Search

Your search keyword '"Lafage-Pochitaloff M"' showing total 15 results
Start Over Author "Lafage-Pochitaloff M" Publication Type Electronic Resources
15 results on '"Lafage-Pochitaloff M"'

1. The CADM1 tumor suppressor gene is a major candidate gene in MDS with deletion of the long arm of chromosome 11

Author

Lafage-Pochitaloff, M., Gerby, B., Baccini, V., Largeaud, L., Fregona, V., Prade, N., Juvin, P.Y., Jamrog, L.A., Bories, P., Hébrard, S., Lagarde, S., Mansat-De Mas, V., Dovey, O.M., Yusa, K., Vassiliou, G.S., Jansen, J.H., Tekath, T., Rombaut, D., Ameye, G., Barin, C., Bidet, A., Boudjarane, J., Collonge-Rame, M.A., Gervais, C., Ittel, A., Lefebvre, C., Luquet, I., Michaux, L., Nadal, N., Antoine-Poirel, H., Radford-Weiss, I., Ribourtout, B., Richebourg, S., Struski, S., Terré, C., Tigaud, I., Penther, D., Eclache, V., Fontenay, M., Broccardo, C., Delabesse, E., Lafage-Pochitaloff, M., Gerby, B., Baccini, V., Largeaud, L., Fregona, V., Prade, N., Juvin, P.Y., Jamrog, L.A., Bories, P., Hébrard, S., Lagarde, S., Mansat-De Mas, V., Dovey, O.M., Yusa, K., Vassiliou, G.S., Jansen, J.H., Tekath, T., Rombaut, D., Ameye, G., Barin, C., Bidet, A., Boudjarane, J., Collonge-Rame, M.A., Gervais, C., Ittel, A., Lefebvre, C., Luquet, I., Michaux, L., Nadal, N., Antoine-Poirel, H., Radford-Weiss, I., Ribourtout, B., Richebourg, S., Struski, S., Terré, C., Tigaud, I., Penther, D., Eclache, V., Fontenay, M., Broccardo, C., and Delabesse, E.

Abstract

Item does not contain fulltext

Published
2022

2. The CADM1 tumor suppressor gene is a major candidate gene in MDS with deletion of the long arm of chromosome 11

Author

Lafage-Pochitaloff, M., Gerby, B., Baccini, V., Largeaud, L., Fregona, V., Prade, N., Juvin, P.Y., Jamrog, L.A., Bories, P., Hébrard, S., Lagarde, S., Mansat-De Mas, V., Dovey, O.M., Yusa, K., Vassiliou, G.S., Jansen, J.H., Tekath, T., Rombaut, D., Ameye, G., Barin, C., Bidet, A., Boudjarane, J., Collonge-Rame, M.A., Gervais, C., Ittel, A., Lefebvre, C., Luquet, I., Michaux, L., Nadal, N., Antoine-Poirel, H., Radford-Weiss, I., Ribourtout, B., Richebourg, S., Struski, S., Terré, C., Tigaud, I., Penther, D., Eclache, V., Fontenay, M., Broccardo, C., Delabesse, E., Lafage-Pochitaloff, M., Gerby, B., Baccini, V., Largeaud, L., Fregona, V., Prade, N., Juvin, P.Y., Jamrog, L.A., Bories, P., Hébrard, S., Lagarde, S., Mansat-De Mas, V., Dovey, O.M., Yusa, K., Vassiliou, G.S., Jansen, J.H., Tekath, T., Rombaut, D., Ameye, G., Barin, C., Bidet, A., Boudjarane, J., Collonge-Rame, M.A., Gervais, C., Ittel, A., Lefebvre, C., Luquet, I., Michaux, L., Nadal, N., Antoine-Poirel, H., Radford-Weiss, I., Ribourtout, B., Richebourg, S., Struski, S., Terré, C., Tigaud, I., Penther, D., Eclache, V., Fontenay, M., Broccardo, C., and Delabesse, E.

Abstract

Contains fulltext : 244555.pdf (Publisher’s version ) (Open Access)

Published
2022

3. The CADM1 tumor suppressor gene is a major candidate gene in MDS with deletion of the long arm of chromosome 11

Author

Lafage-Pochitaloff, M., Gerby, B., Baccini, V., Largeaud, L., Fregona, V., Prade, N., Juvin, P.Y., Jamrog, L.A., Bories, P., Hébrard, S., Lagarde, S., Mansat-De Mas, V., Dovey, O.M., Yusa, K., Vassiliou, G.S., Jansen, J.H., Tekath, T., Rombaut, D., Ameye, G., Barin, C., Bidet, A., Boudjarane, J., Collonge-Rame, M.A., Gervais, C., Ittel, A., Lefebvre, C., Luquet, I., Michaux, L., Nadal, N., Antoine-Poirel, H., Radford-Weiss, I., Ribourtout, B., Richebourg, S., Struski, S., Terré, C., Tigaud, I., Penther, D., Eclache, V., Fontenay, M., Broccardo, C., Delabesse, E., Lafage-Pochitaloff, M., Gerby, B., Baccini, V., Largeaud, L., Fregona, V., Prade, N., Juvin, P.Y., Jamrog, L.A., Bories, P., Hébrard, S., Lagarde, S., Mansat-De Mas, V., Dovey, O.M., Yusa, K., Vassiliou, G.S., Jansen, J.H., Tekath, T., Rombaut, D., Ameye, G., Barin, C., Bidet, A., Boudjarane, J., Collonge-Rame, M.A., Gervais, C., Ittel, A., Lefebvre, C., Luquet, I., Michaux, L., Nadal, N., Antoine-Poirel, H., Radford-Weiss, I., Ribourtout, B., Richebourg, S., Struski, S., Terré, C., Tigaud, I., Penther, D., Eclache, V., Fontenay, M., Broccardo, C., and Delabesse, E.

Abstract

Contains fulltext : 244555.pdf (Publisher’s version ) (Open Access)

Published
2022

4. Dasatinib and low-intensity chemotherapy in elderly patients with Philadelphia chromosome-positive ALL

Author

Rousselot, P, Coudé, M, Gokbuget, N, Gambacorti Passerini, C, Hayette, S, Cayuela, J, Huguet, F, Leguay, T, Chevallier, P, Salanoubat, C, Bonmati, C, Alexis, M, Hunault, M, Glaisner, S, Agape, P, Berthou, C, Jourdan, E, Fernandes, J, Sutton, L, Banos, A, Reman, O, Lioure, B, Thomas, X, Ifrah, N, Lafage-Pochitaloff, M, Bornand, A, Morisset, L, Robin, V, Pfeifer, H, Delannoy, A, Ribera, J, Bassan, R, Delord, M, Hoelzer, D, Dombret, H, Ottmann, O, Rousselot, P, Coudé, M, Gokbuget, N, Gambacorti Passerini, C, Hayette, S, Cayuela, J, Huguet, F, Leguay, T, Chevallier, P, Salanoubat, C, Bonmati, C, Alexis, M, Hunault, M, Glaisner, S, Agape, P, Berthou, C, Jourdan, E, Fernandes, J, Sutton, L, Banos, A, Reman, O, Lioure, B, Thomas, X, Ifrah, N, Lafage-Pochitaloff, M, Bornand, A, Morisset, L, Robin, V, Pfeifer, H, Delannoy, A, Ribera, J, Bassan, R, Delord, M, Hoelzer, D, Dombret, H, and Ottmann, O

Abstract

Prognosis of Philadelphia-positive (Ph1) acutelymphoblastic leukemia (ALL) in the elderly has improved during the imatinib era. We investigated dasatinib, another potent tyrosine kinase inhibitor, in combination with low-intensity chemotherapy. Patients older than age 55 years were included in the European Working Group on Adult ALL(EWALL) study number 01 for Ph+ ALL (EWALL-PH-01 international study) and were treated with dasatinib 140 mg/day (100 mg/day over 70 years) with intrathecal chemotherapy, vincristine, and dexamethasone during induction. Patients in complete remission continued consolidation with dasatinib, sequentially with cytarabine, asparaginase, and methotrexate for 6 months. Maintenance therapy was dasatinib and vincristine/dexamethasone reinductions for 18months followed by dasatinib until relapse or death. Seventy-one patients with amedian age of 69 years were enrolled; 77% had a high comorbidity score.Complete remission ratewas 96% and 65% of patients achieved a3-logreduction inBCR-ABL1transcript levelsduringconsolidation.Only7patientsunderwent allogeneic hematopoietic stemcell transplantation. At 5 years, overall survivalwas 36% and up to 45% taking into account deaths unrelated to disease or treatment as competitors. Thirty-six patients relapsed, 24were tested formutation bySanger sequencing, and 75%were T315I-positive.BCR-ABL1T315Iwastested by allele-specific oligonucleotide reverse transcription-quantitative polymerase chain reaction in 43 patients and detection was associated with short-term relapses. Ten patients (23%) were positive before any therapy and 8 relapsed, all with this mutation. In conclusion, dasatinib combined with low-intensity chemotherapy was well-tolerated and gave long-term survival in 36% of elderly patients with Ph+ ALL. Monitoring of BCRABL1T315I from diagnosis identified patientswith at high risk of early relapse and may help to personalize therapy.

Published
2016

5. Myeloid cell differentiation arrest by miR-125b-1 in myelodysplasic syndrome and acute myeloid leukemia with the t(2;11)(p21;q23) translocation

Author

Bousquet, M. (Marina), Quelen, C. (Cathy), Rosati, R. (Roberto), Mas, V.M.D., Starza, R.L. (Roberta), Bastard, C. (Christian), Lippert, E. (Eric), Talmant, P. (Pascaline), Lafage-Pochitaloff, M. (Marina), Leroux, D. (Dominique), Gervais, C. (Carine), Viguié, F. (Franck), Lai, J.L., Terre, C. (Christine), Beverloo, H.B. (Berna), Sambani, C. (Costantina), Hagemeijer, A. (Anne), Marynen, P. (Peter), Delsol, G. (Georges), Dastugue, N. (Nicole), Mecucci, C. (Cristina), Brousset, P. (Pierre), Bousquet, M. (Marina), Quelen, C. (Cathy), Rosati, R. (Roberto), Mas, V.M.D., Starza, R.L. (Roberta), Bastard, C. (Christian), Lippert, E. (Eric), Talmant, P. (Pascaline), Lafage-Pochitaloff, M. (Marina), Leroux, D. (Dominique), Gervais, C. (Carine), Viguié, F. (Franck), Lai, J.L., Terre, C. (Christine), Beverloo, H.B. (Berna), Sambani, C. (Costantina), Hagemeijer, A. (Anne), Marynen, P. (Peter), Delsol, G. (Georges), Dastugue, N. (Nicole), Mecucci, C. (Cristina), and Brousset, P. (Pierre)

Abstract

Most chromosomal translocations in myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML) involve oncogenes that are either up-regulated or form part of new chimeric genes. The t(2;11)(p21;q23) translocation has been cloned in 19 cases of MDS and AML. In addition to this, we have shown that this translocation is associated with a strong up-regulation of miR-125b (from 6- to 90-fold). In vitro experiments revealed that miR-125b was able to interfere with primary human CD34+cell differentiation, and also inhibited terminal (monocytic and granulocytic) differentiation in HL60 and NB4 leukemic cell lines. Therefore, miR-125b up-regulation may represent a new mechanism of myeloid cell transformation, and myeloid neoplasms carrying the t(2;11) translocation define a new clinicopathological entity.

Published
2008
Full Text
View/download PDF

6. Report of 38 patients with hyperdiploid karyotype in acute myeloid leukemia: A groupe francais de cytogenetique hematologique study

Author

UCL - MD/MINT - Département de médecine interne, Terre, C., Luquet, I., Laie, J. L., Barin, C., Baranger, L., Bilhou-Nabera, C., Lippert, E., Gervais, C., Talmant, P., Cornillet-Lefebvre, P., Perot, C., Nadal, N., Mozziconacci, Marie-Joëlle, Lafage-Pochitaloff, M., Eclache, V., Mugneret, Francine, Lefebvre, Chantal, Herens, C., Speleman, F., Poirel, Hélène, Tigaud, I., Cabrol, C., Rousselot, P., Castaigne, S., Berger, R., 12th Congress of the European-Hematology-Association, UCL - MD/MINT - Département de médecine interne, Terre, C., Luquet, I., Laie, J. L., Barin, C., Baranger, L., Bilhou-Nabera, C., Lippert, E., Gervais, C., Talmant, P., Cornillet-Lefebvre, P., Perot, C., Nadal, N., Mozziconacci, Marie-Joëlle, Lafage-Pochitaloff, M., Eclache, V., Mugneret, Francine, Lefebvre, Chantal, Herens, C., Speleman, F., Poirel, Hélène, Tigaud, I., Cabrol, C., Rousselot, P., Castaigne, S., Berger, R., and 12th Congress of the European-Hematology-Association

Published
2007

7. Abnormalities of the long arm of chromosome 21 in 107 patients with hematopoietic disorders: a collaborative retrospective study of the Groupe Francais de Cytogenetique Hematologique

Author

UCL - Cliniques universitaires Saint-Luc, UCL - MD/MINT - Département de médecine interne, Jeandidier, E, Michaux, Lucienne, Dastugue, N., Mugneret, Francine, Lafage-Pochitaloff, M., Mozziconacci, Marie-Joëlle, Herens, C., Dumoulin, Christine, Talmant, P., Cornillet-Lefebvre, P., Luquet, I., Charrin, C., Barin, C., Collonge-Rame, MA, Perot, C., Van den Akker, J., Gregoire, MJ, Jonveaux, P., Baranger, L., Eclache-Saudreau, V, Pages, MP., Cabrol, C., Terre, C., Berger, R., UCL - Cliniques universitaires Saint-Luc, UCL - MD/MINT - Département de médecine interne, Jeandidier, E, Michaux, Lucienne, Dastugue, N., Mugneret, Francine, Lafage-Pochitaloff, M., Mozziconacci, Marie-Joëlle, Herens, C., Dumoulin, Christine, Talmant, P., Cornillet-Lefebvre, P., Luquet, I., Charrin, C., Barin, C., Collonge-Rame, MA, Perot, C., Van den Akker, J., Gregoire, MJ, Jonveaux, P., Baranger, L., Eclache-Saudreau, V, Pages, MP., Cabrol, C., Terre, C., and Berger, R.

Abstract

Chromosome 21 is frequently rearranged in hematopoietic malignancies. In order to detect new chromosomal aberrations, the Groupe Francais de Cytogenetique Hematologique collected a series of 107 patients with various hematologic disorders and acquired structural abnormalities of the long arm of chromosome 21. The abnormalities were subclassified into 10 groups, according to the location of the 21q breakpoint and the type of abnormality. Band 21q22 was implicated in 72 patients (excluding duplications, triplications, and amplifications). The involvement of the RUNX1 gene was confirmed in 10 novel translocations, but the gene partners were not identified. Eleven novel translocations rearranging band 21q22 with hands 1q25, 2p21, 2q37, 3p21, 3p23, 4q31, 6p24-p25, 6p12, 7p15, 16p11, and 18q21 were detected. Rearrangements of band 21q11 and 21q21 were detected in six novel translocations with 5p15, 6p21, 15q21, 16p13, and 20q11 and with 1p33, 3q27, 5p14, 11q11, and 14q11, respectively. Duplications, triplications, amplifications, and isodicentric chromosomes were detected in eight, three, eight, and three patients, respectively. The present study shows both the wide distribution of the breakpoints on the long arm of chromosome 21 in hematopoietic malignancy and the diversity of the chromosomal rearrangements and the hematologic disorders involved. The findings invite further investigation of the 21q abnormalities to detect their associated molecular rearrangements. (c) 2006 Elsevier Inc. All rights reserved.

Published
2006

8. Identification of a novel CBFB-MYH11 transcript: implications for RT-PCR diagnosis.

Author

Reijden, B.A. van der, Wit, L. de, Poel, S.C. van der, Luiten, E.B., Lafage-Pochitaloff, M., Dastugue, N., Gabert, J., Lowenberg, B., Jansen, J.H., Reijden, B.A. van der, Wit, L. de, Poel, S.C. van der, Luiten, E.B., Lafage-Pochitaloff, M., Dastugue, N., Gabert, J., Lowenberg, B., and Jansen, J.H.

Abstract

Item does not contain fulltext, INTRODUCTION:: The chromosome rearrangements inv(16)(p13q22) or t(16;16)(p13;q22) are present in approximately 10% of all cases with de novo acute myeloid leukemia and define a subgroup with a favorable prognosis. Both aberrations result in a CBFB-MYH11 fusion gene that can be detected by RT-PCR. PATIENTS AND METHODS:: To date, a total of 10 different in-frame CBFB-MYH11 fusion transcripts have been identified. A newly described transcript can not be amplified with the commonly used PCR primers since the MYH11 junction is located outside the amplified region (MYH11 cDNA position 2134). RESULTS:: We describe here a robust two-step RT-PCR assay that reliably detects all known CBFB-MYH11 transcripts types, including the new variant. CONCLUSION:: Because all previously established RT-PCR protocols may miss the new CBFB-MYH11 transcript, we propose to use the improved RT-PCR approach described here for the reliable detection of all known CBFB-MYH11 fusion transcripts.

Published
2001

9. Identification of a novel CBFB-MYH11 transcript: implications for RT-PCR diagnosis.

Author

Reijden, B.A. van der, Wit, L. de, Poel, S.C. van der, Luiten, E.B., Lafage-Pochitaloff, M., Dastugue, N., Gabert, J., Lowenberg, B., Jansen, J.H., Reijden, B.A. van der, Wit, L. de, Poel, S.C. van der, Luiten, E.B., Lafage-Pochitaloff, M., Dastugue, N., Gabert, J., Lowenberg, B., and Jansen, J.H.

Abstract

Item does not contain fulltext, INTRODUCTION:: The chromosome rearrangements inv(16)(p13q22) or t(16;16)(p13;q22) are present in approximately 10% of all cases with de novo acute myeloid leukemia and define a subgroup with a favorable prognosis. Both aberrations result in a CBFB-MYH11 fusion gene that can be detected by RT-PCR. PATIENTS AND METHODS:: To date, a total of 10 different in-frame CBFB-MYH11 fusion transcripts have been identified. A newly described transcript can not be amplified with the commonly used PCR primers since the MYH11 junction is located outside the amplified region (MYH11 cDNA position 2134). RESULTS:: We describe here a robust two-step RT-PCR assay that reliably detects all known CBFB-MYH11 transcripts types, including the new variant. CONCLUSION:: Because all previously established RT-PCR protocols may miss the new CBFB-MYH11 transcript, we propose to use the improved RT-PCR approach described here for the reliable detection of all known CBFB-MYH11 fusion transcripts.

Published
2001

10. Identification of a novel CBFB-MYH11 transcript: implications for RT-PCR diagnosis.

Author

Reijden, B.A. van der, Wit, L. de, Poel, S.C. van der, Luiten, E.B., Lafage-Pochitaloff, M., Dastugue, N., Gabert, J., Lowenberg, B., Jansen, J.H., Reijden, B.A. van der, Wit, L. de, Poel, S.C. van der, Luiten, E.B., Lafage-Pochitaloff, M., Dastugue, N., Gabert, J., Lowenberg, B., and Jansen, J.H.

Abstract

Item does not contain fulltext, INTRODUCTION:: The chromosome rearrangements inv(16)(p13q22) or t(16;16)(p13;q22) are present in approximately 10% of all cases with de novo acute myeloid leukemia and define a subgroup with a favorable prognosis. Both aberrations result in a CBFB-MYH11 fusion gene that can be detected by RT-PCR. PATIENTS AND METHODS:: To date, a total of 10 different in-frame CBFB-MYH11 fusion transcripts have been identified. A newly described transcript can not be amplified with the commonly used PCR primers since the MYH11 junction is located outside the amplified region (MYH11 cDNA position 2134). RESULTS:: We describe here a robust two-step RT-PCR assay that reliably detects all known CBFB-MYH11 transcripts types, including the new variant. CONCLUSION:: Because all previously established RT-PCR protocols may miss the new CBFB-MYH11 transcript, we propose to use the improved RT-PCR approach described here for the reliable detection of all known CBFB-MYH11 fusion transcripts.

Published
2001

11. Characterization of acute promyelocytic leukemia cases lacking the classic t(15;17)

Author

Grimwade, D., Biondi, A., Mozziconacci, M.J., Hagemeijer, A., Berger, R.A., Neat, M., Howe, K., Dastugue, N., Jansen, J.H., Radford-Weiss, I., Lo Coco, F., Lessard, M., Hernandez, J.M., Delabesse, E., Head, D., Liso, V., Sainty, D., Flandrin, G., Solomon, E., Birg, F., Lafage-Pochitaloff, M., Grimwade, D., Biondi, A., Mozziconacci, M.J., Hagemeijer, A., Berger, R.A., Neat, M., Howe, K., Dastugue, N., Jansen, J.H., Radford-Weiss, I., Lo Coco, F., Lessard, M., Hernandez, J.M., Delabesse, E., Head, D., Liso, V., Sainty, D., Flandrin, G., Solomon, E., Birg, F., and Lafage-Pochitaloff, M.

Abstract

Item does not contain fulltext

Published
2000

12. Characterization of acute promyelocytic leukemia cases lacking the classic t(15;17)

Author

Grimwade, D., Biondi, A., Mozziconacci, M.J., Hagemeijer, A., Berger, R.A., Neat, M., Howe, K., Dastugue, N., Jansen, J.H., Radford-Weiss, I., Lo Coco, F., Lessard, M., Hernandez, J.M., Delabesse, E., Head, D., Liso, V., Sainty, D., Flandrin, G., Solomon, E., Birg, F., Lafage-Pochitaloff, M., Grimwade, D., Biondi, A., Mozziconacci, M.J., Hagemeijer, A., Berger, R.A., Neat, M., Howe, K., Dastugue, N., Jansen, J.H., Radford-Weiss, I., Lo Coco, F., Lessard, M., Hernandez, J.M., Delabesse, E., Head, D., Liso, V., Sainty, D., Flandrin, G., Solomon, E., Birg, F., and Lafage-Pochitaloff, M.

Abstract

Item does not contain fulltext

Published
2000

13. Characterization of acute promyelocytic leukemia cases lacking the classic t(15;17)

Author

Grimwade, D., Biondi, A., Mozziconacci, M.J., Hagemeijer, A., Berger, R.A., Neat, M., Howe, K., Dastugue, N., Jansen, J.H., Radford-Weiss, I., Lo Coco, F., Lessard, M., Hernandez, J.M., Delabesse, E., Head, D., Liso, V., Sainty, D., Flandrin, G., Solomon, E., Birg, F., Lafage-Pochitaloff, M., Grimwade, D., Biondi, A., Mozziconacci, M.J., Hagemeijer, A., Berger, R.A., Neat, M., Howe, K., Dastugue, N., Jansen, J.H., Radford-Weiss, I., Lo Coco, F., Lessard, M., Hernandez, J.M., Delabesse, E., Head, D., Liso, V., Sainty, D., Flandrin, G., Solomon, E., Birg, F., and Lafage-Pochitaloff, M.

Abstract

Item does not contain fulltext

Published
2000

14. Genomic acute myeloid leukemia-associated inv(16)(p13q22) breakpoints are tightly clustered.

Author

Reijden, B.A. van der, Dauwerse, H.G., Giles, R.H., Jagmohan-Changur, S, Wijmenga, C., Liu, P.P., Smit, B., Wessels, H.W., Beverstock, G.C., Jotterand-Bellomo, M., Martinet, D., Muhlematter, D., Lafage-Pochitaloff, M., Gabert, J., Reiffers, J., Bilhou-Nabera, C, Ommen, G.J.B. van, Hagemeijer, A., Breuning, M.H., Reijden, B.A. van der, Dauwerse, H.G., Giles, R.H., Jagmohan-Changur, S, Wijmenga, C., Liu, P.P., Smit, B., Wessels, H.W., Beverstock, G.C., Jotterand-Bellomo, M., Martinet, D., Muhlematter, D., Lafage-Pochitaloff, M., Gabert, J., Reiffers, J., Bilhou-Nabera, C, Ommen, G.J.B. van, Hagemeijer, A., and Breuning, M.H.

Abstract

Item does not contain fulltext, The inv(16) and related t(16;16) are found in 10% of all cases with de novo acute myeloid leukemia. In these rearrangements the core binding factor beta (CBFB) gene on 16q22 is fused to the smooth muscle myosin heavy chain gene (MYH11) on 16p13. To gain insight into the mechanisms causing the inv(16) we have analysed 24 genomic CBFB-MYH11 breakpoints. All breakpoints in CBFB are located in a 15-Kb intron. More than 50% of the sequenced 6.2 Kb of this intron consists of human repetitive elements. Twenty-one of the 24 breakpoints in MYH11 are located in a 370-bp intron. The remaining three breakpoints in MYH11 are located more upstream. The localization of three breakpoints adjacent to a V(D)J recombinase signal sequence in MYH11 suggests a V(D)J recombinase-mediated rearrangement in these cases. V(D)J recombinase-associated characteristics (small nucleotide deletions and insertions of random nucleotides) were detected in six other cases. CBFB and MYH11 duplications were detected in four of six cases tested.

Published
1999

15. Genomic acute myeloid leukemia-associated inv(16)(p13q22) breakpoints are tightly clustered.

Author

Reijden, B.A. van der, Dauwerse, H.G., Giles, R.H., Jagmohan-Changur, S, Wijmenga, C., Liu, P.P., Smit, B., Wessels, H.W., Beverstock, G.C., Jotterand-Bellomo, M., Martinet, D., Muhlematter, D., Lafage-Pochitaloff, M., Gabert, J., Reiffers, J., Bilhou-Nabera, C, Ommen, G.J.B. van, Hagemeijer, A., Breuning, M.H., Reijden, B.A. van der, Dauwerse, H.G., Giles, R.H., Jagmohan-Changur, S, Wijmenga, C., Liu, P.P., Smit, B., Wessels, H.W., Beverstock, G.C., Jotterand-Bellomo, M., Martinet, D., Muhlematter, D., Lafage-Pochitaloff, M., Gabert, J., Reiffers, J., Bilhou-Nabera, C, Ommen, G.J.B. van, Hagemeijer, A., and Breuning, M.H.

Abstract

Item does not contain fulltext, The inv(16) and related t(16;16) are found in 10% of all cases with de novo acute myeloid leukemia. In these rearrangements the core binding factor beta (CBFB) gene on 16q22 is fused to the smooth muscle myosin heavy chain gene (MYH11) on 16p13. To gain insight into the mechanisms causing the inv(16) we have analysed 24 genomic CBFB-MYH11 breakpoints. All breakpoints in CBFB are located in a 15-Kb intron. More than 50% of the sequenced 6.2 Kb of this intron consists of human repetitive elements. Twenty-one of the 24 breakpoints in MYH11 are located in a 370-bp intron. The remaining three breakpoints in MYH11 are located more upstream. The localization of three breakpoints adjacent to a V(D)J recombinase signal sequence in MYH11 suggests a V(D)J recombinase-mediated rearrangement in these cases. V(D)J recombinase-associated characteristics (small nucleotide deletions and insertions of random nucleotides) were detected in six other cases. CBFB and MYH11 duplications were detected in four of six cases tested.

Published
1999

Catalog

Books, media, physical & digital resources
See catalog results