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Your search keyword '"Innes, Andrew J."' showing total 7 results
Start Over Author "Innes, Andrew J." Journal leukemia
7 results on '"Innes, Andrew J."'

2. Impact of BCR::ABL1single nucleotide variants on asciminib efficacy

Author

Innes, Andrew J., Hayden, Chloe, Orovboni, Victoria, Claudiani, Simone, Fernando, Fiona, Khan, Afzal, Rees, David, Byrne, Jennifer, Gallipoli, Paolo, Francis, Sebastian, Copland, Mhairi, Horne, Gillian, Raghavan, Manoj, Arnold, Claire, Collins, Angela, Cranfield, Tanya, Cunningham, Nicholas, Danga, Akila, Forsyth, Peter, Frewin, Rebecca, Garland, Paula, Hannah, Guy, Avenoso, Daniele, Hassan, Sandra, Huntly, Brian J. P., Husain, Jissan, Makkuni, Sudhakaran, Rothwell, Kate, Khorashad, Jamshid, Apperley, Jane F., and Milojkovic, Dragana

Abstract

Asciminib is a potent and selective inhibitor of BCR::ABL1, with potential to avoid toxicity resulting from off-target kinase inhibition. Forty-nine patients treated with asciminib under a managed access program in the UK were evaluated for toxicity and response. Intolerance, rather than resistance (65% vs. 35%), was the most common reason for cessation of the last-line of treatment but asciminib was well tolerated, with most patients (29, 59%) remaining on treatment at a median of 14 months follow-up, and only 6 (12%) stopping for intolerance. Of 44 patients assessable for response, 29 (66%) achieved a complete cytogenetic response (CCyR) or better, with poorer responses seen in those stopping their last-line of therapy for resistance. Fewer patients with a prior history of a non-T315I-BCR::ABL1single nucleotide variant (BSNV), or a non-T315I-BSNV detectable at baseline achieved CCyR. Serial tracking of BSNV by next generation sequencing demonstrated clonal expansion of BSNV-harbouring populations, which in some settings was associated with resistance (E459K, F317L, F359I), while in others was seen in the context of ongoing response, often with intensified dosing (T315I, I502F). These data suggest that asciminib exerts selective pressure on some BSNV-harbouring populations in vivo, some of which may respond to intensified dosing.

Published
2024
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3. Results of a national UK physician reported survey of COVID-19 infection in patients with a myeloproliferative neoplasm

Author

Salisbury, Richard A., Curto-Garcia, Natalia, O’Sullivan, Jennifer, Chen, Frederick, Polzella, Paolo, Godfrey, Anna L., Russell, James, Knapper, Steven, Willan, John, Frewin, Rebecca, Joshi, Shivani, Arami, Siamak, Burns, Sarah, Teh, Chun Huat, Wadelin, Frances, Dhanapal, Jaymathi, Neelakantan, Pratap, Milojkovic, Dragana, Psaila, Beth, Szydlo, Richard, Francis, Sebastian, Cargo, Catherine, Jain, Manish, McGregor, Andrew, Wallis, Louise, Duncombe, Andrew, Hussein, Hayder, Dyer, Peter, Munro, Laura, Bond, Lee, McMullin, Mary Frances, Somervaille, Tim C. P., Garg, Mamta, Sekhar, Mallika, Harrison, Claire, Mead, Adam J., and Innes, Andrew J.

Published
2021
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5. COVID-19 vaccine boosted immunity against Omicron in chronic myeloid leukemia patients treated with tyrosine kinase inhibitors

Author

Milojkovic, Dragana, primary, Reynolds, Catherine J., additional, Sandoval, Diana Mūnoz, additional, Pieper, Franziska P., additional, Liu, Siyi, additional, Pade, Corinna, additional, Gibbons, Joseph M., additional, McKnight, Áine, additional, Loaiza, Sandra, additional, Palanicawander, Renuka, additional, Innes, Andrew J., additional, Claudiani, Simone, additional, Apperley, Jane F., additional, Altmann, Daniel M., additional, and Boyton, Rosemary J., additional

Published
2022
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6. Complete remission with incomplete count recovery (CRi) prior to allogeneic HCT for acute myeloid leukaemia is associated with a high non-relapse mortality

Author

Innes, Andrew J., primary, Woolley, Philippa, additional, Szydlo, Richard M., additional, Lozano, Sara, additional, Fernando, Fiona, additional, Bansal, Divya, additional, Palanicawandar, Renuka, additional, Milojkovic, Dragana, additional, May, Philippa C., additional, Nadal-Melsio, Elisabet, additional, Yebra-Fernandez, Eva, additional, Olavarria, Eduardo, additional, Apperley, Jane F., additional, and Pavlů, Jiří, additional

Published
2019
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7. Impact of BCR::ABL1 single nucleotide variants on asciminib efficacy.

Author

Innes AJ, Hayden C, Orovboni V, Claudiani S, Fernando F, Khan A, Rees D, Byrne J, Gallipoli P, Francis S, Copland M, Horne G, Raghavan M, Arnold C, Collins A, Cranfield T, Cunningham N, Danga A, Forsyth P, Frewin R, Garland P, Hannah G, Avenoso D, Hassan S, Huntly BJP, Husain J, Makkuni S, Rothwell K, Khorashad J, Apperley JF, and Milojkovic D

Subjects
Humans, Female, Middle Aged, Male, Aged, Adult, Protein Kinase Inhibitors therapeutic use, Polymorphism, Single Nucleotide, Leukemia, Myelogenous, Chronic, BCR-ABL Positive drug therapy, Leukemia, Myelogenous, Chronic, BCR-ABL Positive genetics, Leukemia, Myelogenous, Chronic, BCR-ABL Positive pathology, Aged, 80 and over, Drug Resistance, Neoplasm genetics, Young Adult, Niacinamide analogs & derivatives, Pyrazoles, Fusion Proteins, bcr-abl genetics, Fusion Proteins, bcr-abl antagonists & inhibitors
Abstract

Asciminib is a potent and selective inhibitor of BCR::ABL1, with potential to avoid toxicity resulting from off-target kinase inhibition. Forty-nine patients treated with asciminib under a managed access program in the UK were evaluated for toxicity and response. Intolerance, rather than resistance (65% vs. 35%), was the most common reason for cessation of the last-line of treatment but asciminib was well tolerated, with most patients (29, 59%) remaining on treatment at a median of 14 months follow-up, and only 6 (12%) stopping for intolerance. Of 44 patients assessable for response, 29 (66%) achieved a complete cytogenetic response (CCyR) or better, with poorer responses seen in those stopping their last-line of therapy for resistance. Fewer patients with a prior history of a non-T315I-BCR::ABL1 single nucleotide variant (BSNV), or a non-T315I-BSNV detectable at baseline achieved CCyR. Serial tracking of BSNV by next generation sequencing demonstrated clonal expansion of BSNV-harbouring populations, which in some settings was associated with resistance (E459K, F317L, F359I), while in others was seen in the context of ongoing response, often with intensified dosing (T315I, I502F). These data suggest that asciminib exerts selective pressure on some BSNV-harbouring populations in vivo, some of which may respond to intensified dosing., (© 2024. The Author(s).)

Published
2024
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