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523 results on '"Dyer, Martin J. S."'

2. Pooled analysis of safety data from clinical trials evaluating acalabrutinib monotherapy in mature B-cell malignancies

Author

Furman, Richard R., Byrd, John C., Owen, Roger G., O’Brien, Susan M., Brown, Jennifer R., Hillmen, Peter, Stephens, Deborah M., Chernyukhin, Nataliya, Lezhava, Tamara, Hamdy, Ahmed M., Izumi, Raquel, Patel, Priti, Baek, Marshall, Christian, Beth, Dyer, Martin J. S., Streetly, Matthew J., Sun, Clare, Rule, Simon, Wang, Michael, Ghia, Paolo, Jurczak, Wojciech, Pagel, John M., and Sharman, Jeff P.

Published
2021
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4. Phase 1b study of tirabrutinib in combination with idelalisib or entospletinib in previously treated B-cell lymphoma

Author

Morschhauser, Franck, Dyer, Martin J. S., Walter, Harriet S., Danilov, Alexey V., Ysebaert, Loic, Hodson, Daniel James, Fegan, Christopher, Rule, Simon A., Radford, John, Cartron, Guillaume, Bouabdallah, Krimo, Davies, Andrew John, Spurgeon, Stephen, Rajakumaraswamy, Nishanthan, Li, Biao, Humeniuk, Rita, Huang, Xi, Bhargava, Pankaj, Jürgensmeier, Juliane M., and Salles, Gilles

Published
2021
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5. Mantle cell lymphomas with concomitant MYC and CCND1 breakpoints are recurrently TdT positive and frequently show high-grade pathological and genetic features

Author

Aukema, Sietse M., Croci, Giorgio A., Bens, Susanne, Oehl-Huber, Kathrin, Wagener, Rabea, Ott, German, Rosenwald, Andreas, Kluin, Philip M., van den Berg, Eva, Bosga-Bouwer, Anneke G., Hoogendoorn, Mels, Hoster, Eva, Bittmann, Iris, Nagel, Inga, Murga Penas, Eva M., Kreuz, Markus, Bausinger, Julia, Belder, Wilfried, Oschlies, Ilske, Dyer, Martin J. S., Jayne, Sandrine, Siebert, Reiner, and Klapper, Wolfram

Published
2021
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8. Genome-wide association study identifies risk loci for progressive chronic lymphocytic leukemia

Author

Lin, Wei-Yu, Fordham, Sarah E., Sunter, Nicola, Elstob, Claire, Rahman, Thahira, Willmore, Elaine, Shepherd, Colin, Strathdee, Gordon, Mainou-Fowler, Tryfonia, Piddock, Rachel, Mearns, Hannah, Barrow, Timothy, Houlston, Richard S., Marr, Helen, Wallis, Jonathan, Summerfield, Geoffrey, Marshall, Scott, Pettitt, Andrew, Pepper, Christopher, Fegan, Christopher, Forconi, Francesco, Dyer, Martin J. S., Jayne, Sandrine, Sellors, April, Schuh, Anna, Robbe, Pauline, Oscier, David, Bailey, James, Rais, Syed, Bentley, Alison, Cawkwell, Lynn, Evans, Paul, Hillmen, Peter, Pratt, Guy, Allsup, David J., and Allan, James M.

Published
2021
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9. Genetic correlation between multiple myeloma and chronic lymphocytic leukaemia provides evidence for shared aetiology

Author

Went, Molly, Sud, Amit, Speedy, Helen, Sunter, Nicola J., Försti, Asta, Law, Philip J., Johnson, David C., Mirabella, Fabio, Holroyd, Amy, Li, Ni, Orlando, Giulia, Weinhold, Niels, van Duin, Mark, Chen, Bowang, Mitchell, Jonathan S., Mansouri, Larry, Juliusson, Gunnar, Smedby, Karin E, Jayne, Sandrine, Majid, Aneela, Dearden, Claire, Allsup, David J., Bailey, James R., Pratt, Guy, Pepper, Chris, Fegan, Chris, Rosenquist, Richard, Kuiper, Rowan, Stephens, Owen W., Bertsch, Uta, Broderick, Peter, Einsele, Hermann, Gregory, Walter M., Hillengass, Jens, Hoffmann, Per, Jackson, Graham H., Jöckel, Karl-Heinz, Nickel, Jolanta, Nöthen, Markus M., da Silva Filho, Miguel Inacio, Thomsen, Hauke, Walker, Brian A., Broyl, Annemiek, Davies, Faith E., Hansson, Markus, Goldschmidt, Hartmut, Dyer, Martin J. S., Kaiser, Martin, Sonneveld, Pieter, Morgan, Gareth J., Hemminki, Kari, Nilsson, Björn, Catovsky, Daniel, Allan, James M., and Houlston, Richard S.

Published
2019
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12. Venetoclax retreatment of patients with chronic lymphocytic leukemia after a previous venetoclax-based regimen

Author

Thompson, Meghan C., primary, Harrup, Rosemary A., additional, Coombs, Catherine C., additional, Roeker, Lindsey E., additional, Pu, Jeffrey J., additional, Choi, Michael Y., additional, Barr, Paul M., additional, Allan, John N., additional, Šimkovič, Martin, additional, Leslie, Lori, additional, Rhodes, Joanna, additional, Chong, Elise A., additional, Kamdar, Manali, additional, Skarbnik, Alan, additional, Lansigan, Frederick, additional, McCall, Brittany, additional, Saja, Khalid, additional, Dyer, Martin J. S., additional, Walter, Harriet S., additional, Lefebure, Marcus, additional, Thadani-Mulero, Maria, additional, Boyer, Michelle, additional, Biondo, Juliana, additional, Sail, Kavita, additional, Manzoor, Beenish S., additional, Furman, Richard, additional, Bantilan, Kurt S., additional, Goy, Andre, additional, Feldman, Tatyana, additional, Labella, Dominic, additional, Schuster, Stephen J., additional, Park, Jae, additional, Palomba, Lia, additional, Zelenetz, Andrew, additional, Eyre, Toby A., additional, Kater, Arnon P., additional, Seymour, John F., additional, and Mato, Anthony R., additional

Published
2022
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14. Computational modeling of DLBCL predicts response to BH3-mimetics.

Author

Cloete, Ielyaas, Smith, Victoria M., Jackson, Ross A., Pepper, Andrea, Pepper, Chris, Vogler, Meike, Dyer, Martin J. S., and Mitchell, Simon

Subjects
B cells, B cell lymphoma, DIFFUSE large B-cell lymphomas, SYSTEMS biology, COMPUTATIONAL biology, PROTEIN-protein interactions, PROTEIN expression
Abstract

In healthy cells, pro- and anti-apoptotic BCL2 family and BH3-only proteins are expressed in a delicate equilibrium. In contrast, this homeostasis is frequently perturbed in cancer cells due to the overexpression of anti-apoptotic BCL2 family proteins. Variability in the expression and sequestration of these proteins in Diffuse Large B cell Lymphoma (DLBCL) likely contributes to variability in response to BH3-mimetics. Successful deployment of BH3-mimetics in DLBCL requires reliable predictions of which lymphoma cells will respond. Here we show that a computational systems biology approach enables accurate prediction of the sensitivity of DLBCL cells to BH3-mimetics. We found that fractional killing of DLBCL, can be explained by cell-to-cell variability in the molecular abundances of signaling proteins. Importantly, by combining protein interaction data with a knowledge of genetic lesions in DLBCL cells, our in silico models accurately predict in vitro response to BH3-mimetics. Furthermore, through virtual DLBCL cells we predict synergistic combinations of BH3-mimetics, which we then experimentally validated. These results show that computational systems biology models of apoptotic signaling, when constrained by experimental data, can facilitate the rational assignment of efficacious targeted inhibitors in B cell malignancies, paving the way for development of more personalized approaches to treatment. [ABSTRACT FROM AUTHOR]

Published
2023
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17. Limitations of Monitoring Disease Progression Using Circulating Tumor DNA in Lymphoma: An Example From Primary Cutaneous DLBCL Leg-type

Author

Trethewey, Christopher S., primary, Walter, Harriet S., additional, Alqahtani, Abdullah N. M., additional, Schmid, Ralf, additional, Guttery, David S., additional, Griffin, Yvette, additional, Ahearne, Matthew J., additional, Saldanha, Gerald S., additional, Jayne, Sandrine P. N., additional, and Dyer, Martin J. S., additional

Published
2022
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20. Ofatumumab retreatment and maintenance in fludarabine-refractory chronic lymphocytic leukaemia patients

Author

Österborg, Anders, Wierda, William G., Mayer, Jiří, Hess, Georg, Hillmen, Peter, Schetelig, Johannes, Schuh, Anna, Smolej, Lukáš, Beck, Christian, Dreyfus, Brigitte, Hellman, Andrzej, Kozlowski, Piotr, Pfreundschuh, Michael, Rizzi, Rita, Spacek, Martin, Phillips, Jennifer L., Gupta, Ira V., Williams, Vanessa, Jewell, Roxanne C., Nebot, Noelia, Lisby, Steen, and Dyer, Martin J. S.

Published
2015
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23. Phase IA/II, multicentre, open-label study of the CD40 antagonistic monoclonal antibody lucatumumab in adult patients with advanced non-Hodgkin or Hodgkin lymphoma

Author

Fanale, Michelle, Assouline, Sarit, Kuruvilla, John, Solal-Céligny, Philippe, Heo, Dae S., Verhoef, Gregor, Corradini, Paolo, Abramson, Jeremy S., Offner, Fritz, Engert, Andreas, Dyer, Martin J. S., Carreon, Daniel, Ewald, Brett, Baeck, Johan, Younes, Anas, and Freedman, Arnold S.

Published
2014
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24. Reconstruction of rearranged T-cell receptor loci by whole genome and transcriptome sequencing gives insights into the initial steps of T-cell prolymphocytic leukemia

Author

Patil, Paurnima, Cieslak, Agata, Bernhart, Stephan H., Toprak, Umut H., Wagener, Rabea, Lopez, Cristina, Wiehle, Laura, Bens, Susanne, Altmueller, Janine, Franitza, Marek, Scholz, Ingrid, Jayne, Sandrine, Ahearne, Matthew J., Scheffold, Annika, Jebaraj, Billy M. C., Schneider, Christof, Costa, Dolors, Braun, Till, Schrader, Alexandra, Campo, Elias, Dyer, Martin J. S., Nuernberg, Peter, Duerig, Jan, Johansson, Patricia, Boettcher, Sebastian, Schlesner, Matthias, Herling, Marco, Stilgenbauer, Stephan, Macintyre, Elizabeth, Siebert, Reiner, Patil, Paurnima, Cieslak, Agata, Bernhart, Stephan H., Toprak, Umut H., Wagener, Rabea, Lopez, Cristina, Wiehle, Laura, Bens, Susanne, Altmueller, Janine, Franitza, Marek, Scholz, Ingrid, Jayne, Sandrine, Ahearne, Matthew J., Scheffold, Annika, Jebaraj, Billy M. C., Schneider, Christof, Costa, Dolors, Braun, Till, Schrader, Alexandra, Campo, Elias, Dyer, Martin J. S., Nuernberg, Peter, Duerig, Jan, Johansson, Patricia, Boettcher, Sebastian, Schlesner, Matthias, Herling, Marco, Stilgenbauer, Stephan, Macintyre, Elizabeth, and Siebert, Reiner

Abstract

T-cell prolymphocytic leukemia (T-PLL) is an aggressive tumor with leukemic presentation of mature T-lymphocytes. Here, we aimed at characterizing the initial events in the molecular pathogenesis of T-PLL and particularly, at determining the point in T-cell differentiation when the hallmark oncogenic events, that is, inv(14)(q11q32)/t(14;14)(q11;q32) and t(X;14)(q28;q11) occur. To this end, we mined whole genome and transcriptome sequencing data of 17 and 11 T-PLL cases, respectively. Mapping of the 14q32.1 locus breakpoints identified only TCL1A, which was moreover significantly overexpressed in T-PLL as compared to benign CD4+ and CD8+ T-cells, as the only common oncogenic target of aberrations. In cases with t(14;14), the breakpoints mapped telomeric and in cases with inv(14) centromeric or in the 3 '-untranslated region of TCL1A. Regarding the T-cell receptor alpha (TRA) locus-TCL1A breakpoint junctions, all 17 breakpoints involved recombination signal sequences and 15 junctions contained nontemplated (N-) nucleotides. All T-PLL cases studied carried in-frame TRA rearrangements on the intact allele, which skewed significantly toward usage of distal/central TRAV/TRAJ gene segments as compared to the illegitimate TRA rearrangements. Our findings suggest that the oncogenic TRA-TCL1A/MTCP1 rearrangements in T-PLL occur during opening of the TRA locus, that is, during the progression from CD4+ immature single positive to early double positive thymocyte stage, just before physiologic TCL1A expression is silenced. The cell carrying such an oncogenic event continues maturation and rearranges the second TRA allele to achieve a functional T-cell receptor. Thereafter, it switches off RAG and DNTT expression in line with the mature T-cell phenotype at presentation of T-PLL.

Published
2020

38. Phase 1b study of tirabrutinib in combination with idelalisib or entospletinib in previously treated B-cell lymphoma

Author

Morschhauser, Franck, primary, Dyer, Martin J. S., additional, Walter, Harriet S., additional, Danilov, Alexey V., additional, Ysebaert, Loic, additional, Hodson, Daniel James, additional, Fegan, Christopher, additional, Rule, Simon A., additional, Radford, John, additional, Cartron, Guillaume, additional, Bouabdallah, Krimo, additional, Davies, Andrew John, additional, Spurgeon, Stephen, additional, Rajakumaraswamy, Nishanthan, additional, Li, Biao, additional, Humeniuk, Rita, additional, Huang, Xi, additional, Bhargava, Pankaj, additional, Jürgensmeier, Juliane M., additional, and Salles, Gilles, additional

Published
2020
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39. Dual dependence on BCL2 and MCL1 in T-cell prolymphocytic leukemia

Author

Smith, Victoria M., primary, Lomas, Oliver, additional, Constantine, Donna, additional, Palmer, Lianne, additional, Schuh, Anna H., additional, Bruce, David, additional, Gonchar, Oksana, additional, Macip, Salvador, additional, Jayne, Sandrine, additional, Dyer, Martin J. S., additional, and Eyre, Toby A., additional

Published
2020
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42. GeneChip analyses point to novel pathogenetic mechanisms in mantle cell lymphoma

Author

Vater, Inga, Wagner, Florian, Kreuz, Markus, Berger, Hilmar, Martín-Subero, José I., Pott, Christiane, Martinez-Climent, Jose A., Klapper, Wolfram, Krause, Kristina, Dyer, Martin J. S., Gesk, Stefan, Harder, Lana, Zamo, Alberto, Dreyling, Martin, Hasenclever, Dirk, Arnold, Norbert, and Siebert, Reiner

Published
2009

49. Genetic correlation between multiple myeloma and chronic lymphocytic leukaemia provides evidence for shared aetiology

Author

Went, Molly, Sud, Amit, Speedy, Helen, Sunter, Nicola J., Försti, Asta, Law, Philip J., Johnson, David C., Mirabella, Fabio, Holroyd, Amy, Li, Ni, Orlando, Giulia, Weinhold, Niels, van Duin, Mark, Chen, Bowang, Mitchell, Jonathan S., Mansouri, Larry, Juliusson, Gunnar, Smedby, Karin E, Jayne, Sandrine, Majid, Aneela, Dearden, Claire, Allsup, David J., Bailey, James R., Pratt, Guy, Pepper, Chris, Fegan, Chris, Rosenquist, Richard, Kuiper, Rowan, Stephens, Owen W., Bertsch, Uta, Broderick, Peter, Einsele, Hermann, Gregory, Walter M., Hillengass, Jens, Hoffmann, Per, Jackson, Graham H., Jöckel, Karl-Heinz, Nickel, Jolanta, Nöthen, Markus M., da Silva Filho, Miguel Inacio, Thomsen, Hauke, Walker, Brian A., Broyl, Annemiek, Davies, Faith E., Hansson, Markus, Goldschmidt, Hartmut, Dyer, Martin J. S., Kaiser, Martin, Sonneveld, Pieter, Morgan, Gareth J., Hemminki, Kari, Nilsson, Björn, Catovsky, Daniel, Allan, James M., Houlston, Richard S., and Hematology

Subjects
Cancer och onkologi, Genetic Linkage, Quantitative Trait Loci, Medizin, Hematology, lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens, lcsh:RC254-282, Leukemia, Lymphocytic, Chronic, B-Cell, Polymorphism, Single Nucleotide, Article, Linkage Disequilibrium, Organ Specificity, Cancer and Oncology, hemic and lymphatic diseases, Case-Control Studies, Databases, Genetic, Humans, Genetic Predisposition to Disease, Hematologi, Multiple Myeloma, Alleles, Genetic Association Studies, Genome-Wide Association Study
Abstract

The clustering of different types of B-cell malignancies in families raises the possibility of shared aetiology. To examine this, we performed cross-trait linkage disequilibrium (LD)-score regression of multiple myeloma (MM) and chronic lymphocytic leukaemia (CLL) genome-wide association study (GWAS) data sets, totalling 11,734 cases and 29,468 controls. A significant genetic correlation between these two B-cell malignancies was shown (R g = 0.4, P = 0.0046). Furthermore, four of the 45 known CLL risk loci were shown to associate with MM risk and five of the 23 known MM risk loci associate with CLL risk. By integrating eQTL, Hi-C and ChIP-seq data, we show that these pleiotropic risk loci are enriched for B-cell regulatory elements and implicate B-cell developmental genes. These data identify shared biological pathways influencing the development of CLL and, MM and further our understanding of the aetiological basis of these B-cell malignancies.

Published
2018

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