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Статті в журналах з теми "PI3K TARGET"
Diacovo, Thomas, Dosh Whye, Evgeni Efimenko, Jianchung Chen, Valeria Tosello, Kim De Keersmaecker, Adam Kashishian та ін. "Therapeutic Utility of PI3Kγ Inhibition in Leukemogenesis and Tumor Cell Survival". Blood 120, № 21 (16 листопада 2012): 1492. http://dx.doi.org/10.1182/blood.v120.21.1492.1492.
Повний текст джерелаBorsari, Chiara, and Matthias P. Wymann. "Targeting Phosphoinositide 3-Kinase – Five Decades of Chemical Space Exploration." CHIMIA 75, no. 12 (December 9, 2021): 1037. http://dx.doi.org/10.2533/chimia.2021.1037.
Повний текст джерелаBarberis, Laura, та Emilio Hirsch. "Targeting phosphoinositide 3-kinase γ to fight inflammation and more". Thrombosis and Haemostasis 99, № 02 (2008): 279–85. http://dx.doi.org/10.1160/th07-10-0632.
Повний текст джерелаMiller, Michelle, Philip Thompson, and Sandra Gabelli. "Structural Determinants of Isoform Selectivity in PI3K Inhibitors." Biomolecules 9, no. 3 (February 26, 2019): 82. http://dx.doi.org/10.3390/biom9030082.
Повний текст джерелаMercurio, Laura, Martina Morelli, Claudia Scarponi, Giovanni Luca Scaglione, Sabatino Pallotta, Cristina Albanesi та Stefania Madonna. "PI3Kδ Sustains Keratinocyte Hyperproliferation and Epithelial Inflammation: Implications for a Topically Druggable Target in Psoriasis". Cells 10, № 10 (2 жовтня 2021): 2636. http://dx.doi.org/10.3390/cells10102636.
Повний текст джерелаLaurent, Pierre-Alexandre, Cédric Garcia, Marie-Pierre Gratacap, Bart Vanhaesebroeck, Pierre Sié, Bernard Payrastre та Anne-Dominique Terrisse. "The class I phosphoinositide 3-kinases α and β control antiphospholipid antibodies-induced platelet activation". Thrombosis and Haemostasis 115, № 06 (2016): 1138–46. http://dx.doi.org/10.1160/th15-08-0661.
Повний текст джерелаKuracha, Murali R., Venkatesh Govindarajan, Brian W. Loggie, Martin Tobi, and 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 (August 2, 2023): 12331. http://dx.doi.org/10.3390/ijms241512331.
Повний текст джерелаXenou, Lydia, та Evangelia A. Papakonstanti. "p110δ PI3K as a therapeutic target of solid tumours". Clinical Science 134, № 12 (червень 2020): 1377–97. http://dx.doi.org/10.1042/cs20190772.
Повний текст джерелаMaffei, Angelo, Giuseppe Lembo, and Daniela Carnevale. "PI3Kinases in Diabetes Mellitus and Its Related Complications." International Journal of Molecular Sciences 19, no. 12 (December 18, 2018): 4098. http://dx.doi.org/10.3390/ijms19124098.
Повний текст джерелаChen, Shiyi, Wenkang Huang, Xiaoyu Li, Lijuan Gao, and 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 (July 13, 2022): 1–10. http://dx.doi.org/10.1155/2022/2156157.
Повний текст джерелаДисертації з теми "PI3K TARGET"
Stamatkin, Christopher W. "PHOSPHATIDYLINOSITOL 3-KINASE (PI3K) AS A THERAPEUTIC TARGET IN NSCLC." UKnowledge, 2014. http://uknowledge.uky.edu/pharmacy_etds/58.
Повний текст джерелаMcCarragher, 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.
Повний текст джерелаCerovac, 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.
Повний текст джерелаULTIMO, 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.
Повний текст джерелаLa 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.
Повний текст джерелаAcute 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.
Повний текст джерелаLonetti, 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/.
Повний текст джерелаVenugopal, 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.
Повний текст джерелаStellwagen, Florian [Verfasser], Jürgen E. [Akademischer Betreuer] Gschwend, Angela [Akademischer Betreuer] Krackhardt, and 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.
Повний текст джерелаGeng, 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.
Повний текст джерелаКниги з теми "PI3K TARGET"
How consumers pick a hotel: Strategic segmentation and target marketing. New York: Haworth Press, 1997.
Знайти повний текст джерелаHow consumers pick a hotel: Strategic segmentation and target marketing. New York: Routledge/Taylor & Francis Group, 2010.
Знайти повний текст джерелаFaithful - Target Club Pick. Simon & Schuster, 2017.
Знайти повний текст джерелаLacy Eye - Target Club Pick. Grand Central Pub, 2016.
Знайти повний текст джерелаChiarella, Jessica. And Again: Target Club Pick. Touchstone Books, 2016.
Знайти повний текст джерелаHouse of Thieves - Target Club Pick. Sourcebooks Landmark, 2016.
Знайти повний текст джерелаFifield, Richard. The Flood Girls - Target Club Pick. Gallery Books, 2016.
Знайти повний текст джерелаJewell, Lisa. The Girls in the Garden: Target Club Pick. Atria Books, 2017.
Знайти повний текст джерелаZevin, Gabrielle. The Storied Life of Aj Fikry-target Club Pick. Algonquin Books, 2014.
Знайти повний текст джерелаReading Planet: Rocket Phonics - Target Practice - Ants! - Pink A. Taylor & Francis Group, 2021.
Знайти повний текст джерелаЧастини книг з теми "PI3K TARGET"
Khwaja, Asim. "PI3K as a Target for Therapy in Haematological Malignancies." In Current Topics in Microbiology and Immunology, 169–88. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/82_2010_71.
Повний текст джерелаMargolin, Kim A. "Targeting the mTOR, PI3K, and AKT Pathways in Melanoma." In 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.
Повний текст джерелаBeagle, Brandon, and David A. Fruman. "The PI3K-AKT-mTOR Signaling Network in AML." In 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.
Повний текст джерелаCastel, Pau, and Maurizio Scaltriti. "Mechanisms of Resistance to PI3K and AKT Inhibitors." In 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.
Повний текст джерелаFernandes, Maria Sofia, João Miguel Sanches, and Raquel Seruca. "Targeting the PI3K Signalling as a Therapeutic Strategy in Colorectal Cancer." In 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.
Повний текст джерелаWymann, Matthias. "PI3Ks—Drug Targets in Inflammation and Cancer." In Subcellular Biochemistry, 111–81. Dordrecht: Springer Netherlands, 2012. http://dx.doi.org/10.1007/978-94-007-3012-0_5.
Повний текст джерелаRoden, Dylan F., Jennifer M. Johnson, Petr Szturz, Paolo Bossi, and Athanassios Argiris. "New and Promising Targeted Therapies in First and Second-Line Settings." In 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.
Повний текст джерелаCarroll, Martin. "Targeting the PI3 Kinase-mTOR Signaling Pathway in AML." In 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.
Повний текст джерелаHarvey, R. Donald, Jeannine Silberman, and Sagar Lonial. "The PI3 Kinase/Akt Pathway as a Therapeutic Target in Multiple Myeloma." In Myeloma Therapy, 309–22. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-564-0_20.
Повний текст джерелаBonavida, 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." In 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.
Повний текст джерелаТези доповідей конференцій з теми "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." In 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.
Повний текст джерелаKolev, Vihren N., Qunli Xu, Jonathan A. Pachter, and David T. Weaver. "Abstract 1525: FAK and PI3K/mTOR inhibitors target cancer stem cells: Implications for SCLC treatment strategies." 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.am2015-1525.
Повний текст джерелаKwan, Suet-Yan, Daisy I. Izaguirre, Xuanjin Cheng, Suet-Ying Kwan, Yvonne TM Tsang, Hoi-Shan Kwan, and Kwong-Kwok Wong. "Abstract 4697: The PI3K/mTOR pathway is a potential therapeutic target in cancers with ARID1A mutations." 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.am2015-4697.
Повний текст джерелаEhrmantrout, Kimberly K., James E. Thompson, and Angie M. Branch. "Abstract 3835: Multiple stimulants target different phosphoinositide 3-kinase (PI3K) classes in breast cancer cell lines." In 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.
Повний текст джерелаKaneda, Megan, Chanae Hardamon, Michael C. Schmid, Michael Bouvet, Franco Novelli, Emilio Hirsch, Andrew Lowy, and Judith A. Varner. "Abstract IA22: Innate immune cell PI3K gamma as a target for suppression of pancreatic ductal adenocarcinoma." In 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.
Повний текст джерелаDansey, Roger. "Abstract IA18: Clinical validation of PI3Kδ as a therapeutic target in B-cell malignancy". У 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.
Повний текст джерелаPetroni, Vanessa, Marie Therese Camilleri Podesta, Anthony George Fenech, and Godfrey Grech. "Abstract B22: Identification of novel drug combinations to target molecular pathways involved in breast cancer." In 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.
Повний текст джерелаBlanco, Elvin, Takafumi Sangai, Funda Meric-Bernstam, and Mauro Ferrari. "Chemotherapeutic Synergy Enhancement Through Micellar Nanotherapeutics." In ASME 2010 First Global Congress on NanoEngineering for Medicine and Biology. ASMEDC, 2010. http://dx.doi.org/10.1115/nemb2010-13263.
Повний текст джерелаBohnacker, 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." 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.am2015-671.
Повний текст джерелаRonecker, Jennifer S., Paul Lee, Sudeepta Sridhara, Michael LaBagnara, Raj Murali, and Meena Jhanwar-Uniyal. "Abstract 1280: The intersection of the PI3K/mTOR and HIPPO pathways: a potential therapeutic target for medulloblastoma." 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.am2016-1280.
Повний текст джерелаЗвіти організацій з теми "PI3K TARGET"
Ilic, Nina. Approaching Resistance to Targeted Inhibition of PI3K in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, October 2011. http://dx.doi.org/10.21236/ada555900.
Повний текст джерелаChen, Xiaole, Peng Wang, Yunquan Luo, Yi-Yu Lu, Wenjun Zhou, Mengdie Yang, Jian Chen, Zhi-Qiang Meng, and Shi-Bing Su. Therapeutic Efficacy Evaluation and Underlying Mechanisms Prediction of Jianpi Liqi Decoction for Hepatocellular Carcinoma. Science Repository, September 2021. http://dx.doi.org/10.31487/j.jso.2021.02.04.sup.
Повний текст джерелаPutriastuti, Massita Ayu Cindy, Vivi Fitriyanti, Vivid Amalia Khusna, and Inka B. Yusgiantoro. Crowdfunding Potential: Willingness to Invest and Donate for Green Project in Indonesia. Purnomo Yusgiantoro Center, August 2022. http://dx.doi.org/10.33116/pycrr-1.
Повний текст джерела