18 results on '"Warren, Louise"'
Search Results
2. Stratification of biological therapies by pathobiology in biologic-naive patients with rheumatoid arthritis (STRAP and STRAP-EU): two parallel, open-label, biopsy-driven, randomised trials
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Zayat, Ahmed, Machado, Ana Rita, Cuervo, Andrea, Mahto, Arti, Cubuk, Cankut, Rawlings, Charlotte, Mosanya, Chijioke, Buckley, Chris, Holroyd, Chris, Maskall, Debbie, Carlucci, Francesco, Thorborn, Georgina, Tan, Gina, Lliso-Ribera, Gloria, Rizvi, Hasan, Peel, Joanna, Fonseca, João Eurico, Isaacs, John, Ramírez, Julio, Meric de Bellefon, Laurent, Fossati-Jimak, Liliane, Githinji, Mary, Congia, Mattia, Millar, Neal, Purkayastha, Nirupam, Celis, Raquel, Seth, Rakhi, Hands-Greenwood, Rebecca, Landewé, Robert, Perniola, Simone, Alivernini, Stefano, Marcia, Stefano, Marini, Stefano, Kelly, Stephen, Romão, Vasco, Rivellese, Felice, Nerviani, Alessandra, Giorli, Giovanni, Warren, Louise, Jaworska, Edyta, Bombardieri, Michele, Lewis, Myles J, Humby, Frances, Pratt, Arthur G, Filer, Andrew, Gendi, Nagui, Cauli, Alberto, Choy, Ernest, McInnes, Iain, Durez, Patrick, Edwards, Christopher J, Buch, Maya H, Gremese, Elisa, Taylor, Peter C, Ng, Nora, Cañete, Juan D, Raizada, Sabrina, McKay, Neil D, Jadon, Deepak, Sainaghi, Pier Paolo, Stratton, Richard, Ehrenstein, Michael R, Ho, Pauline, Pereira, Joaquim P, Dasgupta, Bhaskar, Gorman, Claire, Galloway, James, Chinoy, Hector, van der Heijde, Désirée, Sasieni, Peter, Barton, Anne, and Pitzalis, Costantino
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- 2023
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3. Fidelity evaluation of the dialogue around respiratory illness treatment (DART) program communication training
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Mangione-Smith, Rita, Robinson, Jeffrey D., Zhou, Chuan, Stout, James W., Fiks, Alexander G., Shalowitz, Madeleine, Gerber, Jeffrey S., Burges, Dennis, Hedrick, Benjamin, Warren, Louise, Grundmeier, Robert W., Kronman, Matthew P., Shone, Laura P., Steffes, Jennifer, Wright, Margaret, and Heritage, John
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- 2022
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4. The Sky at Night
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Warren, Louise
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- 2014
5. Understanding your own and otherʼs minds: The relationship to eating disorder related symptoms
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Warren, Louise and Cooper, Myra J.
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- 2011
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6. Reducing Antibiotic Prescribing in Primary Care for Respiratory Illness.
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Kronman, Matthew P., Gerber, Jeffrey S., Grundmeier, Robert W., Zhou, Chuan, Robinson, Jeffrey D., Heritage, John, Stout, James, Burges, Dennis, Hedrick, Benjamin, Warren, Louise, Shalowitz, Madeleine, Shone, Laura P., Steffes, Jennifer, Wright, Margaret, Fiks, Alexander G., and Mangione-Smith, Rita
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- 2020
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7. Role of leadership behaviours in safeguarding supervision: a literature review.
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Warren, Louise
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CHILDREN'S accident prevention , *LEADERSHIP , *MEDICAL care , *SUPERVISION of employees - Abstract
Effective safeguarding supervision reduces risk to children and young people while identifying their needs. Safeguarding supervision also helps front-line practitioners to provide high-quality care, risk analyses and individual action plans. This article is part of a wider study that explores the author's leadership behaviours and their impact on effective safeguarding supervision. The role of the safeguarding leader is evolving and the article explores relevant literature to support or refute the role of the leader in effective safeguarding supervision. A literature review was undertaken using Aveyard (2014)'s critical appraisal tool to provide structure and accuracy. The review showed the interconnection between positive leadership behaviours and effective safeguarding supervision. It also highlighted the positive effect on the practitioner's well-being of being supported by experienced, effective and compassionate leaders. [ABSTRACT FROM AUTHOR]
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- 2018
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8. The relationship between body weight (body mass index) and attachment history in young women
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Cooper, Myra J. and Warren, Louise
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- 2011
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9. Dissimilatory iron(III) reduction by Rhodobacter capsulatus.
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Dobbin, Paul S. and Warren, Louise H.
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MICROBIOLOGY , *BIOENERGETICS - Abstract
Reports that rhodobacter, the photosynthetic proteobacterium is capable of dissimilatory Fe (III) reduction. Activity expressed during anaerobic phototrophic and microaerobic growth; Variety of Fe (III) complexes demonstrated; What rates of reduction appeared to be influenced by; Governing factor for the reduction rate of Fe (III) (maltol)3; Energy-conserving nature of Fe (III) reduction by R. capsulatus demonstration.
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- 1996
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10. Association of Genes within the Major Histocompatibility Complex with Attention Deficit Hyperactivity Disorder.
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Odell, Dennis, Warren, Reed P., Warren, Louise, Burger, Roger A., and Maciulis, Alma
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- 1997
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11. 2:08 20. A Spinal Rehabilitation Program for Idiopathic Low Back Pain Based on Behavioral Learning Theory
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Feary, Joy, Warren, Louise, and Pollock, Raymond
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- 2006
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12. HE COME UP FOR THE DAY.
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Warren, Louise
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- HE Come Up For the Day (Poem), WARREN, Louise
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The poem "HE COME UP FOR THE DAY" by Louise Warren is presented. First Line: He come up for the day. Last Line: it woke him, and he swore, and made for home.
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- 2018
13. Identification of the 1.4 KB and 4.0 KB messages for the lipoprotein associated coagulation inhibitor and expression of the encoded protein
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Girard, Thomas J., Warren, Louise A., Novotny, William F., Bejcek, Bruce E., Miletich, Joseph P., and Broze, George J., Jr.
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- 1989
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14. Confirmation of the association of the C4B null allelle in autism
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Odell, Dennis, Maciulis, Alma, Cutler, Adele, Warren, Louise, McMahon, William M., Coon, Hilary, Stubbs, Gene, Henley, Kathy, and Torres, Anthony
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AUTISM , *AUTOANTIBODIES , *DEVELOPMENTAL disabilities , *HLA histocompatibility antigens - Abstract
Abstract: The objective of this study was to examine and attempt to confirm our previous findings of an increased frequency of the C4B null allele (C4BQ0) in subjects with autism. Newly identified subjects from Utah and Oregon were studied. Families evaluated included 85 who had a child with autism and 69 control families. Of the subjects with autism studied, 42.4% carried at least one C4BQ0, compared with 14.5% of the control subjects (p = 0.00013), with a relative risk of 4.33. Over half of the C4B null alleles in the subjects with autism involved C4A duplications. A marked increase in the ancestral haplotype 44.1 that lacks a C4B gene and has 2 C4A genes was also observed. The results of this study suggest that the human leukocyte antigen class III C4BQ0 significantly increases the risk for autism. [Copyright &y& Elsevier]
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- 2005
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15. The Sought-After Portrait: Marble and Steel in the Service of Francesco I d’Este
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SIMONATO, Lucia, Jennifer Montagu, Pierre Rosenberg, Sergej Androsov, Alan P. Darr, Jeremy Warren, Louise Rice, Giovanna Perini Folesani, Anne-Lise Desmas, Mark S. Weil, L. Simonato et al., MINER, CAROLYN H., and Simonato, Lucia
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- 2015
16. Stratification of biological therapies by pathobiology in biologic-naive patients with rheumatoid arthritis (STRAP and STRAP-EU): two parallel, open-label, biopsy-driven, randomised trials.
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Rivellese F, Nerviani A, Giorli G, Warren L, Jaworska E, Bombardieri M, Lewis MJ, Humby F, Pratt AG, Filer A, Gendi N, Cauli A, Choy E, McInnes I, Durez P, Edwards CJ, Buch MH, Gremese E, Taylor PC, Ng N, Cañete JD, Raizada S, McKay ND, Jadon D, Sainaghi PP, Stratton R, Ehrenstein MR, Ho P, Pereira JP, Dasgupta B, Gorman C, Galloway J, Chinoy H, van der Heijde D, Sasieni P, Barton A, and Pitzalis C
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- Humans, Female, Male, Rituximab therapeutic use, Etanercept therapeutic use, Biological Therapy, Image-Guided Biopsy, Arthritis, Rheumatoid drug therapy, Antirheumatic Agents therapeutic use, Biological Products
- Abstract
Background: Despite highly effective targeted therapies for rheumatoid arthritis, about 40% of patients respond poorly, and predictive biomarkers for treatment choices are lacking. We did a biopsy-driven trial to compare the response to rituximab, etanercept, and tocilizumab in biologic-naive patients with rheumatoid arthritis stratified for synovial B cell status., Methods: STRAP and STRAP-EU were two parallel, open-label, biopsy-driven, stratified, randomised, phase 3 trials done across 26 university centres in the UK and Europe. Biologic-naive patients aged 18 years or older with rheumatoid arthritis based on American College of Rheumatology (ACR)-European League Against Rheumatism classification criteria and an inadequate response to conventional synthetic disease-modifying antirheumatic drugs (DMARDs) were included. Following ultrasound-guided synovial biopsy, patients were classified as B cell poor or B cell rich according to synovial B cell signatures and randomly assigned (1:1:1) to intravenous rituximab (1000 mg at week 0 and week 2), subcutaneous tocilizumab (162 mg per week), or subcutaneous etanercept (50 mg per week). The primary outcome was the 16-week ACR20 response in the B cell-poor, intention-to-treat population (defined as all randomly assigned patients), with data pooled from the two trials, comparing etanercept and tocilizumab (grouped) versus rituximab. Safety was assessed in all patients who received at least one dose of study drug. These trials are registered with the EU Clinical Trials Register, 2014-003529-16 (STRAP) and 2017-004079-30 (STRAP-EU)., Findings: Between June 8, 2015, and July 4, 2019, 226 patients were randomly assigned to etanercept (n=73), tocilizumab (n=74), and rituximab (n=79). Three patients (one in each group) were excluded after randomisation because they received parenteral steroids in the 4 weeks before recruitment. 168 (75%) of 223 patients in the intention-to-treat population were women and 170 (76%) were White. In the B cell-poor population, ACR20 response at 16 weeks (primary endpoint) showed no significant differences between etanercept and tocilizumab grouped together and rituximab (46 [60%] of 77 patients vs 26 [59%] of 44; odds ratio 1·02 [95% CI 0·47-2·17], p=0·97). No differences were observed for adverse events, including serious adverse events, which occurred in six (6%) of 102 patients in the rituximab group, nine (6%) of 108 patients in the etanercept group, and three (4%) of 73 patients in the tocilizumab group (p=0·53)., Interpretation: In this biologic-naive population of patients with rheumatoid arthrtitis, the dichotomic classification into synovial B cell poor versus rich did not predict treatment response to B cell depletion with rituximab compared with alternative treatment strategies. However, the lack of response to rituximab in patients with a pauci-immune pathotype and the higher risk of structural damage progression in B cell-rich patients treated with rituximab warrant further investigations into the ability of synovial tissue analyses to inform disease pathogenesis and treatment response., Funding: UK Medical Research Council and Versus Arthritis., Competing Interests: Declaration of interests AF reports grants or contracts from Janssen, GSK, Mestag, Nascient, Bristol Myers Squibb (BMS), Roche, and UCB, and consulting fees from Janssen and Sonoma. AGP reports grants or contracts from GSK, Pfizer, and Gilead, and consulting fees from Inflection Biosciences. CJE reports payment or honoraria for lectures, presentations, speaker's bureaus, manuscript writing, or educational events from Pfizer, Gilead, Galapagos, AbbVie, Eli Lilly, BMS, Biogen, Celgene, Roche, Sanofi, and UCB Pharma; consulting fees from Gilead, Galapagos, AbbVie, and Eli Lilly; and support for attending meetings or travel from Eli Lilly. CP reports grants or contracts from GSK, Pfizer, BMS, Sanofi, Novartis, Janssen, Exagen, Genentech, and Navidea; trial funding from the UK Medical Research Council and Versus Arthritis; provision of investigational medicinal products for the trial from Pfizer and Roche; consulting fees from AbbVie, Janssen, Exagen, and Kinikska; and support for attending meetings or travel from EULAR, British Society for Rheumatology, and ACR. DvdH reports consulting fees from GSK, Pfizer, Gilead, Galapagos, AbbVie, Eli Lilly, BMS, UCB Pharma, Novartis, Janssen, Argenx, Bayer, and Takeda; is an associate editor for Annals of the Rheumatic Diseases, an editorial board member for the Journal of Rheumatology and RMD Open, an adviser for Axial Spondyloarthritis International Society, and Director of Imaging Rheumatology. EC reports grants or contracts from Pfizer, Biogen, Sanofi, and Bio-Cancer; consulting fees from Gilead, AbbVie, Biogen, Sanofi, UCB Pharma, Janssen, Fresenius Kabi, and R-Pharm; payment or honoraria for lectures, presentations, speaker's bureaus, manuscript writing, or educational events from Galapagos, AbbVie, Eli Lilly, Sanofi, Fresenius Kabi, and Chugai Pharma; support for attending meetings or travel from Galapagos and UCB Pharma. EG reports payment or honoraria for lectures, presentations, speaker's bureaus, manuscript writing, or educational events from Pfizer, Galapagos, AbbVie, Eli Lilly, BMS, Novartis, and Janssen. FR reports consulting fees from Ono Pharmaceutical. HC reports payment or honoraria for lectures, presentations, speaker's bureaus, manuscript writing, or educational events from GSK and UCB Pharma; consulting fees from Pfizer, Galapagos, and Argenx; and participation on a Data Safety Monitoring Board or Advisory Board for AstraZeneca. IM reports grants or contracts from Pfizer, Gilead, AbbVie, Eli Lilly, BMS, UCB Pharma, Novartis, Janssen, AstraZeneca, Amgen, Causeway Therapeutics, Cabaletta, Sanofi Regeneron, Evelo, Compugen, and Moonlake, and is a trustee for Versus Arthritis. JG reports payment or honoraria for lectures, presentations, speaker's bureaus, manuscript writing, or educational events from Pfizer, Galapagos, AbbVie, Eli Lilly, UCB Pharma, Janssen, and Vifor. JPP reports payment or honoraria for lectures, presentations, speaker's bureaus, manuscript writing, or educational events from Pfizer, AbbVie, Eli Lilly; consulting fees from AbbVie; support for attending meetings or travel from AbbVie and Eli Lilly; and participation on a Data Safety Monitoring Board or Advisory Board for AbbVie. MRE reports payment or honoraria for lectures, presentations, speaker's bureaus, manuscript writing, or educational events from GSK, Galapagos, and AbbVie; support for attending meetings or travel from Eli Lilly, AbbVie, and Janssen; and consulting fees from GSK, Fresenius Kabi, and AstraZeneca. MHB reports grants or contracts from Gilead, and payment or honoraria for lectures, presentations, speaker's bureaus, manuscript writing, or educational events from Galapagos, AbbVie, and Boehringer Ingelheim. NN reports support for attending meetings or travel from Janssen. PD reports payment or honoraria for lectures, presentations, speaker's bureaus, manuscript writing, or educational events from Pfizer, Galapagos, AbbVie, and Eli Lilly, and support for attending meetings or travel from Galapagos, AbbVie, and Fresenius Kabi. PCT reports consulting fees from GSK, Pfizer, Gilead, Galapagos, AbbVie, Eli Lilly, Biogen, Sanofi, UCB Pharma, Janssen, Fresenius Kabi, and Nordic Pharma; grants or contracts from Galapagos; payment or honoraria for lectures, presentations, speaker's bureaus, manuscript writing, or educational events from AbbVie; support for attending meetings or travel from Eli Lilly; participation on a Data Safety Monitoring Board or Advisory Board from Moonlake, Kymab, and Immunovant. All other authors declare no competing interests., (Copyright © 2023 The Author(s). Published by Elsevier Ltd. This is an Open Access article under the CC BY 4.0 license. Published by Elsevier Ltd.. All rights reserved.)
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- 2023
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17. Rituximab versus tocilizumab and B-cell status in TNF-alpha inadequate-responder rheumatoid arthritis patients: the R4-RA RCT
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Humby F, Durez P, Buch MH, Lewis MJ, Bombardieri M, John C, Rizvi H, Warren L, Peel J, Fossati-Jimack L, Hands RE, Giorli G, Rivellese F, Cañete JD, Taylor PC, Sasieni P, Fonseca JE, Choy E, and Pitzalis C
- Abstract
Background: Although biological therapies have transformed the outlook for those with rheumatoid arthritis, there is a lack of any meaningful response in approximately 40% of patients. The role of B cells in rheumatoid arthritis pathogenesis is well recognised and is supported by the clinical efficacy of the B-cell-depleting agent rituximab (MabThera, F. Hoffman La-Roche Ltd, Basel, Switzerland). Rituximab is licensed for use in rheumatoid arthritis following failure of conventional synthetic disease-modifying antirheumatic drugs and tumour necrosis factor inhibitor therapy. However, over 50% of patients show low/absent synovial B-cell infiltration, suggesting that, in these patients, inflammation is driven by alternative cell types. This prompted us to test the hypothesis that, in synovial biopsy B-cell-poor patients, tocilizumab (RoActemra, F. Hoffman La-Roche Ltd, Basel, Switzerland) (targeting interleukin 6) is superior to rituximab (targeting CD20
+ /B cells)., Design: The R4–RA (A Randomised, open-labelled study in anti-TNFalpha inadequate responders to investigate the mechanisms for Response, Resistance to Rituximab versus Tocilizumab in Rheumatoid Arthritis patients) trial is a 48-week Phase IV, open-label, randomised controlled trial conducted in 19 European centres that recruited patients failing on or intolerant to conventional synthetic disease-modifying antirheumatic drug therapy and at least one tumour necrosis factor inhibitor., Participants: Synovial tissue was obtained at trial entry and classified histologically as B-cell rich or B-cell poor to inform balanced stratification. Patients were randomised on a 1 : 1 basis to receive standard therapy with rituximab or tocilizumab. B-cell-poor/-rich molecular classification was also carried out. The study was powered to test the superiority of tocilizumab over rituximab at 16 weeks in the B-cell-poor population., Main Outcome Measures: The primary end point was defined as an improvement in the Clinical Disease Activity Index (CDAI) score of ≥ 50% from baseline. In addition, patients were considered to be non-responders if they did not reach an improvement in CDAI score of ≥ 50% and a CDAI score of < 10.1, defined for simplicity as CDAI major treatment response (CDAI-MTR). Secondary outcomes included the assessment of CDAI response in the B-cell-rich cohort, in which the non-inferiority of rituximab compared with tocilizumab was evaluated. Safety data up to week 48 are reported., Results: In total, 164 patients were randomised: 83 patients received rituximab and 81 received tocilizumab. Eighty-one out of 83 rituximab patients and 73 out of 81 tocilizumab patients completed treatment up to week 16 (primary end point). Baseline characteristics were comparable between the treatment groups. In the histologically classified B-cell-poor population ( n = 79), no significant difference was observed in the primary outcome, an improvement in CDAI score of ≥ 50% from baseline (risk ratio 1.25, 95% confidence interval 0.80 to 1.96). A supplementary analysis of the CDAI-MTR, however, did reach statistical significance (risk ratio 1.96, 95% confidence interval 1.01 to 3.78). In addition, when B-cell-poor classification was determined molecularly, both the primary end point and the CDAI-MTR were statistically significant (risk ratio 1.72, 95% confidence interval 1.02 to 2.91, and risk ratio 4.12, 95% confidence interval 1.55 to 11.01, respectively). Moreover, a larger number of secondary end points achieved significance when classified molecularly than when classified histologically. In the B-cell-rich population, there was no significant difference between treatments in the majority of both primary and secondary end points. There were more adverse events and serious adverse events, such as infections, in the tocilizumab group than in the rituximab group., Conclusion: To our knowledge, this is the first biopsy-based, multicentre, randomised controlled trial of rheumatoid arthritis. We were unable to demonstrate that tocilizumab was more effective than rituximab in patients with a B-cell-poor pathotype in our primary analysis. However, superiority was shown in most of the supplementary and secondary analyses using a molecular classification. These analyses overcame possible unavoidable weaknesses in our original study plan, in which the histological method of determining B-cell status may have misclassified some participants and our chosen primary outcome was insufficiently sensitive. Given the significant results observed using the molecular classification, future research will focus on refining this stratification method and evaluating its clinical utility., Trial Registration: Current Controlled Trials ISRCTN97443826., Funding: This project was funded by the Efficacy and Mechanism Evaluation (EME) programme, a Medical Research Council and National Institute for Health and Care Research (NIHR) partnership. This will be published in full in Efficacy and Mechanism Evaluation ; Vol. 9, No. 7. See the NIHR Journals Library website for further project information., (Copyright © Queen’s Printer and Controller of HMSO 2022. This work was produced by Humby et al. under the terms of a commissioning contract issued by the Secretary of State for Health and Social Care. This issue may be freely reproduced for the purposes of private research and study and extracts (or indeed, the full report) may be included in professional journals provided that suitable acknowledgement is made and the reproduction is not associated with any form of advertising. Applications for commercial reproduction should be addressed to: NIHR Journals Library, National Institute for Health and Care Research, Alpha House, University of Southampton Science Park, Southampton SO16 7NS, UK.)- Published
- 2022
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18. First-In-Human Phase I Study of a Next-Generation, Oral, TGFβ Receptor 1 Inhibitor, LY3200882, in Patients with Advanced Cancer.
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Yap TA, Vieito M, Baldini C, Sepúlveda-Sánchez JM, Kondo S, Simonelli M, Cosman R, van der Westhuizen A, Atkinson V, Carpentier AF, Löhr M, Redman R, Mason W, Cervantes A, Le Rhun E, Ochsenreither S, Warren L, Zhao Y, Callies S, Estrem ST, Man M, Gandhi L, Avsar E, and Melisi D
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- Antineoplastic Combined Chemotherapy Protocols adverse effects, Humans, Maximum Tolerated Dose, Paclitaxel therapeutic use, Transforming Growth Factor beta, Antineoplastic Agents adverse effects, Head and Neck Neoplasms, Pancreatic Neoplasms drug therapy
- Abstract
Purpose: A novel, selective, next-generation transforming growth factor beta (TGFβ) receptor type-1 small molecule inhibitor, LY3200882, demonstrated promising preclinical data. This first-in-human trial evaluated safety, tolerability, recommended phase II dose (RP2D), pharmacokinetics, pharmacodynamics, and preliminary antitumor activity of LY3200882 as monotherapy or with other anticancer agents in patients with advanced cancer., Patients and Methods: This phase I multicenter study of oral LY3200882 (NCT02937272) comprised dose escalation, monotherapy expansion in grade 4 glioma, and combination therapy in solid tumors (LY3200882 and PD-L1 inhibitor LY3300054), pancreatic cancer (LY3200882, gemcitabine, and nab-paclitaxel), and head and neck squamous cell cancer (LY3200882, cisplatin, and radiation)., Results: Overall, 139 patients with advanced cancer were treated. The majority (93.5%) of patients experienced ≥1 treatment-emergent adverse events (TEAE), with 39.6% LY3200882-related. Grade 3 LY3200882-related toxicities were only observed in combination therapy arms. One patient in the pancreatic cancer arm experienced cardiovascular toxicity. The LY3200882 monotherapy RP2Ds were established in two schedules: 50 mg twice a day 2-weeks-on/2-weeks-off and 35 mg twice a day 3-weeks-on/1-week-off. Four patients with grade 4 glioma had durable Revised Assessment in Neuro Oncology (RANO) partial responses (PR) with LY3200882 monotherapy ( n = 3) or LY3200882-LY3300054 combination therapy ( n = 1). In treatment-naïve patients with advanced pancreatic cancer, 6 of 12 patients achieved Response Evaluation Criteria in Solid Tumors (RECIST) v1.1 PR and 3 of 12 patients demonstrated stable disease, for an overall 75% disease-control rate with the combination of LY3200882, gemcitabine, and nab-paclitaxel., Conclusions: LY3200882 as monotherapy and combination therapy was safe and well tolerated with preliminary antitumor activity observed in pancreatic cancer. Further studies to evaluate the efficacy of LY3200882 with gemcitabine and nab-paclitaxel in advanced pancreatic cancer are warranted., (©2021 The Authors; Published by the American Association for Cancer Research.)
- Published
- 2021
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