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774 results on '"Oscier, D."'

156. Splenic marginal zone lymphoma proposals for a revision of diagnostic, staging and therapeutic criteria

Author

Matutes, E, primary, Oscier, D, additional, Montalban, C, additional, Berger, F, additional, Callet-Bauchu, E, additional, Dogan, A, additional, Felman, P, additional, Franco, V, additional, Iannitto, E, additional, Mollejo, M, additional, Papadaki, T, additional, Remstein, E D, additional, Salar, A, additional, Solé, F, additional, Stamatopoulos, K, additional, Thieblemont, C, additional, Traverse-Glehen, A, additional, Wotherspoon, A, additional, Coiffier, B, additional, and Piris, M A, additional

Published
2007
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158. CORRESPONDENCE

Author

Oscier, D., primary, Bramble, J., additional, Hodges, E., additional, and Wright, D., additional

Published
2002
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163. Telomere length in myelodysplastic syndromes

Author

Boultwood, J., primary, Fidler, C., additional, Kusec, R., additional, Rack, K., additional, Elliott, P.J. W., additional, Atoyebi, O., additional, Chapman, R., additional, Oscier, D. G., additional, and Wainscoat, J. S., additional

Published
1997
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164. 46 Recent developments in the prognostic classification for MDS: Results of The International Risk Analysis Workshop

Author

Greenberg, P., primary, Cox, C., additional, LeBeau, M., additional, Fenaux, P., additional, Morel, P., additional, Sanz, G., additional, Sanz, M., additional, Vallespi, T., additional, Hamblin, T., additional, Oscier, D., additional, Ohyashiki, K., additional, Toyama, K., additional, Aul, C., additional, Mufti, G., additional, and Bennett, J., additional

Published
1997
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165. 138 Mutant RAS or FMS confer abnormal growth in haematopoietic cells: Poor clinical outcome in myelodysplasia with RAS , FMS and p53 mutations

Author

Padua, R.A., primary, Darley, R., additional, McGlynn, H., additional, Al-Sabah, A., additional, Oscier, D., additional, West, R., additional, Guinn, B., additional, Smith, M., additional, Taylor, C., additional, Pettersson, T., additional, Ridge, S., additional, Carter, G., additional, White, D., additional, and Burnett, A., additional

Published
1997
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168. A randomized trial of hydroxyurea versus VP16 in adult chronic myelomonocytic leukemia. Groupe Francais des Myelodysplasies and European CMML Group

Author

Wattel, E, primary, Guerci, A, additional, Hecquet, B, additional, Economopoulos, T, additional, Copplestone, A, additional, Mahe, B, additional, Couteaux, ME, additional, Resegotti, L, additional, Voglova, V, additional, Foussard, C, additional, Pegourie, B, additional, Michaux, JL, additional, Deconinck, E, additional, Stoppa, AM, additional, Mufti, G, additional, Oscier, D, additional, and Fenaux, P, additional

Published
1996
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181. A randomized trial of hydroxyuea (HY) versus VP16 in advanced adult chronic myelomonocytic leukemia

Author

Wattel, E., primary, Guerci, A., additional, Hecquet, B., additional, Economopoulos, T., additional, Copplestone, A., additional, Resegotti, L., additional, Voglova, V., additional, Foussard, C., additional, Pegourié, B., additional, Michaux, J.L., additional, Deconinck, E., additional, Stoppa, A.M., additional, Mufti, G., additional, Oscier, D., additional, and Fenaux, P., additional

Published
1994
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184. t(8;9) IN CHRONIC MYELOID LEUKAEMIA

Author

Oscier, D. G., primary, Gardiner, Anne, additional, Dyer, Martin, additional, Bellomo, M. Jotterand, additional, Mühlematter, D., additional, Delacrétaz, F., additional, and Schmidt, P. M., additional

Published
1993
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187. Quantification of subclonal distributions of recurrent genomic aberrations in paired pre-treatment and relapse samples from patients with B-cell chronic lymphocytic leukemia.

Author

Knight, S J L, Yau, C, Clifford, R, Timbs, A T, Sadighi Akha, E, Dréau, H M, Burns, A, Ciria, C, Oscier, D G, Pettitt, A R, Dutton, S, Holmes, C C, Taylor, J, Cazier, J-B, and Schuh, A

Subjects
CHRONIC lymphocytic leukemia, CHROMOSOME abnormalities, GENOMICS, B cells, LYMPHOMAS, GENETICS, DISEASES
Abstract

Genome-wide array approaches and sequencing analyses are powerful tools for identifying genetic aberrations in cancers, including leukemias and lymphomas. However, the clinical and biological significance of such aberrations and their subclonal distribution are poorly understood. Here, we present the first genome-wide array based study of pre-treatment and relapse samples from patients with B-cell chronic lymphocytic leukemia (B-CLL) that uses the computational statistical tool OncoSNP. We show that quantification of the proportion of copy number alterations (CNAs) and copy neutral loss of heterozygosity regions (cnLOHs) in each sample is feasible. Furthermore, we (i) reveal complex changes in the subclonal architecture of paired samples at relapse compared with pre-treatment, (ii) provide evidence supporting an association between increased genomic complexity and poor clinical outcome (iii) report previously undefined, recurrent CNA/cnLOH regions that expand or newly occur at relapse and therefore might harbor candidate driver genes of relapse and/or chemotherapy resistance. Our findings are likely to impact on future therapeutic strategies aimed towards selecting effective and individually tailored targeted therapies. [ABSTRACT FROM AUTHOR]

Published
2012
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188. Antigen receptor stereotypy across B-cell lymphoproliferations: the case of IGHV4-59/IGKV3-20 receptors with rheumatoid factor activity.

Author

Kostareli, E, Gounari, M, Janus, A, Murray, F, Brochet, X, Giudicelli, V, Pospisilova, S, Oscier, D, Foroni, L, di Celle, P F, Tichy, B, Pedersen, L B, Jurlander, J, Ponzoni, M, Kouvatsi, A, Anagnostopoulos, A, Thompson, K, Darzentas, N, Lefranc, M-P, and Belessi, C

Subjects
LETTERS to the editor, B cells
Abstract

A letter to the editor commenting on a study related to antigen receptor stereotypy across B-cell lymphoproliferations is presented.

Published
2012
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189. Extreme telomere erosion in ATM-mutated and 11q-deleted CLL patients is independent of disease stage.

Author

Britt-Compton, B, Lin, T T, Ahmed, G, Weston, V, Jones, R E, Fegan, C, Oscier, D G, Stankovic, T, Pepper, C, and Baird, D M

Subjects
LETTERS to the editor, DISEASE progression, CHRONIC lymphocytic leukemia, PATIENTS
Abstract

A letter to the editor is presented which discusses the disease stage independency of chronic lymphocytic leukemia (CLL) patients that showed telomere erosion and loss of heterozygosity that were concomitant with its dysfunction.

Published
2012
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190. 13q deletion anatomy and disease progression in patients with chronic lymphocytic leukemia.

Author

Parker, H., Rose-Zerilli, M. J. J., Parker, A., Chaplin, T., Wade, R., Gardiner, A., Griffiths, M., Collins, A., Young, B. D., Oscier, D. G., and Strefford, J. C.

Subjects
CHRONIC lymphocytic leukemia, LYMPHOPROLIFERATIVE disorders, CANCER patients, DISEASE progression, GENETICS, CHROMOSOME abnormalities, CHROMOSOMES, COMPARATIVE studies, GENES, GENETIC polymorphisms, RESEARCH methodology, MEDICAL cooperation, GENETIC mutation, PROGNOSIS, RESEARCH, RESEARCH funding, EVALUATION research, GENOTYPES
Abstract

Historically, genes targeted by recurrent chromosomal deletions have been identified within the smallest genomic region shared in all patients, the minimally deleted region (MDR). However, deletions this small do not occur in all patients and are a simplification of the impact larger heterogeneous deletions have during carcinogenesis. We use the example of 13q14 deletions in chronic lymphocytic leukemia to show that genes outside MDRs are associated with disease progression. Genomic profiling of 224 patients identified 205 copy number alterations on chromosome 13 in 132 cases. Deletions including DLEU2 were heterogeneous (845 Kb-96.2 Mb) and identified two breakpoint cluster regions within short interspersed nuclear elements proximal to DLEU2 and within long interspersed nuclear elements/L1 repeats distal to GUCY1B2. After defining a deletion class on the basis of size and location, we show that (a) at diagnosis, larger deletions (class II) were associated with a significantly increased risk of disease progression (odds ratio=12.3; P=0.005), (b) in progressive patients, class II deletions were enriched (P=0.02) and (c) this association was independent of IgVH mutational status, ZAP70 expression and ATM/TP53 deletion. Deletion of a 1 Mb gene cluster (48.2-49.2 Mb), including SETDB2, PHF11 and RCBTB1, was significantly associated (P<0.01) with disease progression. Here, we show that the deletion of genes outside MDRs can influence clinical outcome. [ABSTRACT FROM AUTHOR]

Published
2011
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191. Variant IRF4/MUM1 associates with CD38 status and treatment-free survival in chronic lymphocytic leukaemia.

Author

Allan, J. M., Sunter, N. J., Bailey, J. R., Pettitt, A. R., Harris, R. J., Pepper, C., Fegan, C., Hall, A. G., Deignan, L., Bacon, C. M., Pointon, J. C., Houlston, R. S., Broderick, P., Mainou-Fowler, T., Jackson, G. H., Summerfield, G., Evans, P. A., Strefford, J. C., Parker, A., and Oscier, D.

Subjects
LETTERS to the editor, CHRONIC lymphocytic leukemia
Abstract

A letter to the editor is presented related to the treatment of chronic lymphocytic leukemia (CLL).

Published
2010
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195. Cytogenetic Findings and Survival in B-cell Chronic Lymphocytic Leukemia. Second IWCCLL Compilation of Data on 662 Patients

Author

Juliusson, Gunnar, primary, Oscier, David, additional, Juliusson, G., additional, Gahrton, G., additional, Oscier, D., additional, Fitchett, M., additional, Ross, F., additional, Brito-Babapulle, V., additional, Catovsky, D., additional, Knuutila, S., additional, Elonen, E., additional, Lechleitner, M., additional, Tanzer, J., additional, Schoenwald, M., additional, Castoldi, G. L., additional, Cuneo, A., additional, Nowell, P., additional, Peterson, L., additional, and Kay, N., additional

Published
1991
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196. A novel functional assay using etoposide plus nutlin-3a detects and distinguishes between ATM and TP53 mutations in CLL.

Author

Best, O G, Gardiner, A C, Majid, A, Walewska, R, Austen, B, Skowronska, A, Ibbotson, R, Stankovic, T, Dyer, M J S, and Oscier, D G

Subjects
LYMPHOCYTIC leukemia, HUMAN chromosome abnormality diagnosis, GENETIC mutation, P53 protein, DNA damage, DIAGNOSIS
Abstract

This article discusses the etopocide/nutlin-3a functional assay, which is designed to detect the loss or mutation of TP53 protein and ATM genes because of chromosomal abnormalities. A test of TP53 loss can assist in the development of treatments for chronic lymphocytic leukaemia (CLL). While standard fluorescence in situ hybridization, another test for TP53 and ATM loss, can only detect missing genes, this assay can detect mutations.

Published
2008
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197. Splenic marginal zone lymphoma proposals for a revision of diagnostic, staging and therapeutic criteria.

Author

Matutes, E., Oscier, D., Montalban, C., Berger, F., Callet-Bauchu, E., Dogan, A., Felman, P., Franco, V., Iannitto, E., Mollejo, M., Papadaki, T., Remstein, E. D., Salar, A., Solé, F., Stamatopoulos, K., Thieblemont, C., Traverse-Glehen, A., Wotherspoon, A., Coiffier, B., and Piris, M. A.

Subjects
*SPLEEN cancer, *CANCER diagnosis, *CARCINOGENESIS, *CANCER treatment, *MEDICAL literature
Abstract

Since the initial description of splenic marginal zone lymphoma (SMZL) in 1992, an increasing number of publications have dealt with multiple aspects of SMZL diagnosis, molecular pathogenesis and treatment. This process has identified multiple inconsistencies in the diagnostic criteria and lack of clear guidelines for the staging and treatment. The authors of this review have held several meetings and exchanged series of cases with the objective of agreeing on the main diagnostic, staging and therapeutic guidelines for patients with this condition. Specific working groups were created for diagnostic criteria, immunophenotype, staging and treatment. As results of this work, guidelines are proposed for diagnosis, differential diagnosis, staging, prognostic factors, treatment and response criteria. The guidelines proposed here are intended to contribute to the standardization of the diagnosis and treatment of these patients, and should facilitate the future development of clinical trials that could define more precisely predictive markers for histological progression or lack of response, and evaluate new drugs or treatments.Leukemia (2008) 22, 487–495; doi:10.1038/sj.leu.2405068; published online 20 December 2007 [ABSTRACT FROM AUTHOR]

Published
2008
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199. Alemtuzumab in combination with high-dose methylprednisolone is a logical, feasible and highly active therapeutic regimen in chronic lymphocytic leukaemia patients with p53 defects.

Author

Pettitt, A. R., Matutes, E., and Oscier, D.

Subjects
LETTERS to the editor, LEUKEMIA, THERAPEUTICS
Abstract

A letter to the editor is presented in response to an article about the feasibility and efficacy of alemtuzumab combined with methylprednisolone as a therapeutic regimen in chronic lymphocytic leukemia patients with p53 defects.

Published
2006
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200. IgVH genes mutation and usage, ZAP-70 and CD38 expression provide new insights on B-cell prolymphocytic leukemia (B-PLL).

Author

Del Giudice, I, Davis, Z, Matutes, E, Osuji, N, Parry-Jones, N, Morilla, A, Brito-Babapulle, V, Oscier, D, and Catovsky, D

Subjects
LEUKEMIA diagnosis, CANCER diagnosis, IMMUNOGLOBULIN genes, LYMPHOCYTIC leukemia, CELLS
Abstract

B-prolymphocytic leukemia (B-PLL) is a rare disease with poor prognosis. To further characterize the biological features of this disease, we analyzed immunoglobulin heavy chain (IgVH) mutations, ZAP-70 and CD38 in 19 cases with de novo B-PLL. Immunoglobulin heavy chain genes analysis showed an unmutated pattern (>98% homology to germ line) in 9/17 cases (53%), with 100% homology in eight. In the remaining, it ranged from 90 to 97.4%, with three cases slightly mutated (98–95%) and five heavily mutated (<95%). All B-PLL utilized members of VH3 (11/17) and VH4 (6/17) families, with V3-23, V4-59 and V4-34 gene accounting for more than half of them, regardless of mutational status. ZAP-70, assessed by flow cytometry, ranged from 1 to 91% cells, being 20% in 57% of cases. CD38 ranged from 1 to 99% (median 21%). There was no correlation between IgVH status and ZAP-70 or CD38 expression, but male gender and del(17p) were more common in the unmutated group. Neither IgVH mutations, CD38 expression nor del(17p) influenced patients’ outcome. Unexpectedly, ZAP-70+ B-PLL patients survived longer (40 months) than ZAP-70− B-PLL (8 months). B-PLL appears biologically heterogeneous regarding IgVH mutations, ZAP-70 and CD38 expression, showing a pattern distinct from that of other lymphoproliferative disorders.Leukemia (2006) 20, 1231–1237. doi:10.1038/sj.leu.2404238; published online 27 April 2006 [ABSTRACT FROM AUTHOR]

Published
2006
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