18 results on '"Mugneret, F"'
Search Results
2. Genome profiling of acute myelomonocytic leukemia: alteration of the MYB locus in MYST3-linked cases.
- Author
-
Murati, A, Gervais, C, Carbuccia, N, Finetti, P, Cervera, N, Adélaïde, J, Struski, S, Lippert, E, Mugneret, F, Tigaud, I, Penther, D, Bastard, C, Poppe, B, Speleman, F, Baranger, L, Luquet, I, Cornillet-Lefebvre, P, Nadal, N, Nguyen-Khac, F, and Pérot, C
- Subjects
ACUTE myeloid leukemia ,GENOMICS ,DNA microarrays ,ACUTE leukemia ,GENE expression - Abstract
The t(8;16)(p11;p13) is a rare translocation involved in de novo and therapy-related myelomonocytic and monocytic acute leukemia. It fuses two genes encoding histone acetyltransferases (HATs), MYST3 located at 8p11 to CREBBP located at 16p13. Variant translocations involve other HAT-encoding genes such as EP300, MYST4, NCOA2 or NCOA3. MYST3-linked acute myeloid leukemias (AMLs) share specific clinical and biological features and a poor prognosis. Because of its rarity, the molecular biology of MYST3-linked AMLs remains poorly understood. We have established the genome and gene expression profiles of a multicentric series of 61 M4/M5 AMLs including 18 MYST3-linked AMLs by using array comparative genome hybridization (aCGH) (n=52) and DNA microarrays (n=44), respectively. We show that M4/5 AMLs have a variety of rare genomic alterations. One alteration, a gain of the MYB locus, was found recurrently and only in the MYST3-linked AMLs (7/18 vs 0/34). MYST3-AMLs have also a specific a gene expression profile, which includes overexpression of MYB, CD4 and HOXA genes. These features, reminiscent of T-cell acute lymphoid leukemia (ALL), suggest the targeting of a common T-myeloid progenitor.Leukemia (2009) 23, 85–94; doi:10.1038/leu.2008.257; published online 25 September 2008 [ABSTRACT FROM AUTHOR]
- Published
- 2009
- Full Text
- View/download PDF
3. Heterogeneous patterns of amplification of the NUP214-ABL1 fusion gene in T-cell acute lymphoblastic leukemia.
- Author
-
Graux, C, Stevens-Kroef, M, Lafage, M, Dastugue, N, Harrison, C J, Mugneret, F, Bahloula, K, Struski, S, Grégoire, M J, Nadal, N, Lippert, E, Taviaux, S, Simons, A, Kuiper, R P, Moorman, A V, Barber, K, Bosly, A, Michaux, L, Vandenberghe, P, and Lahortiga, I
- Subjects
LYMPHOBLASTIC leukemia ,GENES ,EPISOMES ,T cells ,FLUORESCENCE in situ hybridization - Abstract
Episomes with the NUP214-ABL1 fusion gene have been observed in 6% of T-ALL. In this multicentric study we collected 27 cases of NUP214-ABL1-positive T-ALL. Median age was 15 years with male predominance. Outcome was poor in 12 patients. An associated abnormality involving TLX1 or TLX3 was found in all investigated cases. Fluorescent in situ hybridization revealed a heterogeneous pattern of NUP214-ABL1 amplification. Multiple episomes carrying the fusion were detected in 24 patients. Episomes were observed in a significant number of nuclei in 18 cases, but in only 1–5% of nuclei in 6. In addition, intrachromosomal amplification (small hsr) was identified either as the only change or in association with episomes in four cases and two T-ALL cell lines (PEER and ALL-SIL). One case showed insertion of apparently non-amplified NUP214-ABL1 sequences at 14q12. The amplified sequences were analyzed using array-based CGH.These findings confirm that the NUP214-ABL1 gene requires amplification for oncogenicity; it is part of a multistep process of leukemogenesis; and it can be a late event present only in subpopulations. Data also provide in vivo evidence for a model of episome formation, amplification and optional reintegration into the genome. Implications for the use of kinase inhibitors are discussed.Leukemia (2009) 23, 125–133; doi:10.1038/leu.2008.278; published online 16 October 2008 [ABSTRACT FROM AUTHOR]
- Published
- 2009
- Full Text
- View/download PDF
4. The most frequent t(14;19)(q32;q13)-positive B-cell malignancy corresponds to an aggressive subgroup of atypical chronic lymphocytic leukemia.
- Author
-
Chapiro, E., Radford-Weiss, I., Bastard, C., Luquet, I., Lefebvre, C., Callet-Bauchu, E., Leroux, D., Talmant, P., Mozziconacci, M.-J., Mugneret, F., Struski, S., Raynaud, S., Andrieux, J., Barin, C., Jotterand, M., Mossafa, H., Ramond, S., Terré, C., Lippert, E., and Berger, F.
- Subjects
LETTERS to the editor ,CHRONIC lymphocytic leukemia - Abstract
A letter to the editor is presented which is about t-positive B-cell malignancy in atypical chronic lymphocytic leukemia.
- Published
- 2008
- Full Text
- View/download PDF
5. Acute myeloid leukaemia with 8p11 (MYST3) rearrangement: an integrated cytologic, cytogenetic and molecular study by the groupe francophone de cytogénétique hématologique.
- Author
-
Gervais, C., Murati, A., Helias, C., Struski, S., Eischen, A., Lippert, E., Tigaud, I., Penther, D., Bastard, C., Mugneret, F., Poppe, B., Speleman, F., Talmant, P., Akker, J. VanDen, Baranger, L., Barin, C., Luquet, I., Nadal, N., Nguyen-Khac, F., and Maarek, O.
- Subjects
CASE studies ,ACUTE myeloid leukemia ,CHROMOSOMAL translocation ,CYTOGENETICS ,ACETYLTRANSFERASES ,CARRIER proteins ,HISTONES - Abstract
Thirty cases of acute myeloid leukaemia (AML) with MYST histone acetyltransferase 3 (MYST3) rearrangement were collected in a retrospective study from 14 centres in France and Belgium. The mean age at diagnosis was 59.4 years and 67% of the patients were females. Most cases (77%) were secondary to solid cancer (57%), haematological malignancy (35%) or both (8%), and appeared 25 months after the primary disease. Clinically, cutaneous localization and disseminated intravascular coagulation were present in 30 and 40% of the cases, respectively. AMLs were myelomonocytic (7%) or monocytic (93%), with erythrophagocytosis (75%) and cytoplasmic vacuoles (75%). Immunophenotype showed no particularity compared with monocytic leukaemia without MYST3 abnormality. Twenty-eight cases carried t(8;16)(p11;p13) with MYST3-CREBBP fusion, one case carried a variant t(8;22)(p11;q13) and one case carried a t(8;19)(p11;q13). Type I (MYST3 exon 16-CREBBP exon 3) was the most frequent MYST3-CREBBP fusion transcript (65%). MYST3 rearrangement was associated with a poor prognosis, as 50% of patients deceased during the first 10 months. All those particular clinical, cytologic, cytogenetic, molecular and prognostic characteristics of AML with MYST3 rearrangement may have allowed an individualization into the World Health Organization classification.Leukemia (2008) 22, 1567–1575; doi:10.1038/leu.2008.128; published online 5 June 2008 [ABSTRACT FROM AUTHOR]
- Published
- 2008
- Full Text
- View/download PDF
6. Hyperdiploid karyotypes in acute myeloid leukemia define a novel entity: a study of 38 patients from the Groupe Francophone de Cytogenetique Hematologique (GFCH).
- Author
-
Luquet, I., Laï, J. L., Barin, C., Baranger, L., Bilhou-Nabera, C., Lippert, E., Gervais, C., Talmant, P., Cornillet-Lefebvre, P., Perot, C., Nadal, N., Mozziconacci, M. J., Lafage-Pochitaloff, M., Eclache, V., Mugneret, F., Lefebvre, C., Herens, C., Speleman, F., Poirel, H., and Tigaud, I.
- Subjects
MYELOID leukemia ,CHROMOSOMAL rearrangement ,GENETIC disorders ,KARYOTYPES ,CYTOTAXONOMY - Abstract
A series of 38 patients with acute myeloblastic leukemia (AML) with 49 or more chromosomes and without structural abnormalities was selected within the Groupe Francophone de Cytogénétique Hématologique (GFCH) to better define their characteristics. The median age of the patients was 65 years, and all FAB subtypes were represented. Although all chromosomes were gained, some seems to prevail: chromosome 8 (68%), 21 (47%), 19 (37%), and 13 and 14 (34% each). Since MLL rearrangement leads patients in a group with an unfavorable prognosis, search for cryptic rearrangements of MLL was performed in 34 patients and showed abnormalities in 5 (15%). When we applied the most frequent definition of complex karyotypes (three or more abnormalities), all patients with high hyperdiploid AML fall in the unfavorable category. Among the 18 patients without MLL rearrangement receiving an induction therapy, 16 (89%) reached CR and 6 (33%) were still alive after a 31-month median follow-up (14-61 months). Although this study was retrospective, these results suggest that high hyperdiploid AML without chromosome rearrangement seems to be a subgroup of uncommon AML (less than 1%), and may be better classified in the intermediate prognostic group. [ABSTRACT FROM AUTHOR]
- Published
- 2008
- Full Text
- View/download PDF
7. Clinical, cytogenetic and molecular characteristics of 14 T-ALL patients carrying the TCRβ-HOXA rearrangement: a study of the Groupe Francophone de Cytogénétique Hématologique.
- Author
-
Cauwelier, B., Cavé, H., Gervais, C., Lessard, M., Barin, C., Perot, C., Van den Akker, J., Mugneret, F., Charrin, C., Pagès, M. P., Grégoire, M.-J., Jonveaux, P., Lafage-Pochitaloff, M., Mozzicconacci, M. J., Terré, C., Luquet, I., Cornillet-Lefebvre, P., Laurence, B., Plessis, G., and Lefebvre, C.
- Subjects
CYTOGENETICS ,CELL receptors ,LEUKEMIA ,CARCINOGENESIS ,MOLECULAR genetics ,IN situ hybridization ,BONE marrow ,IMMUNOPHENOTYPING - Abstract
Recently, we and others described a new chromosomal rearrangement, that is, inv(7)(p15q34) and t(7;7)(p15;q34) involving the T-cell receptor beta (TCRβ) (7q34) and the HOXA gene locus (7p15) in 5% of T-cell acute lymphoblastic leukemia (T-ALL) patients leading to transcriptional activation of especially HOXA10. To further address the clinical, immunophenotypical and molecular genetic findings of this chromosomal aberration, we studied 330 additional T-ALLs. This revealed TCRβ-HOXA rearrangements in five additional patients, which brings the total to 14 cases in 424 patients (3.3%). Real-time quantitative PCR analysis for HOXA10 gene expression was performed in 170 T-ALL patients and detected HOXA10 overexpression in 25.2% of cases including all the cases with a TCRβ-HOXA rearrangement (8.2%). In contrast, expression of the short HOXA10 transcript, HOXA10b, was almost exclusively found in the TCRβ-HOXA rearranged cases, suggesting a specific role for the HOXA10b short transcript in TCRβ-HOXA-mediated oncogenesis. Other molecular and/or cytogenetic aberrations frequently found in subtypes of T-ALL (SIL-TAL1, CALM-AF10, HOX11, HOX11L2) were not detected in the TCRβ-HOXA rearranged cases except for deletion 9p21 and NOTCH1 activating mutations, which were present in 64 and 67%, respectively. In conclusion, this study defines TCRβ-HOXA rearranged T-ALLs as a distinct cytogenetic subgroup by clinical, immunophenotypical and molecular genetic characteristics.Leukemia (2007) 21, 121–128. doi:10.1038/sj.leu.2404410; published online 12 October 2006 [ABSTRACT FROM AUTHOR]
- Published
- 2007
- Full Text
- View/download PDF
8. NUP98 rearrangements in hematopoietic malignancies: a study of the Groupe Francophone de Cytogénétique Hématologique.
- Author
-
Romana, S. P., Radford-Weiss, I., Ben Abdelali, R., Schluth, C., Petit, A., Dastugue, N., Talmant, P., Bilhou-Nabera, C., Mugneret, F., Lafage-Pochitaloff, M., Mozziconacci, M.-J., Andrieu, J., Lai, J.-L., Terre, C., Rack, K., Cornillet-Lefebvre, P., Luquet, I., Nadal, N., Nguyen-Khac, F., and Perot, C.
- Subjects
LYMPHOBLASTIC leukemia ,HEMATOPOIETIC stem cell transplantation ,FLUORESCENCE in situ hybridization ,CANCER genetics ,GENETIC regulation ,CHROMOSOMES ,T cells - Abstract
The NUP98 gene is fused with 19 different partner genes in various human hematopoietic malignancies. In order to gain additional clinico-hematological data and to identify new partners of NUP98, the Groupe Francophone de Cytogénétique Hématologique (GFCH) collected cases of hematological malignancies where a 11p15 rearrangement was detected. Fluorescence in situ hybridization (FISH) analysis showed that 35% of these patients (23/66) carried a rearrangement of the NUP98 locus. Genes of the HOXA cluster and the nuclear-receptor set domain (NSD) genes were frequently fused to NUP98, mainly in de novo myeloid malignancies whereas the DDX10 and TOP1 genes were equally rearranged in de novo and in therapy-related myeloid proliferations. Involvement of ADD3 and C6ORF80 genes were detected, respectively, in myeloid disorders and in T-cell acute lymphoblastic leukemia (T-ALL), whereas the RAP1GDS1 gene was fused to NUP98 in T-ALL. Three new chromosomal breakpoints: 3q22.1, 7p15 (in a localization distinct from the HOXA locus) and Xq28 were detected in rearrangements with the NUP98 gene locus. The present study as well as a review of the 73 cases previously reported in the literature allowed us to delineate some chromosomal, clinical and molecular features of patients carrying a NUP98 gene rearrangements.Leukemia (2006) 20, 696–706. doi:10.1038/sj.leu.2404130; published online 9 February 2006 [ABSTRACT FROM AUTHOR]
- Published
- 2006
- Full Text
- View/download PDF
9. Report of 34 patients with clonal chromosomal abnormalities in Philadelphia-negative cells during imatinib treatment of Philadelphia-positive chronic myeloid leukemia.
- Author
-
Terre, C., Eclache, V., Rousselot, P., Imbert, M., Charrin, C., Gervais, C., Mozziconacci, M. J., Maarek, O., Mossafa, H., Auger, N., Dastugue, N., Talmant, P., Van Den Akker, J., Leonard, C., N'Guyen Khac, F., Mugneret, F., Viguié, F., Lafage-Pochitaloff, M., Bastie, J. N., and Roux, G. l.
- Subjects
IMATINIB ,MYELOID leukemia ,PROTEIN-tyrosine kinases ,CHROMOSOMES ,ANTINEOPLASTIC agents ,LEUKEMIA - Abstract
Imatinib mesylate (Gleevec
® ), an inhibitor of the BCR-ABL tyrosine kinase, was introduced recently into the therapy of chronic myeloid leukemia (CML). Several cases of emergence of clonal chromosomal abnormalities after therapy with imatinib have been reported, but their incidence, etiology and prognosis remain to be clarified. We report here a large series of 34 CML patients treated with imatinib who developed Philadelphia (Ph)-negative clones. Among 1001 patients with Ph-positive CML treated with imatinib, 34 (3.4%) developed clonal chromosomal abnormalities in Ph-negative cells. Three patients were treated with imatinib up-front. The most common cytogenetic abnormalities were trisomy 8 and monosomy 7 in twelve and seven patients, respectively. In 15 patients, fluorescent in situ hybridization with specific probes was performed in materials archived before the initiation of imatinib. The Ph-negative clone was related to previous therapy in three patients, and represented a minor pre-existing clone that expanded after the eradication of Ph-positive cells with imatinib in two others. However, in 11 patients, the new clonal chromosomal abnormalities were not detected and imatinib may have had a direct effect. No myelodysplasia was found in our cohort. With a median follow-up of 24 months, one patient showed CML acceleration and two relapsed.Leukemia (2004) 18, 1340-1346. doi:10.1038/sj.leu.2403399 Published online 10 June 2004 [ABSTRACT FROM AUTHOR]- Published
- 2004
- Full Text
- View/download PDF
10. t(5;14)/HOX11L2-positive T-cell acute lymphoblastic leukemia. A collaborative study of the Groupe Français de Cytogénétique Hématologique (GFCH).
- Author
-
Berger, R., Dastugue, N., Busson, M., van den Akker, J., Pérot, C., Ballerini, P., Hagemeijer, A., Michaux, L., Charrin, C., Pages, M.P., Mugneret, F., Andrieux, J., Talmant, P., Hélias, C., Mauvieux, L., Lafage-Pochitaloff, M., Mozziconacci, M-J, Cornillet-Lefebvre, P., Radford, I., and Asnafi, V.
- Subjects
IN situ hybridization ,LYMPHOBLASTIC leukemia ,T cells ,CD antigens ,KARYOTYPES ,CHROMOSOME abnormalities - Abstract
To accurately estimate the incidence of HOX11L2 expression, and determine the associated cytogenetic features, in T-cell acute lymphoblastic leukemia (T-ALL), the Groupe Français de Cytogénétique Hématologique (GFCH) carried out a retrospective study of both childhood and adult patients. In total, 364 patients were included (211 children ?15 years and 153 adults), and 67 (18.5%) [47 children (22.4%) and 20 adults (13.1%)] were shown to either harbor the t(5;14)q35;q32) translocation or express the HOX11L2 gene or both. Most of the common hematological parameters did not show significant differences within positive and negative populations, whereas the incidence of CD1a+/CD10+ and cytoplasmic CD3+ patients was significantly higher in positive than in negative children. Out of the 63 positive patients investigated by conventional cytogenetics, 32 exhibited normal karyotype, whereas the others 31 showed clonal chromosome abnormalities, which did not include classical T-ALL specific translocations. Involvement of the RANBP17/HOX11L2 locus was ascertained by fluorescence in situ hybridization in six variant or alternative (three-way translocation or cytogenetic partner other than 14q32) translocations out of the 223 patients. Our results also show that HOX11L2 expression essentially occurs as a result of a 5q35 rearrangement, but is not associated with another identified T-ALL specific recurrent genetic abnormality, such as SIL-TAL fusion or HOX11 expression.Leukemia (2003) 17, 1851-1857. doi:10.1038/sj.leu.2403061 [ABSTRACT FROM AUTHOR]
- Published
- 2003
- Full Text
- View/download PDF
11. MLL amplification in acute leukaemia: a United Kingdom Cancer Cytogenetics Group (UKCCG) study.
- Author
-
Cuthbert, G, Thompson, K, McCullough, S, Watmore, A, Dickinson, H, Telford, N, Mugneret, F, Harrison, C, Griffiths, M, and Bown, N
- Subjects
GENE amplification ,ACUTE myeloid leukemia - Abstract
The MLL gene, located at 11q23, is frequently rearranged in acute leukaemia as either chimaeric fusion genes or partial tandem duplications. We report a series of 12 acute leukaemia cases with apparent amplification of the MLL gene ascertained using fluorescence in situ hybridisation (FISH). Seven cases showed intrachromosomal amplification of MLL, four cases showed extrachromosomal amplification as double minute chromosomes (dmin) and one case had separate subclones with dmin and homogenously staining region (hsr). Southern blot analysis of the MLL gene showed MLL gene rearrangement in three of the 10 successful cases. These cases do not naturally fall into either of the two recognised categories of MLL rearrangement and may represent a third variety of MLL gene abnormalities. [ABSTRACT FROM AUTHOR]
- Published
- 2000
- Full Text
- View/download PDF
12. Increase therapy-related leukemia secondary to breast cancer.
- Author
-
Carli, P M, Sgro, C, Parchin-Geneste, N, Isambert, N, Mugneret, F, Girodon, F, and Maynadié, M
- Subjects
ACUTE myeloid leukemia ,BREAST tumors - Abstract
Therapy-related leukemia associated with chemotherapy, particularly alkylating agents and topoisomerase II inhibitors, are being reported with increasing frequency in the literature mainly after breast cancer. We also observed an increasing number of such leukemias in the data base of the specialized registry of hematological malignancies of the Côte d'Or department. Between 1980 and 1998, 156 AML and RAEB-t were registered in women in Côte d'Or. Among them, 12 occurred in women with breast cancer history (7.7%). Analysis by period of time shows a significant increase in the proportion of therapy-related leukemia secondary to breast cancer (P < 0.02). Chemotherapy including topoisomerase II inhibitors was used in 10 cases in which mitoxantrone was used in eight cases. In these eight cases, leukemia had clinical and biological characteristics usually described with topoisomerase II inhibitors but 44% were promyelocytic sub-type with the t(15;17) specific karyotypic abnormality. These data on a well-defined population demonstrate the increased proportion of therapy-related leukemia secondary to breast cancer, probably due to the use of mitoxantrone. [ABSTRACT FROM AUTHOR]
- Published
- 2000
- Full Text
- View/download PDF
13. Prolonged remission and autologous recovery in two patients with chronic myelogenous leukemia after graft failure of allogeneic bone marrow transplantation.
- Author
-
Fouillard, L., Deconinck, E., Tiberghien, P., Deschaseaux, M.-L., Solary, E., Mugneret, F., Brion, A., Herve, P., and Cahn, J.-Y.
- Subjects
MYELOID leukemia ,GRAFT versus host disease ,BONE marrow transplantation - Abstract
Two patients with Philadelphia-positive chronic myelogenous leukemia underwent allogeneic bone marrow transplantation from a related HLA mismatched donor (patient 1) or from an unrelated HLA-identical donor (patient 2). Following bone marrow transplantation partial engraftment (patient 1) or graft failure (patient 2) occurred followed by autologous Philadelphia negative hematopoietic recovery either spontaneously (patient 1) or after infusion of autologous bone marrow rescue (patient 2). Neither Philadelphia chromosome, nor ber-abl rearrangement was detectable by PCR analysis up to 7 years (patient 1) and 9 years (patient 2) post-transplantation. These two observations indicate that sustained engraftment of allogeneic bone marrow stem cells following a myeloablative regimen is not necessary to cure chronic myelogenous leukemia. It is hypothesized that the proliferative advantage of Philadelphia-negative progenitors and the anti-leukemic effect of lymphocytes in the graft have resulted in prolonged remission of the patients. [ABSTRACT FROM AUTHOR]
- Published
- 1998
- Full Text
- View/download PDF
14. Ten novel 11q23 chromosomal partner sites. European 11q23 Workshop participants.
- Author
-
Harrison, C J, Cuneo, A, Clark, R, Johansson, B, Lafage-Pochitaloff, M, Mugneret, F, Moorman, A V, and Secker-Walker, L M
- Subjects
GENES ,LEUKEMIA ,CHROMOSOMES ,MYELODYSPLASTIC syndromes ,PROTEINS ,DNA ,LYMPHOBLASTIC leukemia ,ONCOGENES ,MYELOID leukemia ,CHROMOSOME banding ,KARYOTYPES ,CHROMOSOME abnormalities ,TRANSFERASES ,DNA-binding proteins ,TRANSCRIPTION factors ,ACUTE diseases - Abstract
The MLL gene located at 11q23 has been described as a 'promiscuous' gene due its involvement with a large number of genetic partners. The EU Concerted Action Workshop on 11q23 provided 550 cases for study of which 82 showed abnormalities which did not involve the established translocations or deletion of 11q23. In these 'other' cases, which included inversions and duplications, 11q23 was found to be involved with 25 chromosome partners of which 10 had not been previously reported. These were 1q31, 4p11, 6q13, 8q21, 10q22, 10q25, 11q11, 11q21, 13q34 and 18q23. This study demonstrated the value of the Workshop, in confirming the diversity of chromosomal partner sites involved with 11q23 and in the identification of new partners. [ABSTRACT FROM AUTHOR]
- Published
- 1998
- Full Text
- View/download PDF
15. Immunophenotypic patterns and cytogenetic anomalies in acute non-lymphoblastic leukemia subtypes: a prospective study of 432 patients.
- Author
-
Casasnovas, R O, Campos, L, Mugneret, F, Charrin, C, Béné, M C, Garand, R, Favre, M, Sartiaux, C, Chaumarel, I, Bernier, M, Faure, G, and Solary, E
- Subjects
LYMPHOBLASTIC leukemia ,IMMUNOPHENOTYPING ,CHROMOSOME abnormalities - Abstract
This study prospectively analysed the relationships between immunophenotypic and cytogenetic features of blast cells in 432 acute non-lymphoblastic leukemias (ANLL) at presentation. An abnormal karyotype was detected in 232 cases (54%). These abnormalities were related to immunophenotypic markers as detected using a consensual panel of monoclonal antibodies allowing lineage assignment and investigation of myeloid marker expression on blast cells. In univariate analysis, CD9, CD10, CD15, CD34 and TdT expression appeared significantly associated with chromosomal anomalies. Multivariate analysis identified CD34 and CD9 expression as independently predictive of the presence of at least one cytogenetic abnormality (P < 10(-4) and P < 0.03, respectively). Significant associations between immunophenotypic and karyotypic features were observed both within individual FAB subgroups and independently from morphological criteria. Specific features were seen in five ANLL entities: M0 or M1/B lineage antigen positivity/t(9;22) or del(11)(q23); M2/CD13-/t(8;21); M4/CD13+, CD34+, CD36+/inv(16); M4 or M5/lack of B lineage antigen/del(11)(q23) or t(9;11). More practically, and although the relationships demonstrated only represent a fraction of homogeneous immunophenotypic subgroups, identification of such immunophenotypic features should prompt careful karyotypic examination, eventually using molecular biology analysis on non-growing cells. [ABSTRACT FROM AUTHOR]
- Published
- 1998
- Full Text
- View/download PDF
16. Analyses of TET2 mutations in post-myeloproliferative neoplasm acute myeloid leukemias.
- Author
-
Couronné, L., Lippert, E., Andrieux, J., Kosmider, O., Radford-Weiss, I., Penther, D., Dastugue, N., Mugneret, F., Lafage, M., Gachard, N., Nadal, N., Bernard, O. A., Nguyen-Khac, F., and Couronné, L
- Subjects
LETTERS to the editor ,ACUTE myeloid leukemia ,PROTEINS ,RESEARCH ,GENETIC mutation ,RESEARCH methodology ,MYELOPROLIFERATIVE neoplasms ,MEDICAL cooperation ,EVALUATION research ,COMPARATIVE studies ,DNA-binding proteins ,DISEASE complications - Abstract
A letter to the editor is presented that discusses the analyses of TET2 mutations in post-myeloproliferative neoplasm acute myeloid leukemias.
- Published
- 2010
- Full Text
- View/download PDF
17. Epidemiological characteristics of myelodysplastic syndrome in a well-defined French population.
- Author
-
Maynadié, M, Verret, C, Moskovtchenko, P, Mugneret, F, Petrella, T, Caillot, D, Carli, PM, Maynadié, M, and Carli, P M
- Published
- 1996
- Full Text
- View/download PDF
18. Minimally differentiated acute myeloid leukemia (AML-MO) with lymphoid presentation at relapse: a case report.
- Author
-
Ysebaert, L, Carli, P M, Casasnovas, R O, Girodon, F, Caillot, D, Mugneret, F, and Maynadié, M
- Subjects
LEUKEMIA ,DISEASE relapse ,LYMPHOBLASTIC leukemia diagnosis ,BONE marrow ,CELL differentiation ,CELLS ,FLOW cytometry ,GENETICS ,IMMUNOPHENOTYPING ,LYMPHOBLASTIC leukemia ,MYELOID leukemia ,ACUTE diseases ,SECONDARY primary cancer - Abstract
Presents the case study of a person diagnosed with minimally differentiated acute myeloid leukemia at relapse. Treatment given to the patient during the initial diagnosis of leukemia; Relapse of acute leukemia in the patient after ten months of completion of treatment; Diagnosis of B III acute lymphoid leukemia on relapse.
- Published
- 2001
- Full Text
- View/download PDF
Catalog
Discovery Service for Jio Institute Digital Library
For full access to our library's resources, please sign in.