Search Results - "Halford, Sarah E. R."

The clinical efficacy of first-generation carcinoembryonic antigen (CEACAM5)-specific CAR T cells is limited by poor persistence and transient pre-conditioning-dependent respiratory toxicity by Thistlethwaite, Fiona C., Gilham, David E., Guest, Ryan D., Rothwell, Dominic G., Pillai, Manon, Burt, Deborah J., Byatte, Andrea J., Kirillova, Natalia, Valle, Juan W., Sharma, Surinder K., Chester, Kerry A., Westwood, Nigel B., Halford, Sarah E. R., Nabarro, Stephen, Wan, Susan, Austin, Eric, Hawkins, Robert E.

“…The primary aim of this clinical trial was to determine the feasibility of delivering first-generation CAR T cell therapy to patients with advanced, CEACAM5 +…”
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Germline Mutations but Not Somatic Changes at the MYH Locus Contribute to the Pathogenesis of Unselected Colorectal Cancers by Halford, Sarah E.R., Rowan, Andrew J., Lipton, Lara, Sieber, Oliver M., Pack, Kevin, Thomas, Huw J.W., Hodgson, Shirley V., Bodmer, Walter F., Tomlinson, Ian P.M.

“…MYH -associated polyposis is a recently described, autosomal recessive condition comprising multiple colorectal adenomas and cancer. This disease is caused by…”
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A phase I trial of AT9283 (a selective inhibitor of aurora kinases) in children and adolescents with solid tumors: a Cancer Research UK study by Moreno, Lucas, Marshall, Lynley V, Pearson, Andrew D J, Morland, Bruce, Elliott, Martin, Campbell-Hewson, Quentin, Makin, Guy, Halford, Sarah E R, Acton, Gary, Ross, Philip, Kazmi-Stokes, Shamim, Lock, Victoria, Rodriguez, Ana, Lyons, John F, Boddy, Alan V, Griffin, Melanie J, Yule, Murray, Hargrave, Darren

“…A phase I trial of AT9283 (a multitargeted inhibitor of Aurora kinases A and B) was conducted in children and adolescents with solid tumors, to identify…”
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MSI-low, a real phenomenon which varies in frequency among cancer types by Halford, Sarah ER, Sawyer, Elinor J, Lambros, Maryou B, Gorman, Patricia, Macdonald, Nicola D, Talbot, Ian C, Foulkes, William D, Gillett, Cheryl E, Barnes, Diana M, Akslen, Lars A, Lee, Kwok, Jacobs, Ian J, Hanby, Andrew M, Ganesan, Trivadi S, Salvesen, Helga B, Bodmer, Walter F, Tomlinson, Ian PM, Roylance, Rebecca R

“…This study assessed whether low‐level microsatellite instability (MSI‐L) is a phenomenon specific to colorectal cancers or is also present in other tumour…”
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Array-CGH analysis of microsatellite-stable, near-diploid bowel cancers and comparison with other types of colorectal carcinoma by JONES, Angela M, DOUGLAS, Eleanor J, HALFORD, Sarah E. R, FIEGLER, Heike, GORMAN, Patricia A, ROYLANCE, Rebecca R, CARTER, Nigel P, TOMLINSON, Ian P. M

“…Microsatellite-stable, near-diploid (MSI-CIN-) colorectal carcinomas have been reported, but it is not clear as to whether these tumours form a discrete group…”
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Phase I expansion study of the first-in-class monocarboxylate transporter 1 (MCT1) inhibitor AZD3965 in patients with diffuse large B-cell lymphoma (DLBCL) and Burkitt lymphoma (BL) by Halford, Sarah E. R., Walter, Harriet, McKay, Pamela, Townsend, William, Linton, Kim, Heinzmann, Kathrin, Dragoni, Ilaria, Brotherton, Laura, Veal, Gareth, Siskos, Alexandros, Keun, Hector C, Bacon, Chris, Wedge, Steve, Dyer, Martin J.S., Plummer, Elizabeth Ruth

“…Abstract only 3115 Background: Tumours rely on lactate transporters (MCT1-4) to maintain glycolytic flux and avoid intracellular acidification. In…”
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Results of the OPARATIC trial: A phase I dose escalation study of olaparib in combination with temozolomide (TMZ) in patients with relapsed glioblastoma (GBM) by Halford, Sarah E. R., Cruickshank, Garth, Dunn, Laurence, Erridge, Sara, Godfrey, Lisa, Herbert, Christopher, Jefferies, Sarah, Lopez, Juanita Suzanne, McBain, Catherine, Pittman, Marc, Sleigh, Rebecca, Watts, Colin, Webster-Smith, Mark F, Chalmers, Anthony J.

“…Abstract only 2022 Background: Olaparib, a small molecule inhibitor of poly (ADP-ribose) polymerase (PARP), may improve GBM outcomes by enhancing cytotoxic…”
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A first-in-human first-in-class (FIC) trial of the monocarboxylate transporter 1 (MCT1) inhibitor AZD3965 in patients with advanced solid tumours by Halford, Sarah E. R., Jones, Paul, Wedge, Steve, Hirschberg, Sandra, Katugampola, Sidath, Veal, Gareth, Payne, Geoffrey, Bacon, Chris, Potter, Sarah, Griffin, Melanie, Chenard-Poirier, Maxime, Petrides, George, Holder, Graham, Keun, Hector C, Banerji, Udai, Plummer, Elizabeth R.

“…Abstract only 2516 Background: A key metabolic alteration in tumour cells is an increased dependency on the glycolysis, resulting in the production of lactate,…”
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Phase I clinical trials evaluating olaparib in combination with radiotherapy (RT) and/or temozolomide (TMZ) in glioblastoma patients: Results of OPARATIC and PARADIGM phase I and early results of PARADIGM-2 by Chalmers, Anthony J., Short, Susan, Watts, Colin, Herbert, Christopher, Morris, Anna, Stobo, Jamie, Cruickshank, Garth, Dunn, Laurence, Erridge, Sara, Godfrey, Lisa, Jefferies, Sarah, Lopez, Juanita Suzanne, McBain, Catherine, Pittman, Marc, Dillon, Susan, James, Allan, Nowicki, Stefan A, Williamson, Aiofe, Kelly, Caroline, Halford, Sarah E. R.

“…Abstract only…”
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Trends in the characteristics, dose-limiting toxicities and efficacy of phase I oncology trials: The Cancer Research UK experience by Wong, Han Hsi, Barton, Claire, Acton, Gary, McLeod, Robert, Darby-Dowman, Rachel, McQuillan, Janette, Turner, Helen, Wan, Susan, Backholer, Zoe, Peters, Jane, Halford, Sarah E. R.

“…Abstract only…”
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Results of stage 1 of the oparatic trial: A phase I study of olaparib in combination with temozolomide in patients with relapsed glioblastoma by Chalmers, Anthony J., Jackson, Alan, Swaisland, Helen, Stewart, William, Halford, Sarah E. R., Molife, L Rhoda, Hargrave, Darren R, McCormick, Alex

“…Abstract only…”
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A phase I dose escalation study of the tolerability of the oral VEGFR and EGFR inhibitor vandetanib (V) in combination with the oral MEK inhibitor selumetinib (S) in solid tumors by Saka, Wasiru Olugbenga, Pacey, Simon, Blackhall, Fiona Helen, Garcia-Corbacho, Javier, Fusi, Alberto, Karydis, Ioannis, Hategan, Mirela, Laviste, Glenda, Halford, Sarah E. R., Foxton, Caroline, McLeod, Robert, Wan, Susan, Talbot, Denis Charles

“…Abstract only…”
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A phase I trial of the ɣ-secretase inhibitor (GSI) MK-0752 in combination with gemcitabine in patients with pancreatic ductal adenocarcinoma (PDAC) by Cook, Natalie, Basu, Bristi, Smith, Donna-Michelle, Gopinathan, Aarthi, Evans, Thomas Jeff, Steward, William P., Hagemann, Thorsten, Venugopal, Balaji, Tuveson, David A., Hategan, Mirela, Anthoney, David Alan, Farmer, Hayley, Turner, Helen, McLeod, Robert, Halford, Sarah E. R., Jodrell, Duncan Ian

“…Abstract only…”
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A phase I pharmacokinetic (PK) and pharmacodynamic (PD) study of the selective aurora kinase inhibitor GSK1070916A by McNeish, Iain, Anthoney, Alan, Loadman, Paul, Berney, Dan, Joel, Simon, Halford, Sarah E. R., Buxton, Emily, Race, Amanda, Ikram, Mohammed, Scarsbrook, Andrew, Patikis, Angela, Rockall, Andrea, Dobbs, Nicola A, Twelves, Christopher

“…Abstract only 2525 Background: GSK1070916A is a potent and selective inhibitor of Aurora B and C. This phase I study in collaboration with GlaxoSmithKline was…”
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A phase I trial of AT9283 (a selective inhibitor of Aurora kinases) given for 72 hours every 21 days via intravenous infusion in children and adolescents with relapsed and refractory solid tumours by Hargrave, Darren R, Pearson, Andrew DJ, Moreno, Lucas, Morland, Bruce, Elliott, Martin, Makin, Guy, Campbell-Hewson, Quentin, Wyld, Peter J., Halford, Sarah E. R., Lock, Victoria, Lyons, John F., Boddy, Alan V., Yule, Murray

“…Abstract only 9542 Background: AT9283, is a multi-targeted inhibitor, against Aurora A and B, JAK & ABL kinases. Aurora kinases are potential therapeutic…”
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Investigations of the novel checkpoint kinase 1 inhibitor SRA737 in non-small cell lung cancer and colorectal cancer cells of differing tumour protein 53 gene status by Duabil, Ali Jn, Cooper, Christian R, Aldujaily, Esraa, Halford, Sarah Er, Hirschberg, Sandra, Katugampola, Sidath D, Jones, George Dd

“…In response to DNA damage the serine/threonine-specific protein kinase checkpoint kinase 1 (CHK1) is activated allowing cells to enter S phase (S) and G2 phase…”
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