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840 results on '"Vanhaesebroeck, Bart"'

3. Intermittent PI3Kδ inhibition sustains anti-tumour immunity and curbs irAEs.

Author

Eschweiler, Simon, Ramírez-Suástegui, Ciro, Li, Yingcong, King, Emma, Chudley, Lindsey, Thomas, Jaya, Wood, Oliver, von Witzleben, Adrian, Jeffrey, Danielle, McCann, Katy, Simon, Hayley, Mondal, Monalisa, Wang, Alice, Dicker, Martina, Lopez-Guadamillas, Elena, Chou, Ting-Fang, Dobbs, Nicola, Essame, Louisa, Acton, Gary, Kelly, Fiona, Halbert, Gavin, Sacco, Joseph, Schache, Andrew, Shaw, Richard, McCaul, James, Paterson, Claire, Davies, Joseph, Brennan, Peter, Singh, Rabindra, Loadman, Paul, Wilson, William, Hackshaw, Allan, Seumois, Gregory, Okkenhaug, Klaus, Thomas, Gareth, Jones, Terry, Ay, Ferhat, Friberg, Greg, Vanhaesebroeck, Bart, Vijayanand, Pandurangan, Ottensmeier, Christian, and Kronenberg, Mitchell

Subjects
Adenosine, Animals, Antineoplastic Agents, Disease Models, Animal, Head and Neck Neoplasms, Humans, Immunotherapy, Mice, Phosphatidylinositol 3-Kinases, Quinolines, T-Lymphocytes, Regulatory
Abstract

Phosphoinositide 3-kinase δ (PI3Kδ) has a key role in lymphocytes, and inhibitors that target this PI3K have been approved for treatment of B cell malignancies1-3. Although studies in mouse models of solid tumours have demonstrated that PI3Kδ inhibitors (PI3Kδi) can induce anti-tumour immunity4,5, its effect on solid tumours in humans remains unclear. Here we assessed the effects of the PI3Kδi AMG319 in human patients with head and neck cancer in a neoadjuvant, double-blind, placebo-controlled randomized phase II trial (EudraCT no. 2014-004388-20). PI3Kδ inhibition decreased the number of tumour-infiltrating regulatory T (Treg) cells and enhanced the cytotoxic potential of tumour-infiltrating T cells. At the tested doses of AMG319, immune-related adverse events (irAEs) required treatment to be discontinued in 12 out of 21 of patients treated with AMG319, suggestive of systemic effects on Treg cells. Accordingly, in mouse models, PI3Kδi decreased the number of Treg cells systemically and caused colitis. Single-cell RNA-sequencing analysis revealed a PI3Kδi-driven loss of tissue-resident colonic ST2 Treg cells, accompanied by expansion of pathogenic T helper 17 (TH17) and type 17 CD8+ T (TC17) cells, which probably contributed to toxicity; this points towards a specific mode of action for the emergence of irAEs. A modified treatment regimen with intermittent dosing of PI3Kδi in mouse models led to a significant decrease in tumour growth without inducing pathogenic T cells in colonic tissue, indicating that alternative dosing regimens might limit toxicity.

Published
2022

4. A small-molecule PI3Kα activator for cardioprotection and neuroregeneration

Author

Gong, Grace Q., Bilanges, Benoit, Allsop, Ben, Masson, Glenn R., Roberton, Victoria, Askwith, Trevor, Oxenford, Sally, Madsen, Ralitsa R., Conduit, Sarah E., Bellini, Dom, Fitzek, Martina, Collier, Matt, Najam, Osman, He, Zhenhe, Wahab, Ben, McLaughlin, Stephen H., Chan, A. W. Edith, Feierberg, Isabella, Madin, Andrew, Morelli, Daniele, Bhamra, Amandeep, Vinciauskaite, Vanesa, Anderson, Karen E., Surinova, Silvia, Pinotsis, Nikos, Lopez-Guadamillas, Elena, Wilcox, Matthew, Hooper, Alice, Patel, Chandni, Whitehead, Maria A., Bunney, Tom D., Stephens, Len R., Hawkins, Phillip T., Katan, Matilda, Yellon, Derek M., Davidson, Sean M., Smith, David M., Phillips, James B., Angell, Richard, Williams, Roger L., and Vanhaesebroeck, Bart

Published
2023
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9. Targeting PI3Kδ function for amelioration of murine chronic graft-versus-host disease

Author

Paz, Katelyn, Flynn, Ryan, Du, Jing, Tannheimer, Stacey, Johnson, Amy J, Dong, Shuai, Stark, Anne-Katrien, Okkenhaug, Klaus, Panoskaltsis-Mortari, Angela, Sage, Peter T, Sharpe, Arlene H, Luznik, Leo, Ritz, Jerome, Soiffer, Robert J, Cutler, Corey S, Koreth, John, Antin, Joseph H, Miklos, David B, MacDonald, Kelli P, Hill, Geoffrey R, Maillard, Ivan, Serody, Jonathan S, Murphy, William J, Munn, David H, Feser, Colby, Zaiken, Michael, Vanhaesebroeck, Bart, Turka, Laurence A, Byrd, John C, and Blazar, Bruce R

Subjects
Biomedical and Clinical Sciences, Cardiovascular Medicine and Haematology, Immunology, Infectious Diseases, Rare Diseases, Transplantation, Prevention, Stem Cell Research, 5.1 Pharmaceuticals, Development of treatments and therapeutic interventions, Good Health and Well Being, Animals, B-Lymphocytes, Bone Marrow Transplantation, Bronchiolitis Obliterans, Chronic Disease, Class I Phosphatidylinositol 3-Kinases, Disease Models, Animal, Graft vs Host Disease, Humans, Mice, Mice, Inbred BALB C, Mice, Inbred C57BL, Mice, Knockout, Mice, Mutant Strains, Phosphoinositide-3 Kinase Inhibitors, Scleroderma, Localized, T-Lymphocytes, Helper-Inducer, basic (laboratory) research, science, graft-versus-host disease, immunobiology, immunosuppressant - other, basic (laboratory) research/science, Medical and Health Sciences, Surgery, Clinical sciences
Abstract

Chronic graft-versus-host disease (cGVHD) is a leading cause of morbidity and mortality following allotransplant. Activated donor effector T cells can differentiate into pathogenic T helper (Th)-17 cells and germinal center (GC)-promoting T follicular helper (Tfh) cells, resulting in cGVHD. Phosphoinositide-3-kinase-δ (PI3Kδ), a lipid kinase, is critical for activated T cell survival, proliferation, differentiation, and metabolism. We demonstrate PI3Kδ activity in donor T cells that become Tfh cells is required for cGVHD in a nonsclerodermatous multiorgan system disease model that includes bronchiolitis obliterans (BO), dependent upon GC B cells, Tfhs, and counterbalanced by T follicular regulatory cells, each requiring PI3Kδ signaling for function and survival. Although B cells rely on PI3Kδ pathway signaling and GC formation is disrupted resulting in a substantial decrease in Ig production, PI3Kδ kinase-dead mutant donor bone marrow-derived GC B cells still supported BO cGVHD generation. A PI3Kδ-specific inhibitor, compound GS-649443, that has superior potency to idelalisib while maintaining selectivity, reduced cGVHD in mice with active disease. In a Th1-dependent and Th17-associated scleroderma model, GS-649443 effectively treated mice with active cGVHD. These data provide a foundation for clinical trials of US Food and Drug Administration (FDA)-approved PI3Kδ inhibitors for cGVHD therapy in patients.

Published
2019

11. Lack of phosphatidylinositol 3-kinase VPS34 in regulatory T cells leads to a fatal lymphoproliferative disorder without affecting their development

Author

Courreges, Christina JF, primary, Davenport, Elizabeth CM, additional, Bilanges, Benoit, additional, Rebollo-Gomez, Elena, additional, Hukelmann, Jens, additional, Schoenfelder, Priya, additional, Edgar, James R, additional, Sansom, David, additional, Scudamore, Cheryl, additional, Roychoudhuri, Rahul, additional, Garden, Oliver A, additional, Vanhaesebroeck, Bart, additional, and Okkenhaug, Klaus, additional

Published
2024
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15. PI3K-C2β limits mTORC1 signaling and angiogenic growth

Author

Kobialka, Piotr, primary, Llena, Judith, additional, Deleyto-Seldas, Nerea, additional, Munar-Gelabert, Margalida, additional, Dengra, Jose A., additional, Villacampa, Pilar, additional, Albinyà-Pedrós, Alba, additional, Muixi, Laia, additional, Andrade, Jorge, additional, van Splunder, Hielke, additional, Angulo-Urarte, Ana, additional, Potente, Michael, additional, Grego-Bessa, Joaquim, additional, Castillo, Sandra D., additional, Vanhaesebroeck, Bart, additional, Efeyan, Alejo, additional, and Graupera, Mariona, additional

Published
2023
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16. 1032 Early remodelling of CD4 T cell differentiation in lung squamous carcinogenesis

Author

Sahwangarrom, Teerapon, primary, Marin, Claudia Peinador, additional, Gamble, Sam, additional, Whiteman, Zoe, additional, Ung, Seng, additional, Kalinke, Lukas, additional, Alhendi, Ahmed, additional, Pennycuick, Adam, additional, Lopez, Sandra Gomez, additional, Enica, Andrei, additional, Rogers, Amber, additional, Davies, Kate, additional, Foster, Kane, additional, Bentzen, Amalie Kai, additional, Przybilla, Moritz, additional, Gowers, Kate, additional, Teixeira, Vitor, additional, Campbell, Peter, additional, Vanhaesebroeck, Bart, additional, Janes, Sam, additional, and Reading, James L, additional

Published
2023
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19. Somatostatin receptor 2 expression in nasopharyngeal cancer is induced by Epstein Barr virus infection: impact on prognosis, imaging and therapy

Author

Lechner, Matt, Schartinger, Volker H., Steele, Christopher D., Nei, Wen Long, Ooft, Marc Lucas, Schreiber, Liesa-Marie, Pipinikas, Christodoulos P., Chung, Grace Tin-Yun, Chan, Yuk Yu, Wu, Feng, To, Ka-Fai, Tsang, Chi Man, Pearce, Wayne, Morelli, Daniele, Philpott, Martin, Masterson, Liam, Nibhani, Reshma, Wells, Graham, Bell, Christopher G., Koller, Julia, Delecluse, Susanne, Yip, Yim Ling, Liu, Jacklyn, Forde, Cillian T., Forster, Martin D., Jay, Amrita, Dudás, József, Krapp, Annika, Wan, Simon, Uprimny, Christian, Sprung, Susanne, Haybaeck, Johannes, Fenton, Tim R., Chester, Kerry, Thirlwell, Christina, Royle, Gary, Marafioti, Teresa, Gupta, Rajeev, Indrasari, Sagung Rai, Herdini, Camelia, Slim, Mohd Afiq Mohd, Indrawati, I., Sutton, Liam, Fles, Renske, Tan, Bing, Yeong, Joe, Jain, Amit, Han, Shuting, Wang, Haitao, Loke, Kelvin S. H., He, Wan, Xu, Ruilian, Jin, Hongtao, Cheng, Zhiqiang, Howard, David, Hwang, Peter H., Le, Quynh-Thu, Tay, Joshua K., West, Robert B., Tsao, Sai Wah, Meyer, Tim, Riechelmann, Herbert, Oppermann, Udo, Delecluse, Henri-Jacques, Willems, Stefan M., Chua, Melvin L. K., Busson, Pierre, Lo, Kwok Wai, Wollmann, Guido, Pillay, Nischalan, Vanhaesebroeck, Bart, and Lund, Valerie J.

Published
2021
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20. Phosphoinositide 3-kinase p110δ promotes lumen formation through the enhancement of apico-basal polarity and basal membrane organization

Author

Peng, Juan, Awad, Aline, Sar, Sokhavuth, Hamze Komaiha, Ola, Moyano, Romina, Rayal, Amel, Samuel, Didier, Shewan, Annette, Vanhaesebroeck, Bart, Mostov, Keith, and Gassama-Diagne, Ama

Subjects
Biochemistry and Cell Biology, Biological Sciences, Stem Cell Research, Kidney Disease, Stem Cell Research - Nonembryonic - Non-Human, 1.1 Normal biological development and functioning, Underpinning research, Animals, Base Sequence, Cell Adhesion, Cell Membrane, Cell Polarity, Class Ia Phosphatidylinositol 3-Kinase, Collagen, Dogs, Epithelial Cells, Extracellular Matrix, HeLa Cells, Humans, Madin Darby Canine Kidney Cells, Microscopy, Fluorescence, Molecular Sequence Data, Paxillin, Phosphatidylinositol 3-Kinases, Protein Isoforms, RNA, Small Interfering, Signal Transduction, Vinculin, Hela Cells
Abstract

Signalling triggered by adhesion to the extracellular matrix plays a key role in the spatial orientation of epithelial polarity and formation of lumens in glandular tissues. Phosphoinositide 3-kinase signalling in particular is known to influence the polarization process during epithelial cell morphogenesis. Here, using Madin-Darby canine kidney epithelial cells grown in 3D culture, we show that the p110δ isoform of phosphoinositide 3-kinase co-localizes with focal adhesion proteins at the basal surface of polarized cells. Pharmacological, siRNA- or kinase-dead-mediated inhibition of p110δ impair the early stages of lumen formation, resulting in inverted polarized cysts, with no laminin or type IV collagen assembly at cell/extracellular matrix contacts. p110δ also regulates the organization of focal adhesions and membrane localization of dystroglycan. Thus, we uncover a previously unrecognized role for p110δ in epithelial cells in the orientation of the apico-basal axis and lumen formation.

Published
2015

28. Supplementary Figure 1 from Plasma Metabolomic Changes following PI3K Inhibition as Pharmacodynamic Biomarkers: Preclinical Discovery to Phase I Trial Evaluation

Author

Ang, Joo Ern, primary, Pandher, Rupinder, primary, Ang, Joo Chew, primary, Asad, Yasmin J., primary, Henley, Alan T., primary, Valenti, Melanie, primary, Box, Gary, primary, de Haven Brandon, Alexis, primary, Baird, Richard D., primary, Friedman, Lori, primary, Derynck, Mika, primary, Vanhaesebroeck, Bart, primary, Eccles, Suzanne A., primary, Kaye, Stan B., primary, Workman, Paul, primary, de Bono, Johann S., primary, and Raynaud, Florence I., primary

Published
2023
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29. Supplementary Figure from HER2 Mediates PSMA/mGluR1-Driven Resistance to the DS-7423 Dual PI3K/mTOR Inhibitor in PTEN Wild-type Prostate Cancer Models

Author

Gómez, Valentí, primary, Galazi, Myria, primary, Weitsman, Gregory, primary, Monypenny, James, primary, Al-Salemee, Fahad, primary, Barber, Paul R., primary, Ng, Kenrick, primary, Beatson, Richard, primary, Szokol, Bálint, primary, Orfi, László, primary, Mullen, Greg, primary, Vanhaesebroeck, Bart, primary, Chowdhury, Simon, primary, Leung, Hing Y., primary, and Ng, Tony, primary

Published
2023
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30. Supplementary Table 3 from Plasma Metabolomic Changes following PI3K Inhibition as Pharmacodynamic Biomarkers: Preclinical Discovery to Phase I Trial Evaluation

Author

Ang, Joo Ern, primary, Pandher, Rupinder, primary, Ang, Joo Chew, primary, Asad, Yasmin J., primary, Henley, Alan T., primary, Valenti, Melanie, primary, Box, Gary, primary, de Haven Brandon, Alexis, primary, Baird, Richard D., primary, Friedman, Lori, primary, Derynck, Mika, primary, Vanhaesebroeck, Bart, primary, Eccles, Suzanne A., primary, Kaye, Stan B., primary, Workman, Paul, primary, de Bono, Johann S., primary, and Raynaud, Florence I., primary

Published
2023
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31. Supplementary Table 1 from Plasma Metabolomic Changes following PI3K Inhibition as Pharmacodynamic Biomarkers: Preclinical Discovery to Phase I Trial Evaluation

Author

Ang, Joo Ern, primary, Pandher, Rupinder, primary, Ang, Joo Chew, primary, Asad, Yasmin J., primary, Henley, Alan T., primary, Valenti, Melanie, primary, Box, Gary, primary, de Haven Brandon, Alexis, primary, Baird, Richard D., primary, Friedman, Lori, primary, Derynck, Mika, primary, Vanhaesebroeck, Bart, primary, Eccles, Suzanne A., primary, Kaye, Stan B., primary, Workman, Paul, primary, de Bono, Johann S., primary, and Raynaud, Florence I., primary

Published
2023
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32. Supplementary Table 5 from Plasma Metabolomic Changes following PI3K Inhibition as Pharmacodynamic Biomarkers: Preclinical Discovery to Phase I Trial Evaluation

Author

Ang, Joo Ern, primary, Pandher, Rupinder, primary, Ang, Joo Chew, primary, Asad, Yasmin J., primary, Henley, Alan T., primary, Valenti, Melanie, primary, Box, Gary, primary, de Haven Brandon, Alexis, primary, Baird, Richard D., primary, Friedman, Lori, primary, Derynck, Mika, primary, Vanhaesebroeck, Bart, primary, Eccles, Suzanne A., primary, Kaye, Stan B., primary, Workman, Paul, primary, de Bono, Johann S., primary, and Raynaud, Florence I., primary

Published
2023
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33. Data from Plasma Metabolomic Changes following PI3K Inhibition as Pharmacodynamic Biomarkers: Preclinical Discovery to Phase I Trial Evaluation

Author

Ang, Joo Ern, primary, Pandher, Rupinder, primary, Ang, Joo Chew, primary, Asad, Yasmin J., primary, Henley, Alan T., primary, Valenti, Melanie, primary, Box, Gary, primary, de Haven Brandon, Alexis, primary, Baird, Richard D., primary, Friedman, Lori, primary, Derynck, Mika, primary, Vanhaesebroeck, Bart, primary, Eccles, Suzanne A., primary, Kaye, Stan B., primary, Workman, Paul, primary, de Bono, Johann S., primary, and Raynaud, Florence I., primary

Published
2023
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34. Supplementary Table 4 from Plasma Metabolomic Changes following PI3K Inhibition as Pharmacodynamic Biomarkers: Preclinical Discovery to Phase I Trial Evaluation

Author

Ang, Joo Ern, primary, Pandher, Rupinder, primary, Ang, Joo Chew, primary, Asad, Yasmin J., primary, Henley, Alan T., primary, Valenti, Melanie, primary, Box, Gary, primary, de Haven Brandon, Alexis, primary, Baird, Richard D., primary, Friedman, Lori, primary, Derynck, Mika, primary, Vanhaesebroeck, Bart, primary, Eccles, Suzanne A., primary, Kaye, Stan B., primary, Workman, Paul, primary, de Bono, Johann S., primary, and Raynaud, Florence I., primary

Published
2023
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35. Supplementary Table 2 from Plasma Metabolomic Changes following PI3K Inhibition as Pharmacodynamic Biomarkers: Preclinical Discovery to Phase I Trial Evaluation

Author

Ang, Joo Ern, primary, Pandher, Rupinder, primary, Ang, Joo Chew, primary, Asad, Yasmin J., primary, Henley, Alan T., primary, Valenti, Melanie, primary, Box, Gary, primary, de Haven Brandon, Alexis, primary, Baird, Richard D., primary, Friedman, Lori, primary, Derynck, Mika, primary, Vanhaesebroeck, Bart, primary, Eccles, Suzanne A., primary, Kaye, Stan B., primary, Workman, Paul, primary, de Bono, Johann S., primary, and Raynaud, Florence I., primary

Published
2023
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36. Regulation of p110δ PI 3-Kinase Gene Expression

Author

Kok, Klaartje, Nock, Gemma E, Verrall, Elizabeth AG, Mitchell, Michael P, Hommes, Daan W, Peppelenbosch, Maikel P, and Vanhaesebroeck, Bart

Subjects
Biochemistry and Cell Biology, Bioinformatics and Computational Biology, Biological Sciences, Clinical Research, Genetics, Underpinning research, 1.1 Normal biological development and functioning, 5' Untranslated Regions, Animals, Base Sequence, Binding Sites, Cell Line, Class I Phosphatidylinositol 3-Kinases, DNA Methylation, Exons, Gene Expression Regulation, Enzymologic, Genes, Reporter, Histones, Humans, Isoenzymes, Leukocytes, Mice, Molecular Sequence Data, Phosphatidylinositol 3-Kinases, Promoter Regions, Genetic, RNA Stability, Sequence Analysis, DNA, Signal Transduction, Transcription Initiation Site, General Science & Technology
Abstract

BackgroundDespite an intense interest in the biological functions of the phosphoinositide 3-kinase (PI3K) signalling enzymes, little is known about the regulation of PI3K gene expression. This also applies to the leukocyte-enriched p110delta catalytic subunit of PI3K, an enzyme that has attracted widespread interest because of its role in immunity and allergy.Principal findingsWe show that p110delta expression is mainly regulated at the transcriptional level. In fibroblasts, lymphocytes and myeloid cells, p110delta gene transcription appears to be constitutive and not subject to acute stimulation. 5'RACE experiments revealed that p110delta mRNA transcripts contain distinct upstream untranslated exons (named exon -1, -2a, -2b, -2c and -2d), which are located up to 81 kb upstream of the translational start codon in exon 1. The levels of all the different p110delta transcripts are higher in leukocytes compared to non-leukocytes, with the p110delta transcript containing exon -2a most abundantly expressed. We have identified a highly conserved transcription factor (TF) binding cluster in the p110delta gene which has enhanced promoter activity in leukocytes compared to non-leukocytes. In human, this TF cluster is located immediately upstream of exon -2a whilst in mouse, it is located within exon -2a.ConclusionThis study identifies a conserved PIK3CD promoter region that may account for the predominant leukocyte expression of p110delta.

Published
2009

37. Organismal metabolism regulates the expansion of oncogenic PIK3CAmutant clones in normal esophagus

Author

Herms, Albert, Colom, Bartomeu, Piedrafita, Gabriel, Kalogeropoulou, Argyro, Banerjee, Ujjwal, King, Charlotte, Abby, Emilie, Murai, Kasumi, Caseda, Irene, Fernandez-Antoran, David, Ong, Swee Hoe, Hall, Michael W. J., Bryant, Christopher, Sood, Roshan K., Fowler, Joanna C., Pol, Albert, Frezza, Christian, Vanhaesebroeck, Bart, and Jones, Philip H.

Abstract

Oncogenic PIK3CAmutations generate large clones in aging human esophagus. Here we investigate the behavior of Pik3camutant clones in the normal esophageal epithelium of transgenic mice. Expression of a heterozygous Pik3caH1047Rmutation drives clonal expansion by tilting cell fate toward proliferation. CRISPR screening and inhibitor treatment of primary esophageal keratinocytes confirmed the PI3K–mTOR pathway increased mutant cell competitive fitness. The antidiabetic drug metformin reduced mutant cell advantage in vivo and in vitro. Conversely, metabolic conditions such as type 1 diabetes or diet-induced obesity enhanced the competitive fitness of Pik3caH1047Rcells. Consistently, we found a higher density of PIK3CAgain-of-function mutations in the esophagus of individuals with high body mass index compared with those with normal weight. We conclude that the metabolic environment selectively influences the evolution of the normal epithelial mutational landscape. Clinically feasible interventions to even out signaling imbalances between wild-type and mutant cells may limit the expansion of oncogenic mutants in normal tissues.

Published
2024
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39. Clinical spectrum and features of activated phosphoinositide 3-kinase δ syndrome: A large patient cohort study

Author

Coulter, Tanya I., Chandra, Anita, Bacon, Chris M., Babar, Judith, Curtis, James, Screaton, Nick, Goodlad, John R., Farmer, George, Steele, Cathal Laurence, Leahy, Timothy Ronan, Doffinger, Rainer, Baxendale, Helen, Bernatoniene, Jolanta, Edgar, J. David M., Longhurst, Hilary J., Ehl, Stephan, Speckmann, Carsten, Grimbacher, Bodo, Sediva, Anna, Milota, Tomas, Faust, Saul N., Williams, Anthony P., Hayman, Grant, Kucuk, Zeynep Yesim, Hague, Rosie, French, Paul, Brooker, Richard, Forsyth, Peter, Herriot, Richard, Cancrini, Caterina, Palma, Paolo, Ariganello, Paola, Conlon, Niall, Feighery, Conleth, Gavin, Patrick J., Jones, Alison, Imai, Kohsuke, Ibrahim, Mohammad A.A., Markelj, Gašper, Abinun, Mario, Rieux-Laucat, Frédéric, Latour, Sylvain, Pellier, Isabelle, Fischer, Alain, Touzot, Fabien, Casanova, Jean-Laurent, Durandy, Anne, Burns, Siobhan O., Savic, Sinisa, Kumararatne, D.S., Moshous, Despina, Kracker, Sven, Vanhaesebroeck, Bart, Okkenhaug, Klaus, Picard, Capucine, Nejentsev, Sergey, Condliffe, Alison M., and Cant, Andrew James

Published
2017
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42. Endothelial phosphoinositide 3-kinase-β inactivation confers protection from immune-mediated vascular injury

Author

Masoud, Andrew G., primary, Lin, Jiaxin, additional, Zhu, Lin F., additional, Tao, Kesheng, additional, Ness, Nathan W., additional, Kassiri, Zamaneh, additional, Moore, Ronald B., additional, Vanhaesebroeck, Bart, additional, West, Lori, additional, Anderson, Colin C., additional, Oudit, Gavin Y., additional, and Murray, Allan G., additional

Published
2023
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44. NFκB-Mediated Expression of Phosphoinositide 3-Kinase δ Is Critical for Mesenchymal Transition in Retinal Pigment Epithelial Cells

Author

Han, Haote, primary, Yang, Yanhui, additional, Han, Zhuo, additional, Wang, Luping, additional, Dong, Lijun, additional, Qi, Hui, additional, Liu, Bing, additional, Tian, Jingkui, additional, Vanhaesebroeck, Bart, additional, Kazlauskas, Andrius, additional, Zhang, Guoming, additional, Zhang, Shaochong, additional, and Lei, Hetian, additional

Published
2023
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45. Genome Editing of Pik3cd Impedes Abnormal Retinal Angiogenesis

Author

Wu, Wenyi, primary, Ma, Gaoen, additional, Qi, Hui, additional, Dong, Lijun, additional, Chen, Fang, additional, Wang, Yun, additional, Mao, Xingxing, additional, Guo, Xiaoqing, additional, Cui, Jing, additional, Matsubara, Joanne Aiko, additional, Vanhaesebroeck, Bart, additional, Yan, Xiaohe, additional, Zhao, Guoming, additional, Zhang, Shaochong, additional, and Lei, Hetian, additional

Published
2023
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50. Long‐term treatment of cancer‐prone germline PTEN mutant mice with low‐dose rapamycin extends lifespan and delays tumour development

Author

Tibarewal, Priyanka, primary, Rathbone, Victoria, additional, Constantinou, Georgia, additional, Pearce, Wayne, additional, Adil, Mahreen, additional, Varyova, Zofia, additional, Folkes, Lisa, additional, Hampson, Alix, additional, Classen, Gala Anastasia Electra, additional, Alves, Adriana, additional, Carvalho, Sara, additional, Scudamore, Cheryl L, additional, and Vanhaesebroeck, Bart, additional

Published
2022
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