Academic literature on the topic 'PI3K'

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Journal articles on the topic "PI3K"

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Hus, Iwona, Bartosz Puła, and Tadeusz Robak. "PI3K Inhibitors for the Treatment of Chronic Lymphocytic Leukemia: Current Status and Future Perspectives." Cancers 14, no. 6 (2022): 1571. http://dx.doi.org/10.3390/cancers14061571.

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Phosphoinositide 3-kinases (PI3Ks) signaling regulates key cellular processes, such as growth, survival and apoptosis. Among the three classes of PI3K, class I is the most important for the development, differentiation and activation of B and T cells. Four isoforms are distinguished within class I (PI3Kα, PI3Kβ, PI3Kδ and PI3Kγ). PI3Kδ expression is limited mainly to the B cells and their precursors, and blocking PI3K has been found to promote apoptosis of chronic lymphocytic leukemia (CLL) cells. Idelalisib, a selective PI3Kδ inhibitor, was the first-in-class PI3Ki introduced into CLL treatme
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Bohat, Ritu, Xiaofang Liang, Chunyu Xu, et al. "Abstract 4444: Targeting PI3K isoforms to improve the effectiveness of T cell mediated immunotherapy." Cancer Research 83, no. 7_Supplement (2023): 4444. http://dx.doi.org/10.1158/1538-7445.am2023-4444.

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Abstract Hyperactivation of the PI3K pathway has been reported to correlate with resistance to immune checkpoint blockade therapy (ICB) in melanoma, highlighting the therapeutic potential of combining PI3K inhibition (PI3Ki) with ICB. To maximize the clinical benefit of PI3Ki-based immune oncology (IO) combination, we characterized the role of PI3K isoforms in tumor and T cells and determined the immunological impacts of PI3Ki alone or in combination with ICB. Inhibitions of PI3K were achieved by either genetic knockdown (KD) or the bioactive compound in PTEN-present (B16/MC38), PTEN-absent (B
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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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Hawkins, P. T., K. E. Anderson, K. Davidson, and L. R. Stephens. "Signalling through Class I PI3Ks in mammalian cells." Biochemical Society Transactions 34, no. 5 (2006): 647–62. http://dx.doi.org/10.1042/bst0340647.

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It is now accepted that activation of Class I PI3Ks (phosphoinositide 3-kinases) is one of the most important signal transduction pathways used by cell-surface receptors to control intracellular events. The receptors which access this pathway include those that recognize growth factors, hormones, antigens and inflammatory stimuli, and the cellular events known to be regulated include cell growth, survival, proliferation and movement. We have learnt a great deal about the family of Class I PI3K enzymes themselves and the structural adaptations which allow a variety of cell-surface receptors to
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Garcia, Analia, Soochong Kim, Kamala Bhavaraju, Simone M. Schoenwaelder та Satya P. Kunapuli. "Role of phosphoinositide 3-kinase β in platelet aggregation and thromboxane A2 generation mediated by Gi signalling pathways". Biochemical Journal 429, № 2 (2010): 369–77. http://dx.doi.org/10.1042/bj20100166.

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PI3Ks (phosphoinositide 3-kinases) play a critical role in platelet functional responses. PI3Ks are activated upon P2Y12 receptor stimulation and generate pro-aggregatory signals. P2Y12 receptor has been shown to play a key role in the platelet aggregation and thromboxane A2 generation caused by co-stimulation with Gq or Gz, or super-stimulation of Gi pathways. In the present study, we evaluated the role of specific PI3K isoforms α, β, γ and δ in platelet aggregation, thromboxane A2 generation and ERK (extracellular-signal-regulated kinase) activation. Our results show that loss of the PI3K si
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Stypik, Mariola, Stanisław Michałek, Nina Orłowska та ін. "Design, Synthesis, and Development of Pyrazolo[1,5-a]pyrimidine Derivatives as a Novel Series of Selective PI3Kδ Inhibitors: Part II—Benzimidazole Derivatives". Pharmaceuticals 15, № 8 (2022): 927. http://dx.doi.org/10.3390/ph15080927.

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Phosphoinositide 3-kinase (PI3K) is the family of lipid kinases participating in vital cellular processes such as cell proliferation, growth, migration, or cytokines production. Due to the high expression of these proteins in many human cells and their involvement in metabolism regulation, normal embryogenesis, or maintaining glucose homeostasis, the inhibition of PI3K (especially the first class which contains four subunits: α, β, γ, δ) is considered to be a promising therapeutic strategy for the treatment of inflammatory and autoimmune diseases such as systemic lupus erythematosus (SLE) or m
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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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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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Huang, Yi Elaine, Miho Iijima, Carole A. Parent, Satoru Funamoto, Richard A. Firtel, and Peter Devreotes. "Receptor-mediated Regulation of PI3Ks Confines PI(3,4,5)P3 to the Leading Edge of Chemotaxing Cells." Molecular Biology of the Cell 14, no. 5 (2003): 1913–22. http://dx.doi.org/10.1091/mbc.e02-10-0703.

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Recent studies have demonstrated that PH domains specific for PI(3,4,5)P3 accumulate at the leading edge of a number of migrating cells and that PI3Ks and PTEN associate with the membrane at the front and back, respectively, of chemotaxing Dictyostelium discoideum cells. However, the dependence of chemoattractant induced changes in PI(3,4,5)P3 on PI3K and PTEN activities have not been defined. We find that bulk PI(3,4,5)P3 levels increase transiently upon chemoattractant stimulation, and the changes are greater and more prolonged in pten– cells. PI3K activation increases within 5 s of chemoatt
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Lin, Shu, Zuwen Zhou, Rui Tan та ін. "Abstract 5453: FCN-289, a novel, potent and selective PI3Kδ inhibitor for the treatment of B-cell malignancies". Cancer Research 82, № 12_Supplement (2022): 5453. http://dx.doi.org/10.1158/1538-7445.am2022-5453.

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Abstract Phosphoinositide 3-kinase (PI3K)/AKT/mTOR pathway plays critical roles in cell growth, differentiation, motility, survival, and intracellular trafficking, and is one of the most frequently dysregulated pathways in human cancers including B-cell malignancies. There are 3 classes of PI3K, among which Class I PI3Ks including PI3Kα, β, γ, and δ isoforms are the mostly studied and plays key roles in physiological functions. PI3Kα has a role in insulin-dependent signaling, PI3Kβ functions in platelet aggregation, thrombosis and insulin signaling, and PI3Kγ/δ are expressed mainly in leukocyt
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Dissertations / Theses on the topic "PI3K"

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Balakrishnan, Sanjeevi. "Establishing a biological role for class II phosphoinositide 3-kinase (PI3K) enzyme PI3K-C2??" Thesis, Imperial College London, 2012. http://hdl.handle.net/10044/1/39135.

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Phosphoinositide 3-Kinase (PI3K) enzymes control a variety of cellular processes and their deregulation has been extensively investigated in disease conditions including renal disease, autoimmunity and chronic inflammation. Whilst PI3K enzymes have been the subject of intense research activity, the precise biological role of PI3K-C2?? enzyme remains unclear. PI3K-C2??-/- mice developed focal segmental glomerulosclerosis, damaging podocyte morphology and affecting function. My thesis explored the contribution of the PI3K-C2?? enzyme in the pathology of chronic diseases. PI3K-C2??flx/+ mice were
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Hale, Benjamin G. "Influenza A viruses and PI3K signalling." Thesis, University of St Andrews, 2007. http://hdl.handle.net/10023/483.

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The influenza A virus non-structural (NS1) protein is multifunctional, and during virus-infection NS1 interacts with several factors in order to manipulate host-cell processes. This study reports that NS1 binds directly to p85β, a regulatory subunit of phosphoinositide 3-kinase (PI3K), but not to the related p85α. Expression of NS1 was sufficient to activate PI3K and cause the phosphorylation of a downstream mediator of PI3K signalling, Akt. However, in virus-infected MDCK cells, the kinetics of Akt phosphorylation did not correlate with NS1 expression, and suggested that negative regulation o
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Hale, Benjamin G. "Influenza A viruses and PI3K signalling /." St Andrews, 2008. http://hdl.handle.net/10023/483.

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White, Angela R. "Shared PI3K signaling abnormalities in brain tumors and epilepsy: PI3K inhibition in PTEN-deficient disorders of the brain." University of Cincinnati / OhioLINK, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1603712831970142.

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Castel, Morales Pau. "Molecular mechanisms of resistance to PI3K inhibitors." Doctoral thesis, Universitat de Barcelona, 2016. http://hdl.handle.net/10803/396640.

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The development of high-throughput sequencing technologies has prompted the evaluation of large cohorts of different tumor types. The results from these comprehensive genomic studies have revealed the most commonly mutated genes across human cancers, providing further understanding of the pathogenesis, molecular classification, and therapeutic strategies for this disease. PIK3CA, the gene encoding the PI3Kα isoform, is among the most frequently mutated genes in breast, head and neck, colorectal, and lung cancer, among others. Activating mutations in PIK3CA promote hyperactivation of the PI3
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Figueiredo, Ana Raquel Martins. "Role of PI3K in pericytes during angiogenesis." Doctoral thesis, Universitat de Barcelona, 2017. http://hdl.handle.net/10803/404276.

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Pericytes (PCs) are important regulators of the vascular development promoting vessel growth and stabilization. They have recently emerged as a therapeutic target to promote or inhibit angiogenesis. Therefore, advancing our basic understanding on PCs biology and its molecular regulators during physiological angiogenesis is essential to develop PC-related therapies. One of the major pathways leading to cellular proliferation, migration, and survival is relayed by PI3K. Data from our laboratory and others have demonstrated isoform selectivity stimulating PI3K signalling in the regulation of both
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Fedrigo, Carlos Alexandre. "Inibição da via PI3K-Akt em gliomas." Pontifícia Universidade Católica do Rio Grande do Sul, 2012. http://hdl.handle.net/10923/4518.

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Made available in DSpace on 2013-08-07T19:05:17Z (GMT). No. of bitstreams: 1 000439149-Texto+Completo-0.pdf: 1490829 bytes, checksum: bd616615ee5265db0a960d6f77c8581d (MD5) Previous issue date: 2012<br>Glioblastoma multiforme (GMB) is the most malignant and common type of all astrocytic tumours. Current standard treatment for GBM patients involves maximum surgical resection of the tumour, followed by radiotherapy and chemotherapy, usually containing the alkylating agent Temozolomide (TMZ). Despite this aggressive combination therapy, the survival rate of GBM patients is still low. This work
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Ramos, Delgado Carmen Fernanda. "Exploring PI3K signalling dynamics in pancreatic cancer." Thesis, Toulouse 3, 2020. http://www.theses.fr/2020TOU30152.

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Les PI3K sont des enzymes qui phosphorylent le groupe hydroxyl en position 3 des phosphatidylinositols comme le PIP2 ou le PI. Ces lipides sont impliqués dans de nombreux processus cellulaires tels que la croissance, la prolifération, la motilité, l'autophagie et le trafic cellulaire. Chez les mammifères, il y a 8 isoformes de PI3K et elles sont regroupées en trois classes (I, II et III) en fonction de leur structure et spécificité du substrat. Les PI3K de classe I sont les mieux caractérisées et impliquées dans le cancer. Les rôles oncogéniques des PI3K de classe II et III restent méconnus. L
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Karnes, Jonathan Burgess. "PI3K Class IIalpha Is Required for Autophagy." Thesis, Van Andel Research Institute, 2017. http://pqdtopen.proquest.com/#viewpdf?dispub=10268645.

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<p> Autophagy is a cellular recycling process in which cytoplasmic proteins and organelles are sequestered in a double membrane vesicle, delivered to the lysosome, and degraded following fusion of the two vesicles. A key part of the initiation signaling for autophagy is the generation of phosphoinositol 3-phosphate (P13P) by class III phosphoinositol 3-kinase also knows as Vps 34. In humans there are eight P13K isoforms divided into three classes, four class I enzymes, three class II enzymes, and a single class III enzyme. Of these eight enzymes, only the class III isoform is thought to partic
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Zunder, Eli Richard. "A yeast screen for PI3K inhibitor resistance." Diss., Search in ProQuest Dissertations & Theses. UC Only, 2009. http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqdiss&rft_dat=xri:pqdiss:3339211.

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Books on the topic "PI3K"

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Dominguez-Villar, Margarita, ed. PI3K and AKT Isoforms in Immunity. Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-06566-8.

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Dey, Nandini, Pradip De, and Brian Leyland-Jones, eds. PI3K-mTOR in Cancer and Cancer Therapy. Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-34211-5.

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Ding, Lili. The roles of ERK1/2 and PI3K in abnormal vascular functions in angiotensin II-infused hypertensive rats. Brock University, Faculty of Applied Health Science, 2005.

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Cheng, Peter. Hydroacoustic estimation of Fraser River pink salmon abundance and distribution at Mission, B.C., in 1987. Pacific Salmon Commission, 1991.

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Dallas, Karl. Bricks in the wall. Shapolsky, 1988.

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Bourdon, Roger J. The Pick operating system: A practical guide. Addison-Wesley, 1987.

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Sisk, Jonathan E. Exploring the PICK operating system. 2nd ed. Hayden Books, 1988.

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Steve, VanArsdale, ed. Exploring the Pick operating system. 2nd ed. Hayden Books, 1989.

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White, Bruce A. Genetic stock identification of Fraser River pink salmon: Methodology and management application. Pacific Salmon Commission, 1996.

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Fraser River Action Plan (Canada). Fraser River pink. Fraser River Action Plan, Fishery Management Group, 1995.

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Book chapters on the topic "PI3K"

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Okkenhaug, Klaus. "PI3K." In Encyclopedia of Medical Immunology. Springer New York, 2014. http://dx.doi.org/10.1007/978-0-387-84828-0_44.

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Donato, Dominique M., Steven K. Hanks, Kenneth A. Jacobson, et al. "PI3K." In Encyclopedia of Signaling Molecules. Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_101039.

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Isabelle, Plo. "PI3K Signaling." In Encyclopedia of Cancer. Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27841-9_4569-2.

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Plo, Isabelle. "PI3K Signaling." In Encyclopedia of Cancer. Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-46875-3_4569.

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Plo, Isabelle. "PI3K Signaling." In Encyclopedia of Cancer. Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_4569.

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Tibbetts, Randal S., and Robert T. Abraham. "PI3K-Related Kinases." In Signaling Networks and Cell Cycle Control. Humana Press, 2000. https://doi.org/10.1007/978-1-59259-218-0_15.

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Thomas, Hala Elnakat, Sónia R. Pereira da Veiga, George Thomas, and Sara C. Kozma. "The PI3K-mTOR Pathway." In mTOR Inhibition for Cancer Therapy: Past, Present and Future. Springer Paris, 2016. http://dx.doi.org/10.1007/978-2-8178-0492-7_2.

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Hawkins, Phillip T., Len R. Stephens, Sabine Suire, and Michael Wilson. "PI3K Signaling in Neutrophils." In Current Topics in Microbiology and Immunology. Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/82_2010_40.

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Platt, Craig. "Activated PI3K-Delta Syndrome." In Genetic Syndromes. Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-319-66816-1_2-1.

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Caux, Manuella, Gaetan Chicanne, and Sonia Severin. "Class III PI3K Biology." In Current Topics in Microbiology and Immunology. Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-06566-8_3.

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Conference papers on the topic "PI3K"

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COMA, SILVIA, David T. Weaver та Jonathan A. Pachter. "Abstract 663: The dual PI3K-δ/PI3K-γ inhibitor duvelisib inhibits signaling and proliferation of solid tumor cells expressing PI3K-δ and/or PI3K-γ". У Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-663.

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Scott, William J., Ningshu Liu, Andreas Hägebarth, et al. "Abstract 4851: Second generation 2,3-dihydroimidazo[1,2-c]quinazoline PI3K inhibitors: development of BAY 1082439, a novel balanced PI3Ká / PI3Kâ inhibitor." 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.am2016-4851.

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Cantley, L., and C. Cantley Lewis. "Abstract MS1-1: Targeting PI3K." In Abstracts: Thirty-Fifth Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 4‐8, 2012; San Antonio, TX. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/0008-5472.sabcs12-ms1-1.

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Adams, Julian. "Abstract IA19: Targeting PI3K-δ and PI3K-γ in hematological malignancies with duvelisib (IPI-145)". 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-ia19.

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Blanco Aparicio, Carmen, Oliver Renner, Elena Gomez-Casero, et al. "Abstract A275: Co-targeting PIM and PI3K/mTOR pathways with a single molecule: Novel orally available combined PIM/PI3K and PIM/PI3K/mTOR kinase inhibitors." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Oct 19-23, 2013; Boston, MA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1535-7163.targ-13-a275.

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Cantley, Lewis C. "Abstract IA22: PI3K and cancer metabolism." In Abstracts: Third AACR International Conference on Frontiers in Basic Cancer Research - September 18-22, 2013; National Harbor, MD. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.fbcr13-ia22.

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Spoerke, Jill, Carol O'Brien, Jenny Wu, et al. "Abstract 4821: Biomarker evaluation In phase I clinical trials of selective PI3K and PI3K/mTOR inhibitors." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-4821.

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Spoerke, Jill, Rupal Desai, Rajesh Patel, et al. "Abstract 4567: Biomarker evaluation in phase I clinical trials of selective PI3K and PI3K/mTOR inhibitors." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-4567.

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Nakanishi, Yoshito, Jill M. Spoerke, Mika Derynck, et al. "Abstract B03: Pharmacodynamic biomarker evaluation in phase I clinical trials of selective PI3K and PI3K/mTOR inhibitors." 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-b03.

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Sherris, David, Philip A. Dennis, Willie Wilson, et al. "Abstract A23: Differentiation of PI3K/Akt/mTOR inhibition in cancer models using dual dissociative TORC1/TORC2 (P529), single dissociative TORC1 (rapalogs) and catalytic inhibitors (PI3K/Akt, PI3K/mTOR)." 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-a23.

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Reports on the topic "PI3K"

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Patumraj, Suthiluk, and Sheepsumon Viboolvorakul. Protective effects of exercise training against vascular and neuronal dysfunction in aging brain. Department of Physiology, Faculty of Medicine, Chulalongkorn University, 2019. https://doi.org/10.58837/chula.res.2019.11.

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During advancing age, reduction of microvessels in the brain contributes insufficiency tissue perfusion. Mounting evidence indicates that microvascular deterioration in aged brain relates to oxidative stress. Nuclear factor erythroid-related factor 2 (Nrf2) plays an important role in cellular antioxidant defense. Regular physical exercise is well known to have beneficial effect to brain health, including promoted blood flow and augmented angiogenesis, in aging individuals. However, the underlying mechanism of regular physical exercise in improvement of brain microvascular density during advanc
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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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Gan, Yena, Jinwei Huang, Duoduo Li, et al. PI3K/AKT/mTOR pathway and oral diseases: a bibliometric analysis from 2008 to 2025. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, 2025. https://doi.org/10.37766/inplasy2025.6.0066.

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ธราภิวัฒนานนท์, ทิพวรรณ, ประสิทธิ์ ภวสันต์ та ทัศนีย์ ยงชัยตระกูล. การตอบสนองของเซลล์โพรงฟันต่ออินเตอร์ลิวคิน-6 : รายงานวิจัย. จุฬาลงกรณ์มหาวิทยาลัย, 2007. https://doi.org/10.58837/chula.res.2007.16.

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อันตรายต่อโพรงฟัน จะเหนี่ยวนำให้มีการหลั่งสารที่เกี่ยวกับการอักเสบ และเกิดการละลายตัวของเนื้อฟันจากภายในโพรงฟัน (internal resorption) คณะผู้วิจัยได้ตั้งสมมติฐานว่าอินเตอร์ลิวคิน-6 (IL-6) ที่เพิ่มขึ้นในภาวะที่มีการอักเสบของโพรงฟัน มีผลต่อเซลล์โพรงฟัน โดยรบกวนสมดุลของ รีเซบเตอร์ แอคติเวเตอร์ ออฟ นิวเคลีย แฟคเตอร์ แคปปาบี ไลแกนส์ (RANKL) และออสติโอโปรติเจริน (OPG) ซึ่งมีผลกระตุ้นการเกิดเซลล์สลายกระดูก และย่อยสลายเนื้อฟัน การศึกษาด้วยอาร์ที พีซีอาร์ และเวสเทอร์นอนาไลซิส พบว่าอินเตอร์ลิวคิน-6 (1 และ 10 นาโนกรัม/มิลลิลิตร) กระตุ้นการสร้าง RANKL ทั้งในระดับอาร์เอ็นเอและโปรตีน แต่ไม่มีผลต่อ OPG และมาโ
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ภวสันต์, ประสิทธิ์, та ทัศนีย์ ยงชัยตระกูล. อิทธิพลของ TNF-Alfla ต่อการสร้าง MMP-13, RANKL และ M-CSF ในเซลล์เพาะเลี้ยงเอ็นยึดปริทันต์ : รายงานผลการวิจัย. จุฬาลงกรณ์มหาวิทยลัย, 2006. https://doi.org/10.58837/chula.res.2006.9.

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วัตถุประสงค์: เซลล์เอ็นยึดปริทันต์สามารถตอบสนองต่อเชื้อแบคทีเรียและไซโตไคน์ ในภาวะที่มีการอักเสบ โดยหลั่งเอนไซม์ เมทริกซ์เมแทโลโปรทีเนส-13 (MMP-13) เพิ่มขึ้น และสร้างโปรตีนนิวเคลียแฟคเตอร์แคปปาบีไลแกนด์ (RANKL) ซึ่งช่วยกระตุ้นการเกิดเซลล์สลายกระดูก (osteoclasts) ร่วมด้วย แต่การเกิดเซลล์สลายกระดูกจำเป็นต้องมี แมคโครฟาจ-โคโลนี สติมูเลติง แฟคเตอร์ (M-CSF) ร่วมด้วย เราจึงศึกษาว่า เซลล์เอ็นยึดปริทันต์สามารถสร้าง M-CSF และ MMP-13 ในการตอบสนองต่อไซโตไคน์ที่เกี่ยวกับการอักเสบในรอยโรคปริทันต์ คือ ทูเมอร์เนโครสิส แฟคเตอร์ แอลฟา (TNF[alpha]) หรือไม่ วิธีการวิจัย: กระตุ้นเซลล์เพาะเลี้ยงเอ็นยึดปริทันต์ด้วย
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Akasheh, Rand, Mahenge Cuthbert, Faiza Kalam, Anita Adib, Stephanie Schulte, and Ting-Yuan David Cheng. Body Size and Body Composition in Relation to the PI3K/AKT/MTOR Pathway Informing Cancer Risk and Outcomes: A Systematic Review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, 2024. http://dx.doi.org/10.37766/inplasy2024.5.0036.

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Hang, Fei, Rishalaiti Tayier, Ang Li, Yanjie Yuan, and Shunhua Wu. PTEN regulates arsenic-inducedn autophagy in PI3K/AKT/mTOR signaling pathway; A systematic review and meta-analysis of in vivo and in vitro studies. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, 2021. http://dx.doi.org/10.37766/inplasy2021.1.0012.

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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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Poloboc, Alina. Fancy Pink Goat. Intellectual Archive, 2023. http://dx.doi.org/10.32370/iaj.2998.

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"Fancy Pink Goat" is a contemporary art piece from the Fancy Collection, created in Spain in 2022. It is a vividly colorful painting dominated by pink and blue, which are the signature colors of the artist`s style. The painting features a fancy goat walking through the jungle with its elegant collar and abstract, long legs. Surrounding the Fancy Pink Goat are a variety of other unusual creatures inhabiting the jungle and keeping the goat company. The artist`s signature red high-heeled shoes are also present, adding a touch of sophistication and style to the painting. This artwork is an impress
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Zelenak, Andrew J. Covercoat Pick-and-Place Robot Design. Office of Scientific and Technical Information (OSTI), 2013. http://dx.doi.org/10.2172/1089458.

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