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330 results on '"Greaves, M. P."'

35. Single-cell analysis identifies CRLF2rearrangements as both early and late events in Down syndrome and non-Down syndrome acute lymphoblastic leukaemia

Author

Potter, N., Jones, L., Blair, H., Strehl, S., Harrison, C. J., Greaves, M., Kearney, L., and Russell, L. J.

Abstract

Deregulated expression of the type I cytokine receptor, CRLF2, is observed in 5–15% of precursor B-cell acute lymphoblastic leukaemia (B-ALL). We have previously reported the genomic landscape of patients with CRLF2rearrangements (CRLF2-r) using both whole genome and exome sequencing, which identified a number of potential clonal and sub-clonal genomic alterations. In this study, we aimed to assess when the CRLF2-r; IGH-CRLF2or P2RY8-CRLF2, arose during the evolution of both Down syndrome-ALL (DS-ALL) and non-DS-ALL. Using fluorescence in situ hybridisation, we were able to track up to four structural variants in single cells from 47 CRLF2-r B-ALL patients, which in association with our multiplex single-cell analysis of a further four patients, permitted simultaneous tracking of copy number alterations, structural and single nucleotide variants within individual cells. We observed CRLF2-r arising as both early and late events in DS and non-DS-ALL patients. Parallel evolution of discrete clones was observed in the development of CRLF2-r B-ALL, either involving the CRLF2-r or one of the other tracked abnormalities. In-depth single-cell analysis identified both linear and branching evolution with early clones harbouring a multitude of abnormalities, including the CRLF2-r in DS-ALL patients.

Published
2019
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41. Towards the biocontrol of bindweeds with a mycoherbicide

Author

Défago, G., Ammon, H. U., Cagán, L., Draeger, B., Greaves, M. P., Guntli, D., Hoeke, D., Klimes, L., Lawrie, J., Moënne-Loccoz, Y., Nicolet, B., Pfirter, H. A., Tabacchi, Raphael, Tóth, P., Défago, G., Ammon, H. U., Cagán, L., Draeger, B., Greaves, M. P., Guntli, D., Hoeke, D., Klimes, L., Lawrie, J., Moënne-Loccoz, Y., Nicolet, B., Pfirter, H. A., Tabacchi, Raphael, and Tóth, P.

Abstract

Within the framework of the European COST Action 816, afive-year collaboration between scientists from five Europeancountries has made an important contribution to biologicalcontrol of field and hedge bindweeds (Convolvulus arvensis and Calystegia sepium, respectively). A fungus Stagonosporaconvolvuli strain LA39, able to infect both field and hedgebindweed, was found in the UK and its biocontrol efficacyimproved by optimising mass production, formulation and storagetechniques. This fungus controlled bindweeds in both a cemeteryand in maize crops. Its use fits best in an integrated pestmanagement system where a green cover controls most of the weedsexcept the bindweeds. DNA marker analyses indicate that thefungus reproduces sexually, which could be used to furtherimprove this mycoherbicide. In addition, the insect Melanagromyzaalbocilia, which itself exhibits biocontrol potential againstbindweeds, may be used in combination with LA39 to improve theability of the fungus to penetrate the stem of bindweeds.Overall, the results suggest that S. convolvuli LA39 haspromising potential as a bioherbicide for control of field andhedge bindweed.

Published
2010

43. A genome-wide association study identifies risk loci for childhood acute lymphoblastic leukemia at 10q26.13 and 12q23.1

Author

Vijayakrishnan, J, Kumar, R, Henrion, M Y R, Moorman, A V, Rachakonda, P S, Hosen, I, da Silva Filho, M I, Holroyd, A, Dobbins, S E, Koehler, R, Thomsen, H, Irving, J A, Allan, J M, Lightfoot, T, Roman, E, Kinsey, S E, Sheridan, E, Thompson, P D, Hoffmann, P, Nöthen, M M, Heilmann-Heimbach, S, Jöckel, K H, Greaves, M, Harrison, C J, Bartram, C R, Schrappe, M, Stanulla, M, Hemminki, K, and Houlston, R S

Abstract

Genome-wide association studies (GWASs) have shown that common genetic variation contributes to the heritable risk of childhood acute lymphoblastic leukemia (ALL). To identify new susceptibility loci for the largest subtype of ALL, B-cell precursor ALL (BCP-ALL), we conducted a meta-analysis of two GWASs with imputation using 1000 Genomes and UK10K Project data as reference (totaling 1658 cases and 7224 controls). After genotyping an additional 2525 cases and 3575 controls, we identify new susceptibility loci for BCP-ALL mapping to 10q26.13 (rs35837782, LHPP, P=1.38 × 10−11) and 12q23.1 (rs4762284, ELK3, P=8.41 × 10−9). We also provide confirmatory evidence for the existence of independent risk loci at 9p21.3, but show that the association marked by rs77728904 can be accounted for by linkage disequilibrium with the rare high-impact CDKN2A p.Ala148Thr variant rs3731249. Our data provide further insights into genetic susceptibility to ALL and its biology.

Published
2017
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