Relevant bibliographies by topics / PI3K TARGET

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'PI3K TARGET'

Author: Grafiati
Published: 11 September 2023
Last updated: 31 July 2025

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Journal articles on the topic "PI3K TARGET"

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Wang, Bi-Dar, Alyssa Lucero, Siyoung Ha та Reyhaneh Yarmohammadi. "PI3Kδ as a Novel Therapeutic Target for Aggressive Prostate Cancer". Cancers 17, № 10 (2025): 1610. https://doi.org/10.3390/cancers17101610.

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Phosphoinositide 3-kinases (PI3Ks) signaling represents an important pathway regulating cell proliferation, survival, invasion, migration, and metabolism. Notably, PI3K/AKT/mTOR signaling is frequently dysregulated in the majority of malignancies. Among the class IA PI3Ks (PI3Kα/β/δ), emerging evidence has implicated that PI3Kδ is not only overexpressed in leukocytes but also in solid tumors, including prostate cancer. The critical role of PI3Kδ in tumorigenesis and in the creation of a suppressive tumor microenvironment, along with the recent finding of PI3Kδ splice isoforms in promoting tumo
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Diacovo, Thomas, Dosh Whye, Evgeni Efimenko та ін. "Therapeutic Utility of PI3Kγ Inhibition in Leukemogenesis and Tumor Cell Survival". Blood 120, № 21 (2012): 1492. http://dx.doi.org/10.1182/blood.v120.21.1492.1492.

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Abstract Abstract 1492 Aberrant activation of the PI3K/Akt signaling pathway is a frequent event in cancer including various types of leukemia. Consequently, much emphasis has been placed on developing inhibitors that target this pathway. However, this would require an in depth knowledge of the role that specific class I PI3K isoforms (α, β, γ, δ)play in the pathogenesis of a particular hematological malignancy. For instance, PI3Kδ has been shown to be essential for the growth and survival of tumors derived from B cells such as chronic lymphocytic leukemia (CLL). Such knowledge has lead to dev
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Borsari, Chiara, and Matthias P. Wymann. "Targeting Phosphoinositide 3-Kinase – Five Decades of Chemical Space Exploration." CHIMIA 75, no. 12 (2021): 1037. http://dx.doi.org/10.2533/chimia.2021.1037.

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Phosphoinositide 3-kinase (PI3K) takes a key role in a plethora of physiologic processes and controls cell growth, metabolism, immunity, cardiovascular and neurological function, and more. The discovery of wortmannin as the first potent PI3K inhibitor (PI3Ki) in the 1990s provided rapid identification of PI3K-dependent processes, which drove the assembly of the PI3K/protein kinase B (PKB/Akt)/target of rapamycin (mTOR) pathway. Genetic mouse models and first PI3K isoform-specific inhibitors pinpointed putative therapeutic applications. The recognition of PI3K as target for cancer therapy drove
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Varkaris, Andreas, Ferran Fece de la Cruz, Elizabeth Martin, et al. "Abstract GS03-10: Allosteric PI3K-alpha inhibition overcomes on-target resistance to orthosteric inhibitors mediated by secondary PIK3CA mutations." Cancer Research 84, no. 9_Supplement (2024): GS03–10—GS03–10. http://dx.doi.org/10.1158/1538-7445.sabcs23-gs03-10.

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Abstract Background: PIK3CA mutations occur in ~40% of HR-positive breast cancers, where alpelisib, an orthosteric PI3Kα inhibitor, is FDA-approved in combination with fulvestrant. Although prior studies have identified potential resistance mechanisms, such as PTEN loss, clinical acquired resistance to orthosteric PI3Kα inhibitors and the role of next-generation allosteric PI3Kα inhibitors remain poorly understood. Methods: To identify on-target and off-target alterations potentially mediating resistance to PI3Kα inhibitors, we used a targeted next-generation sequencing assay (Guardant360; Gua
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Wen, Hanning, Shuai Mao, Mahamadou Djibo та ін. "Abstract 3001: Highly selective and oral bioavailable PI3Kγ inhibitor for cancer immunotherapy by targeting myeloid-derived suppressor cells in tumor". Cancer Research 85, № 8_Supplement_1 (2025): 3001. https://doi.org/10.1158/1538-7445.am2025-3001.

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Abstract Introduction: Phosphoinositide 3-kinases (PI3Ks) are crucial for cell growth, survival, and metabolism, with dysregulated signaling common in cancer. The PI3K family includes four isoforms—PI3Kα, PI3Kβ, PI3Kδ, and PI3Kγ—each with distinct roles, where pan-PI3K inhibition often results in toxicity due to broad isoform expression. Existing various PI3K isoform inhibitors, despite in vitro specificity, often act as pan-inhibitors at high in vivo clinical effective concentrations (1μ M to 5μ M). We developed a highly selective PI3Kγ inhibitor that retains its specificity even at therapeut
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Barberis, 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.

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SummaryThe family of class I phosphoinositide-3-kinase (PI3K) is composed of four lipid kinases involved at multiple levels in innate and adaptive immune responses. Class I PI3Ks are divided into two subclasses, IA and IB, sharing a similar catalytic core. Whereas class IA PI3Ks are primarily activated by receptor tyrosine kinases, the unique element of class IB PI3K (PI3Kγ) is activated by G protein coupled receptors (GPCRs), like chemokine receptors. PI3Kγ is mainly expressed in leukocytes where it plays a significant role in chemotaxis. Here, we report recent advances in the analysis of the
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Miller, Michelle, Philip Thompson, and Sandra Gabelli. "Structural Determinants of Isoform Selectivity in PI3K Inhibitors." Biomolecules 9, no. 3 (2019): 82. http://dx.doi.org/10.3390/biom9030082.

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Phosphatidylinositol 3-kinases (PI3Ks) are important therapeutic targets for the treatment of cancer, thrombosis, and inflammatory and immune diseases. The four highly homologous Class I isoforms, PI3Kα, PI3Kβ, PI3Kγ and PI3Kδ have unique, non-redundant physiological roles and as such, isoform selectivity has been a key consideration driving inhibitor design and development. In this review, we discuss the structural biology of PI3Ks and how our growing knowledge of structure has influenced the medicinal chemistry of PI3K inhibitors. We present an analysis of the available structure-selectivity
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Laurent, Pierre-Alexandre, Cédric Garcia, Marie-Pierre Gratacap та ін. "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.

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SummaryAntiphospholipid syndrome (APS) is an autoimmune disease characterised by the presence of antiphospholipid antibodies (aPL) associated with increased thrombotic risk and pregnancy morbidity. Although aPL are heterogeneous auto-antibodies, the major pathogenic target is the plasma protein β2-glycoprotein 1. The molecular mechanisms of platelet activation by aPL remain poorly understood. Here, we explored the role of the class IA phosphoinositide 3-kinase (PI3K) α and β isoforms in platelet activation by aPL. Compared to control IgG from healthy individuals, the IgG fraction isolated from
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Mercurio, Laura, Martina Morelli, Claudia Scarponi та ін. "PI3Kδ Sustains Keratinocyte Hyperproliferation and Epithelial Inflammation: Implications for a Topically Druggable Target in Psoriasis". Cells 10, № 10 (2021): 2636. http://dx.doi.org/10.3390/cells10102636.

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The phosphatidylinositol 3-kinase (PI3K)-dependent signaling pathway is aberrantly activated in psoriatic lesions and contributes to disease pathogenesis. Among PI3Ks enzymes, PI3Kα, β, and δ isoforms are known to bind the p85 regulatory subunit and mediate activation of AKT and other downstream effectors. In this study, we deepened our understanding of the expression and function of PI3Kδ in skin lesions of patients affected by psoriasis. For the first time, we found that PI3Kδ is overexpressed in psoriatic plaques, and its expression is not only confined to infiltrating immune cells but also
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Kuracha, 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 (2023): 12331. http://dx.doi.org/10.3390/ijms241512331.

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The phosphatidylinositol (PI3K)/AKT/mTOR axis represents an important therapeutic target to treat human cancers. A well-described downstream target of the PI3K pathway is the forkhead box O (FOXO) transcription factor family. FOXOs have been implicated in many cellular responses, including drug-induced resistance in cancer cells. However, FOXO-dependent acute phase resistance mediated by pictilisib, a potent small molecule PI3K inhibitor (PI3Ki), has not been studied. Here, we report that pictilisib-induced adaptive resistance is regulated by the FOXO-dependent rebound activity of receptor tyr
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Dissertations / Theses on the topic "PI3K TARGET"

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Stamatkin, Christopher W. "PHOSPHATIDYLINOSITOL 3-KINASE (PI3K) AS A THERAPEUTIC TARGET IN NSCLC." UKnowledge, 2014. http://uknowledge.uky.edu/pharmacy_etds/58.

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Deregulated activation of phosphatidylinositol 3-kinase (PI3K) pathway is central to many human malignancies. The functions of this pathway are critical for normal cell metabolism, proliferation, and survival. In lung cancers, the PI3K pathway activity is often aberrantly driven by multiple mutations, including EGFR, KRAS, and PIK3CA. Molecules targeting the PI3K pathway are intensely investigated as potential anti-cancer agents. Although inhibitors of the pathway are currently in clinical trials, rational and targeted use of these compounds, alone or in combination, requires an understanding
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McCarragher, 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.

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Cerovac, 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.

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ULTIMO, 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.

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Acute Lymphoblastic Leukemia (ALL) is a malignant disorder characterized by the abnormal clonal proliferation of B-cell progenitors (B-ALL) or immature stage thymocytes (T-ALL). Constitutive activation of the PI3K/Akt/mTOR network is a common feature of B- and T-ALL, influencing cell growth and survival. The PI3K/Akt/mTOR inhibitors are currently being developed for clinical use either as single agents or in combination with conventional chemotherapy for T-ALL patient treatment. In this study it has been investigated the effects of a panel of PI3K/Akt/mTOR inhibitors on healthy human CD4+ T-c
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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.

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In Europa, la sopravvivenza a 5 anni dei pazienti affetti da leucemia mieloide acuta (LMA) è solo del 20%. La duplicazione interna in tandem del gene FLT3 (FLT3-ITD), che codifica per il recettore della tirosina chinasi FLT3, è la mutazione più frequente (~ 25%) nella LMA con cariotipo normale, dove porta all'attivazione costitutiva della chinasi FLT3. Nonostante risultati iniziali molto promettenti con inibitori di FLT3 (FLT3i) nei pazienti con questa mutazione, pochi pazienti hanno remissioni prolungate, evidenziando la necessità di nuove e più efficaci terapie. La persistenza delle cellule
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Lonetti, Annalisa <1982&gt. "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.

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Class I phosphatidylinositol 3-kinases (PI3Ks) are heterodimeric lipid kinases consisting of a regulatory subunit and one of four catalytic subunits (p110α, p110β, p110γ or p110δ). p110γ/p110δ PI3Ks are highly enriched in leukocytes. In general, PI3Ks regulate a variety of cellular processes including cell proliferation, survival and metabolism, by generating the second messenger phosphatidylinositol-3,4,5-trisphosphate (PtdIns(3,4,5)P3). Their activity is tightly regulated by the phosphatase and tensin homolog (PTEN) lipid phosphatase. PI3Ks are widely implicated in human cancers, and in part
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Lonetti, Annalisa <1982&gt. "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/.

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Class I phosphatidylinositol 3-kinases (PI3Ks) are heterodimeric lipid kinases consisting of a regulatory subunit and one of four catalytic subunits (p110α, p110β, p110γ or p110δ). p110γ/p110δ PI3Ks are highly enriched in leukocytes. In general, PI3Ks regulate a variety of cellular processes including cell proliferation, survival and metabolism, by generating the second messenger phosphatidylinositol-3,4,5-trisphosphate (PtdIns(3,4,5)P3). Their activity is tightly regulated by the phosphatase and tensin homolog (PTEN) lipid phosphatase. PI3Ks are widely implicated in human cancers, and in part
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Venugopal, 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.

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In this study, we investigated differential activation and the role of two mTOR complexes in cell migration of prostate cancer cells. Specific knock-down of endogenous RAPTOR and RICTOR by siRNA resulted in decreased cell migration in LNCaP, DU145, and PC3 cells indicating that both mTORC1 and mTORC2 are required for cell migration. EGF treatment induced the activation of both mTORC1 and mTORC2 as determined by complex-specific phosphorylation of mTOR protein. Specific knock-down or inhibition of Rac1 activity in PC3 cells blocked EGF-induced activation of mTORC2, but had no effect on mTORC1 a
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Stellwagen, 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.

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Geng, 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.

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Endometrial cancer (EC) is the fourth most common cancer in women in developed countries, such as North America, Europe and Australia. Patients with low-grade, early-stage disease usually have a favourable survival rate. However, patients that present at an advanced stage of disease have an average survival of only 12 months. Current treatments for these patients are radiation and chemotherapy, which offer limited clinical benefit. There is no efficient treatment for advanced EC. Improved therapeutic approaches are needed for the treatment of recurrent and metastatic endometrial cancer. Recent
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Books on the topic "PI3K TARGET"

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Faithful - Target Club Pick. Simon & Schuster, 2017.

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Chiarella, Jessica. And Again: Target Club Pick. Touchstone Books, 2016.

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Lacy Eye - Target Club Pick. Grand Central Pub, 2016.

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Fifield, Richard. The Flood Girls - Target Club Pick. Gallery Books, 2016.

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House of Thieves - Target Club Pick. Sourcebooks Landmark, 2016.

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Jewell, Lisa. The Girls in the Garden: Target Club Pick. Atria Books, 2017.

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Zevin, Gabrielle. The Storied Life of Aj Fikry-target Club Pick. Algonquin Books, 2014.

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Reading Planet: Rocket Phonics - Target Practice - Ants! - Pink A. Taylor & Francis Group, 2021.

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Kleanthous, Grace. Reading Planet: Rocket Phonics - Target Practice - Ed's Neck - Pink B. Rising Stars UK Ltd., 2023.

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How consumers pick a hotel: Strategic segmentation and target marketing. Haworth Press, 1997.

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Book chapters on the topic "PI3K TARGET"

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Khwaja, Asim. "PI3K as a Target for Therapy in Haematological Malignancies." In Current Topics in Microbiology and Immunology. Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/82_2010_71.

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Margolin, Kim A. "Targeting the mTOR, PI3K, and AKT Pathways in Melanoma." In Targeted Therapeutics in Melanoma. Springer New York, 2011. http://dx.doi.org/10.1007/978-1-61779-407-0_8.

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Beagle, Brandon, and David A. Fruman. "The PI3K-AKT-mTOR Signaling Network in AML." In Targeted Therapy of Acute Myeloid Leukemia. Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1393-0_17.

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Castel, Pau, and Maurizio Scaltriti. "Mechanisms of Resistance to PI3K and AKT Inhibitors." In Resistance to Targeted Anti-Cancer Therapeutics. Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67932-7_6.

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Fernandes, 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. Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-030-02771-1_4.

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Wymann, Matthias. "PI3Ks—Drug Targets in Inflammation and Cancer." In Subcellular Biochemistry. Springer Netherlands, 2012. http://dx.doi.org/10.1007/978-94-007-3012-0_5.

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Roden, 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. Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-63234-2_18.

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AbstractDeeper understanding of the molecular pathogenesis of malignancies, including head and neck squamous cell carcinoma (HNSCC), has led to the investigation of several novel targeted therapies. These therapeutic approaches may eventually replace or complement existing treatment modalities, such as surgery, radiation therapy, and traditional cytotoxic chemotherapy. Epidermal growth factor receptor (EGFR) inhibitors, and specifically cetuximab, are as of now the only class of targeted agents, excluding immune checkpoint inhibitors, with approval in the treatment of HNSCC. Beyond EGFR inhibi
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Carroll, Martin. "Targeting the PI3 Kinase-mTOR Signaling Pathway in AML." In Targeted Therapy of Acute Myeloid Leukemia. Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1393-0_18.

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Harvey, R. Donald, Jeannine Silberman, and Sagar Lonial. "The PI3 Kinase/Akt Pathway as a Therapeutic Target in Multiple Myeloma." In Myeloma Therapy. Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-564-0_20.

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Bonavida, 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. Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-17807-3_9.

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Conference papers on the topic "PI3K TARGET"

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Herzog, Lee-or, Bianca J. Lee, Thanh-Trang Vo, 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.

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Kolev, 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.

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Kwan, Suet-Yan, Daisy I. Izaguirre, Xuanjin Cheng, et al. "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.

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Ehrmantrout, 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.

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Kaneda, Megan, Chanae Hardamon, Michael C. Schmid, et al. "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.

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Blanco, 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.

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Current chemotherapeutic regimens involve the administration of a combination of agents with hopes of gaining synergistic cell-killing effects observed in vitro. However, drug synergy is rarely realized clinically given the different pharmacokinetic profiles of the drugs. Recent findings show that a combination of rapamycin and paclitaxel proves highly effective at hindering growth of tumors wherein the phosphatidylinositol 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) pathway. Our objective was to fabricate a micellar nanotherapeutic platform capable of delivering a multitude of ag
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Dansey, 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.

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Petroni, 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.

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Bohnacker, Thomas, Florent Beaufils, Andrea E. Prota, 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.

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Ronecker, 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.

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Reports on the topic "PI3K TARGET"

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Ilic, Nina. Approaching Resistance to Targeted Inhibition of PI3K in Breast Cancer. Defense Technical Information Center, 2011. http://dx.doi.org/10.21236/ada555900.

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Chen, Xiaole, Peng Wang, Yunquan Luo, et al. Therapeutic Efficacy Evaluation and Underlying Mechanisms Prediction of Jianpi Liqi Decoction for Hepatocellular Carcinoma. Science Repository, 2021. http://dx.doi.org/10.31487/j.jso.2021.02.04.sup.

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Objective: The aim of this study was to assess the therapeutic effects of Jianpi Liqi decoction (JPLQD) in hepatocellular carcinoma (HCC) and explore its underlying mechanisms. Methods: The characteristics and outcomes of HCC patients with intermediate stage B who underwent sequential conventional transcatheter arterial chemoembolization (cTACE) and radiofrequency ablation (RFA) only or in conjunction with JPLQD were analysed retrospectively. The plasma proteins were screened using label-free quantitative proteomics analysis. The effective mechanisms of JPLQD were predicted through network pha
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Goswami, Partha. The Software-defined Vehicle: Its Current Trajectory and Execution Challenges. SAE International, 2024. http://dx.doi.org/10.4271/epr2024027.

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&lt;div class="section abstract"&gt;&lt;div class="htmlview paragraph"&gt;Original equipment manufacturers, Tier 1 suppliers, and the rest of the value chain, including the semiconductor industry, are reshaping their product portfolios, development processes, and business models to support this transformation to software-defined vehicles (SDVs). The focus on software is rippling out through the automotive sector, forcing the industry to rethink organization, leadership, processes, and future roadmaps.&lt;/div&gt;&lt;div class="htmlview paragraph"&gt;&lt;b&gt;The Software-defined Vehicle: Its C
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Putriastuti, 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, 2022. http://dx.doi.org/10.33116/pycrr-1.

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Highlights • Individual investors prefer to have an investment with high ROI rather than a low-profit investment with environmental and social benefits. • Males invest and donate more money than females in terms of quantity and frequency. • People with a level of education above an associate degree (D3) have a significantly higher level of willingness to invest and donate to green project, compared to people with a lower level of education. • In general, people with a higher income level have a higher willingness to invest. However, there is no proof on the relationship between level of income
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