Mallika Singh et al. « Abstract IA17 : Strategies to target the mTORC1/eIF4F axis in B-cell leukemia and lymphoma ». Dans Abstracts : AACR Special Conference on Targeting PI3K/mTOR Signaling ; November 30-December 8, 2018 ; Boston, MA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1557-3125.pi3k-mtor18-ia17.
Texte intégralKolev, Vihren N., Qunli Xu, Jonathan A. Pachter et David T. Weaver. « Abstract 1525 : FAK and PI3K/mTOR inhibitors target cancer stem cells : Implications for SCLC treatment strategies ». Dans 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.am2015-1525.
Texte intégralKwan, Suet-Yan, Daisy I. Izaguirre, Xuanjin Cheng, Suet-Ying Kwan, Yvonne TM Tsang, Hoi-Shan Kwan et Kwong-Kwok Wong. « Abstract 4697 : The PI3K/mTOR pathway is a potential therapeutic target in cancers with ARID1A mutations ». Dans 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.am2015-4697.
Texte intégralEhrmantrout, Kimberly K., James E. Thompson et Angie M. Branch. « Abstract 3835 : Multiple stimulants target different phosphoinositide 3-kinase (PI3K) classes in breast cancer cell lines ». Dans Proceedings : AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011 ; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-3835.
Texte intégralKaneda, Megan, Chanae Hardamon, Michael C. Schmid, Michael Bouvet, Franco Novelli, Emilio Hirsch, Andrew Lowy et Judith A. Varner. « Abstract IA22 : Innate immune cell PI3K gamma as a target for suppression of pancreatic ductal adenocarcinoma ». Dans Abstracts : AACR Special Conference on Pancreatic Cancer : Innovations in Research and Treatment ; May 18-21, 2014 ; New Orleans, LA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.panca2014-ia22.
Texte intégralDansey, Roger. « Abstract IA18 : Clinical validation of PI3Kδ as a therapeutic target in B-cell malignancy ». Dans Abstracts : AACR Special Conference : Targeting the PI3K-mTOR Network in Cancer ; September 14-17, 2014 ; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-8514.pi3k14-ia18.
Texte intégralPetroni, Vanessa, Marie Therese Camilleri Podesta, Anthony George Fenech et Godfrey Grech. « Abstract B22 : Identification of novel drug combinations to target molecular pathways involved in breast cancer ». Dans Abstracts : AACR Special Conference : Targeting the PI3K-mTOR Network in Cancer ; September 14-17, 2014 ; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-8514.pi3k14-b22.
Texte intégralBlanco, Elvin, Takafumi Sangai, Funda Meric-Bernstam et Mauro Ferrari. « Chemotherapeutic Synergy Enhancement Through Micellar Nanotherapeutics ». Dans ASME 2010 First Global Congress on NanoEngineering for Medicine and Biology. ASMEDC, 2010. http://dx.doi.org/10.1115/nemb2010-13263.
Texte intégralBohnacker, Thomas, Florent Beaufils, Andrea E. Prota, John E. Burke, Anna Melone, Alison J. Inglis, Ludovico Fusco et al. « Abstract 671 : BKM120-mediated G2 arrest : Structural and functional segregation of off-target action and PI3K inhibition ». Dans 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.am2015-671.
Texte intégralRonecker, Jennifer S., Paul Lee, Sudeepta Sridhara, Michael LaBagnara, Raj Murali et Meena Jhanwar-Uniyal. « Abstract 1280 : The intersection of the PI3K/mTOR and HIPPO pathways : a potential therapeutic target for medulloblastoma ». Dans 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.am2016-1280.
Texte intégralRapports d'organisations sur le sujet "PI3K TARGET"
Ilic, Nina. Approaching Resistance to Targeted Inhibition of PI3K in Breast Cancer. Fort Belvoir, VA : Defense Technical Information Center, octobre 2011. http://dx.doi.org/10.21236/ada555900.
Texte intégralChen, Xiaole, Peng Wang, Yunquan Luo, Yi-Yu Lu, Wenjun Zhou, Mengdie Yang, Jian Chen, Zhi-Qiang Meng et Shi-Bing Su. Therapeutic Efficacy Evaluation and Underlying Mechanisms Prediction of Jianpi Liqi Decoction for Hepatocellular Carcinoma. Science Repository, septembre 2021. http://dx.doi.org/10.31487/j.jso.2021.02.04.sup.
Texte intégralPutriastuti, Massita Ayu Cindy, Vivi Fitriyanti, Vivid Amalia Khusna et Inka B. Yusgiantoro. Crowdfunding Potential : Willingness to Invest and Donate for Green Project in Indonesia. Purnomo Yusgiantoro Center, août 2022. http://dx.doi.org/10.33116/pycrr-1.
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