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14 results on '"Ladon, Dariusz"'

1. TP53 mutation in therapy-related myeloid neoplasm defines a distinct molecular subtype

Author

Hiwase, Devendra, Hahn, Christopher, Tran, Elizabeth Ngoc Hoa, Chhetri, Rakchha, Baranwal, Anmol, Al-Kali, Aref, Sharplin, Kirsty, Ladon, Dariusz, Hollins, Rachel, Greipp, Patricia, Kutyna, Monika, Alkhateeb, Hassan, Badar, Talha, Wang, Paul, Ross, David M., Singhal, Deepak, Shanmuganathan, Naranie, Bardy, Peter, Beligaswatte, Ashanka, Yeung, David, Litzow, Mark R., Mangaonkar, Abhishek, Giri, Pratyush, Lee, Cindy, Yong, Angie, Horvath, Noemi, Singhal, Nimit, Gowda, Raghu, Hogan, William, Gangat, Naseema, Patnaik, Mrinal, Begna, Kebede, Tiong, Ing S., Wei, Andrew, Kumar, Sharad, Brown, Anna, Scott, Hamish, Thomas, Daniel, Kok, Chung H., Tefferi, Ayalew, and Shah, Mithun Vinod

Published
2023
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2. TP53mutation in therapy-related myeloid neoplasm defines a distinct molecular subtype

Author

Hiwase, Devendra, Hahn, Christopher, Tran, Elizabeth Ngoc Hoa, Chhetri, Rakchha, Baranwal, Anmol, Al-Kali, Aref, Sharplin, Kirsty, Ladon, Dariusz, Hollins, Rachel, Greipp, Patricia, Kutyna, Monika, Alkhateeb, Hassan, Badar, Talha, Wang, Paul, Ross, David M., Singhal, Deepak, Shanmuganathan, Naranie, Bardy, Peter, Beligaswatte, Ashanka, Yeung, David, Litzow, Mark R., Mangaonkar, Abhishek, Giri, Pratyush, Lee, Cindy, Yong, Angie, Horvath, Noemi, Singhal, Nimit, Gowda, Raghu, Hogan, William, Gangat, Naseema, Patnaik, Mrinal, Begna, Kebede, Tiong, Ing S., Wei, Andrew, Kumar, Sharad, Brown, Anna, Scott, Hamish, Thomas, Daniel, Kok, Chung H., Tefferi, Ayalew, and Shah, Mithun Vinod

Abstract

[Display omitted]

Published
2023
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3. Unraveling facets of MECOM-associated syndrome: somatic genetic rescue, clonal hematopoiesis, and phenotype expansion

Author

Venugopal, Parvathy, Arts, Peer, Fox, Lucy C., Simons, Annet, Hiwase, Devendra K., Bardy, Peter G., Swift, Annette, Ross, David M., van Vulpen, Lize F. D., Buijs, Arjan, Bolton, Kelly L., Getta, Bartlomiej, Furlong, Eliska, Carter, Tina, Krapels, Ingrid, Hoeks, Marlijn, Al Kindy, Adila, Al Kindy, Farah, de Munnik, Sonja, Evans, Pamela, Frank, Mahalia S. B., Bournazos, Adam, Cooper, Sandra T., Ha, Thuong Thi, Jackson, Matilda R., Arriola-Martinez, Luis, Phillips, Kerry, Brennan, Yvonne, Bakshi, Madhura, Ambler, Karen, Gao, Song, Kassahn, Karin S., Kenyon, Rosalie, Hung, Kevin, Babic, Milena, McGovern, Alan, Rawlings, Lesley, Vakulin, Cassandra, Dejong, Lucas, Fathi, Rema, McRae, Simon, Myles, Nicholas, Ladon, Dariusz, Jongmans, Marjolijn, Kuiper, Roland P., Poplawski, Nicola K., Barbaro, Pasquale, Blombery, Piers, Brown, Anna L., Hahn, Christopher N., and Scott, Hamish S.

Published
2024
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4. DNA methylation-based profiling for paediatric CNS tumour diagnosis and treatment: a population-based study

Author

Pickles, Jessica C, Fairchild, Amy R, Stone, Thomas J, Brownlee, Lorelle, Merve, Ashirwad, Yasin, Shireena A, Avery, Aimee, Ahmed, Saira W, Ogunbiyi, Olumide, Gonzalez Zapata, Jamie, Peary, Abigail F, Edwards, Marie, Wilkhu, Lisa, Dryden, Carryl, Ladon, Dariusz, Kristiansen, Mark, Rowe, Catherine, Kurian, Kathreena M, Nicoll, James A R, Mitchell, Clare, Bloom, Tabitha, Hilton, David A, Al-Sarraj, Safa, Doey, Lawrence, Johns, Paul N, Bridges, Leslie R, Chakrabarty, Aruna, Ismail, Azzam, Rathi, Nitika, Syed, Khaja, Lammie, G Alistair, Limback-Stanic, Clara, Smith, Colin, Torgersen, Antonia, Rae, Frances, Hill, Rebecca M, Clifford, Steven C, Grabovska, Yura, Williamson, Daniel, Clarke, Matthew, Jones, Chris, Capper, David, Sill, Martin, von Deimling, Andreas, Pfister, Stefan M, Jones, David T W, Hargrave, Darren, Chalker, Jane, and Jacques, Thomas S

Abstract

Marked variation exists in the use of genomic data in tumour diagnosis, and optimal integration with conventional diagnostic technology remains uncertain despite several studies reporting improved diagnostic accuracy, selection for targeted treatments, and stratification for trials. Our aim was to assess the added value of molecular profiling in routine clinical practice and the impact on conventional and experimental treatments.

Published
2020
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5. Comparison of World Health Organization and International Consensus Classification Guidelines for Myeloid Neoplasms Harboring TP53-Mutations Using an Independent International Cohort

Author

Shah, Mithun V, Kutyna, Monika, Shah, Syed, Tran, Elizabeth Ngoc Hoa, Baranwal, Anmol, Ladon, Dariusz, Al-Kali, Aref, Brown, Anna, Chen, Dong, Greipp, Patricia, Begna, Kebede, Litzow, Mark R., Hogan, William J., Bardy, Peter, Kumar, Sharad, Yeung, David T, Patnaik, Mrinal M., Foran, James M., He, Rong, Gangat, Naseema, Scott, Hamish S, Arana Yi, Cecilia Y., Alkhateeb, Hassan, Mangaonkar, Abhishek A, Thomas, Daniel, Hahn, Christopher Norman, Orazi, Attilio, Arber, Daniel A., Kok, Chung Hoow, Tefferi, Ayalew, and Hiwase, Devendra

Abstract

BACKGROUND:Recently proposed World Health Organization (WHO, 5 thedition) and International Consensus Classification (ICC) recognized myeloid neoplasms (MN) harboring TP53-mutated ( TP53mut) as a separate entity. However, there are critical differences between the two classifications regarding allelic-status, variance allele frequency (VAF) cut-off and blast categories, that may lead to under- or overestimation of the risk.

Published
2023
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6. TP53 Mutation Status Defines a Distinct Clinicopathological Entity of Therapy-Related Myeloid Neoplasm, Characterized By Genomic Instability and Extremely Poor Outcome

Author

Shah, Mithun V., Hahn, Christopher N, Tran, Elizabeth Ngoc Hoa, Sharplin, Kirsty M, Chhetri, Rakchha, Baranwal, Anmol, Kutyna, Monika M, Wang, Paul, Ladon, Dariusz, Al-Kali, Aref, Alkhateeb, Hassan B., Ross, David M, Yeung, David T, Shanmuganathan, Naranie, Litzow, Mark R., Mangaonkar, Abhishek A., Hogan, William J., Gangat, Naseema, Patnaik, Mrinal M.M., Kebede, Begna, Kumar, Sharad, Singhal, Deepak, Brown, Anna L., Scott, Hamish S, Thomas, Daniel, Kok, Chung Hoow, Tefferi, Ayalew, and Hiwase, Devendra

Published
2022
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7. TP53Mutation Status Defines a Distinct Clinicopathological Entity of Therapy-Related Myeloid Neoplasm, Characterized By Genomic Instability and Extremely Poor Outcome

Author

Shah, Mithun V., Hahn, Christopher N, Tran, Elizabeth Ngoc Hoa, Sharplin, Kirsty M, Chhetri, Rakchha, Baranwal, Anmol, Kutyna, Monika M, Wang, Paul, Ladon, Dariusz, Al-Kali, Aref, Alkhateeb, Hassan B., Ross, David M, Yeung, David T, Shanmuganathan, Naranie, Litzow, Mark R., Mangaonkar, Abhishek A., Hogan, William J., Gangat, Naseema, Patnaik, Mrinal M.M., Kebede, Begna, Kumar, Sharad, Singhal, Deepak, Brown, Anna L., Scott, Hamish S, Thomas, Daniel, Kok, Chung Hoow, Tefferi, Ayalew, and Hiwase, Devendra

Published
2022
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8. Personalized Prediction Model to Risk Stratify Patients with Therapy-Related Myeloid Neoplasms

Author

Kok, Chung Hoow, Tran, Elizabeth Ngoc Hoa, Ladon, Dariusz, Chhetri, Rakchha, Baranwal, Anmol, Sharplin, Kirsty M, Alkhateeb, Hassan B., Singhal, Deepak, Al-Kali, Aref, Gangat, Naseema, Yeung, David T, Litzow, Mark R., Ross, David M, Hogan, William J., Kebede, Ashanka Begna, Mangaonkar, Abhishek A., Patnaik, Mrinal M., Tefferi, Ayalew, Shanmuganathan, Naranie, Kumar, Sharad, Thomas, Daniel, Shah, Mithun V., and Hiwase, Devendra

Published
2022
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9. Personalized Prediction Model to Risk Stratify Patients with Therapy-Related Myeloid Neoplasms

Author

Kok, Chung Hoow, Tran, Elizabeth Ngoc Hoa, Ladon, Dariusz, Chhetri, Rakchha, Baranwal, Anmol, Sharplin, Kirsty M, Alkhateeb, Hassan B., Singhal, Deepak, Al-Kali, Aref, Gangat, Naseema, Yeung, David T, Litzow, Mark R., Ross, David M, Hogan, William J., Kebede, Ashanka Begna, Mangaonkar, Abhishek A., Patnaik, Mrinal M., Tefferi, Ayalew, Shanmuganathan, Naranie, Kumar, Sharad, Thomas, Daniel, Shah, Mithun V., and Hiwase, Devendra

Published
2022
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10. Long Terminal Repeat CRISPR-CAR-Coupled “Universal” T Cells Mediate Potent Anti-leukemic Effects

Author

Georgiadis, Christos, Preece, Roland, Nickolay, Lauren, Etuk, Aniekan, Petrova, Anastasia, Ladon, Dariusz, Danyi, Alexandra, Humphryes-Kirilov, Neil, Ajetunmobi, Ayokunmi, Kim, Daesik, Kim, Jin-Soo, and Qasim, Waseem

Abstract

Gene editing can be used to overcome allo-recognition, which otherwise limits allogeneic T cell therapies. Initial proof-of-concept applications have included generation of such “universal” T cells expressing chimeric antigen receptors (CARs) against CD19 target antigens combined with transient expression of DNA-targeting nucleases to disrupt the T cell receptor alpha constant chain (TRAC). Although relatively efficient, transgene expression and editing effects were unlinked, yields variable, and resulting T cell populations heterogeneous, complicating dosing strategies. We describe a self-inactivating lentiviral “terminal” vector platform coupling CAR expression with CRISPR/Cas9 effects through incorporation of an sgRNA element into the ΔU3 3′ long terminal repeat (LTR). Following reverse transcription and duplication of the hybrid ΔU3-sgRNA, delivery of Cas9 mRNA resulted in targeted TRAClocus cleavage and allowed the enrichment of highly homogeneous (>96%) CAR+(>99%) TCR−populations by automated magnetic separation. Molecular analyses, including NGS, WGS, and Digenome-seq, verified on-target specificity with no evidence of predicted off-target events. Robust anti-leukemic effects were demonstrated in humanized immunodeficient mice and were sustained longer than by conventional CAR+TCR+T cells. Terminal-TRAC (TT) CAR T cells offer the possibility of a pre-manufactured, non-HLA-matched CAR cell therapy and will be evaluated in phase 1 trials against B cell malignancies shortly.

Published
2018
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12. TT52CAR19: Phase 1 Trial of CRISPR/Cas9 Edited Allogeneic CAR19 T Cells for Paediatric Relapsed/Refractory B-ALL

Author

Ottaviano, Giorgio, Georgiadis, Christos, Syed, Farhatullah, Gkazi, Soragia Athina, Zhan, Hong, Etuk, Annie, Chu, Jan, Pinner, Danielle, Inglott, Sarah, Gilmour, Kimberly, Adams, Stuart, Kricke, Susanne, Izotova, Natalia, Ladon, Dariusz, Kubat, Agnieszka, Veys, Paul, Vora, Ajay, Rao, Kanchan, and Qasim, Waseem

Abstract

Qasim: Autolus: Current equity holder in publicly-traded company; Novartis: Honoraria; Servier: Research Funding; Tessa: Membership on an entity's Board of Directors or advisory committees.

Published
2021
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13. Progression Free Survival (PFS) in Alemtuzumab Based RIC Allogeneic Transplantation for Myeloma Is Improved with Use of Pre-Emptive DLI (pDLI).

Author

Ramasamy, Karthik, Mahmood, Shameem, Pearce, Laurence, Lim, ZiYi, Ladon, Dariusz, Pagliuca, Antonio, Devereux, Stephen, Mufti, Ghulam J., and Schey, Stephen

Abstract

Allogeneic transplantation is the only potentially curative treatment option for myeloma (MM). While reduced intensity conditioning (RIC) regimens are associated with lower transplant related morbidity and mortality (TRM), this approach is offset by an increase in relapse rates in myeloma. Method & Materials: We conducted a prospective study on the use of pDLI in myeloma patients with declining donor T cell chimerism following alemtuzumab based RIC allogeneic transplants. 19 consecutive patients were recruited. Patients received 100mg of Alemtuzumab 1H in total over 5 days in vivo as part of the pre-transplant conditioning regimen. There were 8 females and 11 males with a median age of 54 years (range: 41–63). Median lines of prior therapy was 2 (1–4), and 17(84%) had at least one prior autograft. 15 patients were transplanted with related donors and 4 unrelated. The median followed up of the cohort was 25.5 months (4–82). Fractionated peripheral blood (PB) and unfractionated bone marrow (BM) chimerism was performed on day 30, 60, 100 and 3–6 monthly thereafter using promega powerplex 16 genetic identity system. The samples were electrophoresed on an ABI 3130 XL capillary sequencer and analysed using Genemapper 4.0 software. Metaphase cytogenetics of unfractionated BM overnight cultures and Y-FISH for sex mismatch transplants was performed at various time points. Escalating doses of pDLI was given to patients with falling donor T cell chimerism (<50%) after Day 100. The starting dose of DLI was 1 × 105 CD3 cells/kg. 6 patients received pDLI with a median number of pDLI infusions of 2.5 (1–4). Overall survival (OS) and PFS was calculated from date of transplant using Kaplan-Meier cumulative survival plot using SPSS 14.0 software in pDLI receiving (Cohort I) and non-pDLI receiving cohort (Cohort II). Results: 17 patients (84%) responded with CR rate at 100 days of 57%. One patient had primary graft failure and 1 patient had stable disease for a year post transplant. Median OS and PFS for all patients was 24 months (17.6–30.3) and 12 months (7.7–16.2) respectively. TRM at 2 years was 15.5%. In Cohort I, 13 patients did not receive pDLI. 1 patients (7.6%) experienced limited chronic graft versus host disease (cGVHD) with no cases of acute GVHD. In Cohort II, escalated doses of pDLI were administered to 6 patients at declining levels of donor CD3 chimerism in PB without evidence of morphological or cytogenetic relapse. 2/6(33.3%) patients developed cGVHD post DLI. Full donor chimerism was achieved in 4/6 patients, all of whom are long-term survivors. Median OS in Cohort I is 24 months (8.9–41.0) and 17 months (11.3–22.6) in Cohort II (p=NS). Median PFS in Cohort I is 25 months vs 9 months in Cohort II (p= 0.02). Cytogenetics was not helpful in determining requirement for DLI even in sex-mismatched patients. The presence of GvHD did not have a significant impact on OS. Conclusion: pDLI administration guided by PB CD3 chimerism significantly improves PFS in Alemtuzumab conditioned RIC transplants for myeloma. Monitoring CD3 chimerism and early application of pDLI improves survival with a 5-year survival rate of 20% in multiply treated high risk patients.

Published
2007
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14. Progression Free Survival (PFS) in Alemtuzumab Based RIC Allogeneic Transplantation for Myeloma Is Improved with Use of Pre-Emptive DLI (pDLI).

Author

Ramasamy, Karthik, Mahmood, Shameem, Pearce, Laurence, Lim, ZiYi, Ladon, Dariusz, Pagliuca, Antonio, Devereux, Stephen, Mufti, Ghulam J., and Schey, Stephen

Abstract

Allogeneic transplantation is the only potentially curative treatment option for myeloma (MM). While reduced intensity conditioning (RIC) regimens are associated with lower transplant related morbidity and mortality (TRM), this approach is offset by an increase in relapse rates in myeloma.

Published
2007
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