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1. NUP98 is rearranged in 3.8% of pediatric AML forming a clinical and molecular homogenous group with a poor prognosis

Author

Struski, S, Lagarde, S, Bories, P, Puiseux, C, Prade, N, Cuccuini, W, Pages, M-P, Bidet, A, Gervais, C, Lafage-Pochitaloff, M, Roche-Lestienne, C, Barin, C, Penther, D, Nadal, N, Radford-Weiss, I, Collonge-Rame, M-A, Gaillard, B, Mugneret, F, Lefebvre, C, Bart-Delabesse, E, Petit, A, Leverger, G, Broccardo, C, Luquet, I, Pasquet, M, and Delabesse, E

Published
2017
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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, Berger, F, Felman, P, Merle-Béral, H, Bernard, O A, Davi, F, Berger, R, and Nguyen-Khac, F

Published
2008
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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, Maarek, O, Herens, C, Sainty, D, Flandrin, G, Birnbaum, D, Mozziconacci, M-J, and Lessard, M

Published
2008
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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, Tigaud, I, Cabrol, C, Rousselot, P, Daliphard, S, Imbert, M, Garand, R, Geneviève, F, Berger, R, and Terre, C

Published
2008
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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, Lefebvre, C, Leroux, D, Antoine-Poirel, H, Graux, C, Mauvieux, L, Heimann, P, Chalas, C, Clappier, E, Verhasselt, B, Benoit, Y, Moerloose, B D, Poppe, B, Van Roy, N, Keersmaecker, K D, Cools, J, Sigaux, F, Soulier, J, Hagemeijer, A, Paepe, A D, Dastugue, N, Berger, R, and Speleman, F

Published
2007
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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, Perot, C, Van den Akker, J, Fert-Ferrer, S, Cabrol, C, Charrin, C, Tigaud, I, Poirel, H, Vekemans, M, Bernard, O A, and Berger, R

Published
2006
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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, Khac, F N'Guyen, Mugneret, F, Viguié, F, Lafage-Pochitaloff, M, Bastie, J N, Roux, G L, Nicolini, F, Maloisel, F, Vey, N, Laurent, G, Recher, C, Vigier, M, Yacouben, Y, Giraudier, S, Vernant, J P, Salles, B, Roussi, J, Castaigne, S, Leymarie, V, Flandrin, G, and Lessard, M

Published
2004
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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, Asnafi, V, Bilhou-Nabera, C, Nguyen Khac, F, Léonard, C, Speleman, F, Poppe, B, Bastard, C, Taviaux, S, Quilichini, B, Herens, C, Grégoire, M-J, Cavé, H, and Bernard, O A

Published
2003
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18. NUP98 is rearranged in 3.8% of pediatric AML forming a clinical and molecular homogenous group with a poor prognosis

Author

Struski, S, primary, Lagarde, S, additional, Bories, P, additional, Puiseux, C, additional, Prade, N, additional, Cuccuini, W, additional, Pages, M-P, additional, Bidet, A, additional, Gervais, C, additional, Lafage-Pochitaloff, M, additional, Roche-Lestienne, C, additional, Barin, C, additional, Penther, D, additional, Nadal, N, additional, Radford-Weiss, I, additional, Collonge-Rame, M-A, additional, Gaillard, B, additional, Mugneret, F, additional, Lefebvre, C, additional, Bart-Delabesse, E, additional, Petit, A, additional, Leverger, G, additional, Broccardo, C, additional, Luquet, I, additional, Pasquet, M, additional, and Delabesse, E, additional

Published
2016
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19. NUP98is rearranged in 3.8% of pediatric AML forming a clinical and molecular homogenous group with a poor prognosis

Author

Struski, S, Lagarde, S, Bories, P, Puiseux, C, Prade, N, Cuccuini, W, Pages, M-P, Bidet, A, Gervais, C, Lafage-Pochitaloff, M, Roche-Lestienne, C, Barin, C, Penther, D, Nadal, N, Radford-Weiss, I, Collonge-Rame, M-A, Gaillard, B, Mugneret, F, Lefebvre, C, Bart-Delabesse, E, Petit, A, Leverger, G, Broccardo, C, Luquet, I, Pasquet, M, and Delabesse, E

Abstract

Pediatric acute myeloid leukemia (AML) is a rare disease whose prognosis is highly variable according to factors such as chromosomal abnormalities. Recurrent genomic rearrangements are detected in half of pediatric AML by karyotype. NUcleoPorin 98(NUP98) gene is rearranged with 31 different fusion partner genes. These rearrangements are frequently undetected by conventional cytogenetics, as the NUP98gene is located at the end of the chromosome 11 short arm (11p15). By screening a series of 574 pediatric AML, we detected a NUP98rearrangement in 22 cases (3.8%), a frequency similar to CBFB-MYH11fusion gene (4.0%). The most frequent NUP98fusion gene partner is NSD1. These cases are homogeneous regarding their biological and clinical characteristics, and associated with bad prognosis only improved by bone marrow transplantation. We detailed the biological characteristics of these AML by exome sequencing which demonstrated few recurrent mutations (FLT3ITD, WT1, CEBPA, NBPF14, BCRand ODF1). The analysis of the clonal structure in these cases suggests that the mutation order in the NUP98-rearranged pediatric AML begins with the NUP98rearrangement leading to epigenetic dysregulations then followed by mutations of critical hematopoietic transcription factors and finally, activation of the FLT3 signaling pathway.

Published
2017
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20. Molecular analysis of T-cell receptor transcripts in a human T-cell leukemia bearing a t(1;14) and an inv(7); cell surface expression of a TCR-beta chain in the absence of alpha chain

Author

Olivier Bernard, Groettrup M, Mugneret F, Berger R, and Azogui O

Subjects
Adult, Chromosomes, Human, Pair 14, Male, Base Sequence, Transcription, Genetic, Receptors, Antigen, T-Cell, alpha-beta, Molecular Sequence Data, Gene Expression, DNA, Neoplasm, Gene Rearrangement, T-Lymphocyte, Translocation, Genetic, Blotting, Southern, Phenotype, Chromosomes, Human, Pair 1, Chromosome Inversion, Humans, Leukemia-Lymphoma, Adult T-Cell, Amino Acid Sequence, RNA, Neoplasm, Chromosomes, Human, Pair 7
Abstract

The polymerase chain reaction (PCR) was used to amplify cDNA in order to characterize normal and hybrid T-cell receptor (TCR) gene rearrangements derived from a T-cell acute lymphoblastic leukemia (T-ALL) bearing a chromosome 7 inversion. The nucleotide sequence analysis of the amplified product showed the presence of an out-of-frame V beta/J gamma/C gamma transcript and an in-frame V gamma/J gamma/C beta transcript which result from an interlocus recombination between the TCR-beta and gamma loci and the transcription of the reciprocal hybrid TCR gene. The sequence analysis of the reciprocal DNA segment directly involved in the breakpoint of the inversion showed a recombination between a J gamma-sequence heptamer signal and a coding J beta gene segment. The exonuclease nibbling of each DNA extremity and the non-templated nucleotide insertion observed at both coding and reciprocal joints demonstrate that the inversion is mediated by the lymphocyte recombinase complex. During T-cell differentiation, TCR-beta genes are rearranged prior to TCR-alpha genes. In the present case of T-ALL, we have shown that TCR-delta genes are rearranged at both loci, excluding productive rearrangements of TCR-alpha genes. The molecular analysis of the normal TCR genes derived from the leukemic cells revealed the presence of productively rearranged TCR-beta, gamma, and delta genes. Cell surface staining of these cells showed the presence of CD3 molecules and of a TCR-beta chain corresponding to the normal beta allele expressed in a disulfide-linked complex with a protein which is not TCR-alpha, gamma, or delta. This could represent the cell surface expression of the hybrid TCR-V gamma/C beta protein or the expression of a TCR-beta homodimer.

Published
1993

21. 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, primary, Laï, J L, additional, Barin, C, additional, Baranger, L, additional, Bilhou-Nabera, C, additional, Lippert, E, additional, Gervais, C, additional, Talmant, P, additional, Cornillet-Lefebvre, P, additional, Perot, C, additional, Nadal, N, additional, Mozziconacci, M J, additional, Lafage-Pochitaloff, M, additional, Eclache, V, additional, Mugneret, F, additional, Lefebvre, C, additional, Herens, C, additional, Speleman, F, additional, Poirel, H, additional, Tigaud, I, additional, Cabrol, C, additional, Rousselot, P, additional, Daliphard, S, additional, Imbert, M, additional, Garand, R, additional, Geneviève, F, additional, Berger, R, additional, and Terre, C, additional

Published
2007
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22. 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, primary, Cavé, H, additional, Gervais, C, additional, Lessard, M, additional, Barin, C, additional, Perot, C, additional, Van den Akker, J, additional, Mugneret, F, additional, Charrin, C, additional, Pagès, M P, additional, Grégoire, M-J, additional, Jonveaux, P, additional, Lafage-Pochitaloff, M, additional, Mozzicconacci, M J, additional, Terré, C, additional, Luquet, I, additional, Cornillet-Lefebvre, P, additional, Laurence, B, additional, Plessis, G, additional, Lefebvre, C, additional, Leroux, D, additional, Antoine-Poirel, H, additional, Graux, C, additional, Mauvieux, L, additional, Heimann, P, additional, Chalas, C, additional, Clappier, E, additional, Verhasselt, B, additional, Benoit, Y, additional, Moerloose, B D, additional, Poppe, B, additional, Van Roy, N, additional, Keersmaecker, K D, additional, Cools, J, additional, Sigaux, F, additional, Soulier, J, additional, Hagemeijer, A, additional, Paepe, A D, additional, Dastugue, N, additional, Berger, R, additional, and Speleman, F, additional

Published
2006
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23. Der(16)t(1;16)(q10;p10) in multiple myeloma: a new non-random abnormality that is frequently associated with Burkitt's-type translocations.

Author

Mugneret F, Sidaner I, Favre B, Manone L, Maynadié M, Caillot D, and Solary E

Subjects
Adult, Aged, Aneuploidy, Bone Marrow pathology, Burkitt Lymphoma genetics, Burkitt Lymphoma pathology, Clone Cells pathology, Female, Humans, In Situ Hybridization, Fluorescence, Karyotyping, Male, Middle Aged, Multiple Myeloma pathology, Trisomy, Tumor Cells, Cultured, Chromosomes, Human, Pair 1 ultrastructure, Chromosomes, Human, Pair 16 ultrastructure, Monosomy, Multiple Myeloma genetics, Translocation, Genetic
Abstract

Aneuploidy is a frequent feature in multiple myeloma. Cytogenetic analyses have shown that a 14q+ chromosome resulting from either a t(8;14)(q24;q32) or a t(11;14)(q13;q32) was the most consistent abnormality but no specific chromosomal aberration has been identified in this disease. Bone marrow cells from 121 consecutive patients with multiple myeloma were analyzed cytogenetically by standard banding techniques including RHG, GTG and CBG banding. Cells were cultured for 24-96 h in the presence or in the absence of interleukin-6. Clonal abnormalities were detected in 41 of the 121 patients (34%). A der(16)t(1;16)(q10;p10) abnormality was identified in nine of these 41 patients (22%). Der(16) was identified at diagnosis in five patients, during disease progression in two additional patients, and at the time of a relapse in the two last cases. The t(1;15)(q10;p10) translocation was always unbalanced, resulting in a monosomy 16q in all cases. The CBG banding did not demonstrate dicentric chromosomes and the whole chromosome painting confirmed the der(16). A large number of other chromosomal abnormalities were associated with der(16), including chromosomal rearrangements involving the 8q24 band in five cases. Four of these five cases were Burkitt's-type translocations. This observation suggests that der(16)t(1;16)(q10;p10) could be one of the most frequent chromosomal abnormalities that can be identified in multiple myeloma cells.

Published
1995

24. Molecular analysis of T-cell receptor transcripts in a human T-cell leukemia bearing a t(1;14) and an inv(7); cell surface expression of a TCR-beta chain in the absence of alpha chain.

Author

Bernard O, Groettrup M, Mugneret F, Berger R, and Azogui O

Subjects
Adult, Amino Acid Sequence, Base Sequence, Blotting, Southern, DNA, Neoplasm analysis, DNA, Neoplasm genetics, Gene Expression genetics, Gene Rearrangement, T-Lymphocyte genetics, Humans, Male, Molecular Sequence Data, Phenotype, RNA, Neoplasm analysis, RNA, Neoplasm genetics, Receptors, Antigen, T-Cell, alpha-beta analysis, Chromosome Inversion, Chromosomes, Human, Pair 1 physiology, Chromosomes, Human, Pair 14 physiology, Chromosomes, Human, Pair 7 physiology, Leukemia-Lymphoma, Adult T-Cell genetics, Receptors, Antigen, T-Cell, alpha-beta genetics, Transcription, Genetic genetics, Translocation, Genetic genetics
Abstract

The polymerase chain reaction (PCR) was used to amplify cDNA in order to characterize normal and hybrid T-cell receptor (TCR) gene rearrangements derived from a T-cell acute lymphoblastic leukemia (T-ALL) bearing a chromosome 7 inversion. The nucleotide sequence analysis of the amplified product showed the presence of an out-of-frame V beta/J gamma/C gamma transcript and an in-frame V gamma/J gamma/C beta transcript which result from an interlocus recombination between the TCR-beta and gamma loci and the transcription of the reciprocal hybrid TCR gene. The sequence analysis of the reciprocal DNA segment directly involved in the breakpoint of the inversion showed a recombination between a J gamma-sequence heptamer signal and a coding J beta gene segment. The exonuclease nibbling of each DNA extremity and the non-templated nucleotide insertion observed at both coding and reciprocal joints demonstrate that the inversion is mediated by the lymphocyte recombinase complex. During T-cell differentiation, TCR-beta genes are rearranged prior to TCR-alpha genes. In the present case of T-ALL, we have shown that TCR-delta genes are rearranged at both loci, excluding productive rearrangements of TCR-alpha genes. The molecular analysis of the normal TCR genes derived from the leukemic cells revealed the presence of productively rearranged TCR-beta, gamma, and delta genes. Cell surface staining of these cells showed the presence of CD3 molecules and of a TCR-beta chain corresponding to the normal beta allele expressed in a disulfide-linked complex with a protein which is not TCR-alpha, gamma, or delta. This could represent the cell surface expression of the hybrid TCR-V gamma/C beta protein or the expression of a TCR-beta homodimer.

Published
1993

25. P-glycoprotein expression and in vitro reversion of doxorubicin resistance by verapamil in clinical specimens from acute leukaemia and myeloma.

Author

Solary E, Bidan JM, Calvo F, Chauffert B, Caillot D, Mugneret F, Gauville C, Tsuruo T, Carli PM, and Guy H

Subjects
ATP Binding Cassette Transporter, Subfamily B, Member 1, Drug Resistance, Humans, Leukemia, Myeloid, Acute drug therapy, Multiple Myeloma drug therapy, Precursor Cell Lymphoblastic Leukemia-Lymphoma drug therapy, Doxorubicin metabolism, Leukemia, Myeloid, Acute metabolism, Membrane Glycoproteins metabolism, Multiple Myeloma metabolism, Neoplasm Proteins metabolism, Precursor Cell Lymphoblastic Leukemia-Lymphoma metabolism, Verapamil pharmacology
Abstract

The expression of the P-glycoprotein which is associated with the development of multidrug resistance in various cell lines was investigated in 87 fresh acute leukaemia and multiple myeloma samples using the specific mouse monoclonal antibody MRK16 in an indirect immunofluorescence assay. Considering a 10% positive cell cut-off value, a heterogeneous expression of P-glycoprotein was observed in 5/22 (22.7%) de novo acute leukaemias, 7/22 (31.8%) relapse or secondary acute leukaemias, 14/27 (51.8%) acute transformation of myeloproliferative or myelodysplastic syndromes and 5/16 (31.2%) multiple myelomas. This expression was not associated with specific cytogenetic abnormalities, especially alterations of chromosome 7q. Verapamil, a calcium channel blocker, has been demonstrated to circumvent the multidrug resistance in cell lines, possibly by interfering with P-glycoprotein function. Using the microculture tetrazolium assay, verapamil was demonstrated to increase the sensitivity of fresh leukaemic or myeloma cells to doxorubicin in 19/43 (43.1%) samples. The doxorubicin IC50 level and the capacity of verapamil to increase the sensitivity of blast cells to doxorubicin in vitro did not correlate with the expression of P-glycoprotein. We conclude that high non-cytotoxic concentrations of verapamil were able to increase the in vitro doxorubicin sensitivity of fresh acute leukaemia and myeloma cells without detectable expression of the P-glycoprotein.

Published
1991

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