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4 results on '"Lubbert M."'

1. Long-term results of all-trans retinoic acid and arsenic trioxide in non-high-risk acute promyelocytic leukemia: update of the APL0406 Italian-German randomized trial

Author

Cicconi, L, Platzbecker, U, Avvisati, G, Paoloni, F, Thiede, C, Vignetti, M, Fazi, P, Ferrara, F, Divona, M, Albano, F, Efficace, F, Sborgia, M, Di Bona, E, Breccia, M, Borlenghi, E, Cairoli, R, Rambaldi, A, Melillo, L, La Nasa, G, Fiedler, W, Brossart, P, Hertenstein, B, Salih, H, Annibali, O, Wattad, M, Lubbert, M, Brandts, C, Hanel, M, Rollig, C, Schmitz, N, Lin, H, Frairia, C, Fozza, C, Maria D’Arco, A, Di Renzo, N, Cortelezzi, A, Fabbiano, F, Dohner, K, Ganser, A, Dohner, H, Amadori, S, Mandelli, F, Teresa Voso, M, Ehninger, G, Schlenk, R, Lo-Coco, F, Cicconi L, Platzbecker U, Avvisati G, Paoloni F, Thiede C, Vignetti M, Fazi P, Ferrara F, Divona M, Albano F, Efficace F, Sborgia M, Di Bona E, Breccia M, Borlenghi E, Cairoli R, Rambaldi A, Melillo L, La Nasa G, Fiedler W, Brossart P, Hertenstein B, Salih HR, Annibali O, Wattad M, Lubbert M, Brandts C, Hanel M, Rollig C, Schmitz N, Lin H, Frairia C, Fozza C, Maria D’Arco A, Di Renzo N, Cortelezzi A, Fabbiano F, Dohner K, Ganser A, Dohner H, Amadori S, Mandelli F, Teresa Voso M, Ehninger G, Schlenk RF, Lo-Coco F., Cicconi, L, Platzbecker, U, Avvisati, G, Paoloni, F, Thiede, C, Vignetti, M, Fazi, P, Ferrara, F, Divona, M, Albano, F, Efficace, F, Sborgia, M, Di Bona, E, Breccia, M, Borlenghi, E, Cairoli, R, Rambaldi, A, Melillo, L, La Nasa, G, Fiedler, W, Brossart, P, Hertenstein, B, Salih, H, Annibali, O, Wattad, M, Lubbert, M, Brandts, C, Hanel, M, Rollig, C, Schmitz, N, Lin, H, Frairia, C, Fozza, C, Maria D’Arco, A, Di Renzo, N, Cortelezzi, A, Fabbiano, F, Dohner, K, Ganser, A, Dohner, H, Amadori, S, Mandelli, F, Teresa Voso, M, Ehninger, G, Schlenk, R, Lo-Coco, F, Cicconi L, Platzbecker U, Avvisati G, Paoloni F, Thiede C, Vignetti M, Fazi P, Ferrara F, Divona M, Albano F, Efficace F, Sborgia M, Di Bona E, Breccia M, Borlenghi E, Cairoli R, Rambaldi A, Melillo L, La Nasa G, Fiedler W, Brossart P, Hertenstein B, Salih HR, Annibali O, Wattad M, Lubbert M, Brandts C, Hanel M, Rollig C, Schmitz N, Lin H, Frairia C, Fozza C, Maria D’Arco A, Di Renzo N, Cortelezzi A, Fabbiano F, Dohner K, Ganser A, Dohner H, Amadori S, Mandelli F, Teresa Voso M, Ehninger G, Schlenk RF, and Lo-Coco F.

Published
2020

2. Comprehensive mutational analysis of primary and relapse acute promyelocytic leukemia

Author

Madan, V, Shyamsunder, P, Han, L, Mayakonda, A, Nagata, Y, Sundaresan, J, Kanojia, D, Yoshida, K, Ganesan, S, Hattori, N, Fulton, N, Tan, K, Alpermann, T, Kuo, M, Rostami, S, Matthews, J, Sanada, M, Liu, L, Shiraishi, Y, Miyano, S, Chendamarai, E, Hou, H, Malnassy, G, Ma, T, Garg, M, Ding, L, Sun, Q, Chien, W, Ikezoe, T, Lill, M, Biondi, A, Larson, R, Powell, B, Lubbert, M, Chng, W, Tien, H, Heuser, M, Ganser, A, Koren-Michowitz, M, Kornblau, S, Kantarjian, H, Nowak, D, Hofmann, W, Yang, H, Stock, W, Ghavamzadeh, A, Alimoghaddam, K, Haferlach, T, Ogawa, S, Shih, L, Mathews, V, Koeffler, H, Madan V., Shyamsunder P., Han L., Mayakonda A., Nagata Y., Sundaresan J., Kanojia D., Yoshida K., Ganesan S., Hattori N., Fulton N., Tan K. -T., Alpermann T., Kuo M. -C., Rostami S., Matthews J., Sanada M., Liu L. -Z., Shiraishi Y., Miyano S., Chendamarai E., Hou H. -A., Malnassy G., Ma T., Garg M., Ding L. -W., Sun Q. -Y., Chien W., Ikezoe T., Lill M., Biondi A., Larson R. A., Powell B. L., Lubbert M., Chng W. J., Tien H. -F., Heuser M., Ganser A., Koren-Michowitz M., Kornblau S. M., Kantarjian H. M., Nowak D., Hofmann W. -K., Yang H., Stock W., Ghavamzadeh A., Alimoghaddam K., Haferlach T., Ogawa S., Shih L. -Y., Mathews V., Koeffler H. P., Madan, V, Shyamsunder, P, Han, L, Mayakonda, A, Nagata, Y, Sundaresan, J, Kanojia, D, Yoshida, K, Ganesan, S, Hattori, N, Fulton, N, Tan, K, Alpermann, T, Kuo, M, Rostami, S, Matthews, J, Sanada, M, Liu, L, Shiraishi, Y, Miyano, S, Chendamarai, E, Hou, H, Malnassy, G, Ma, T, Garg, M, Ding, L, Sun, Q, Chien, W, Ikezoe, T, Lill, M, Biondi, A, Larson, R, Powell, B, Lubbert, M, Chng, W, Tien, H, Heuser, M, Ganser, A, Koren-Michowitz, M, Kornblau, S, Kantarjian, H, Nowak, D, Hofmann, W, Yang, H, Stock, W, Ghavamzadeh, A, Alimoghaddam, K, Haferlach, T, Ogawa, S, Shih, L, Mathews, V, Koeffler, H, Madan V., Shyamsunder P., Han L., Mayakonda A., Nagata Y., Sundaresan J., Kanojia D., Yoshida K., Ganesan S., Hattori N., Fulton N., Tan K. -T., Alpermann T., Kuo M. -C., Rostami S., Matthews J., Sanada M., Liu L. -Z., Shiraishi Y., Miyano S., Chendamarai E., Hou H. -A., Malnassy G., Ma T., Garg M., Ding L. -W., Sun Q. -Y., Chien W., Ikezoe T., Lill M., Biondi A., Larson R. A., Powell B. L., Lubbert M., Chng W. J., Tien H. -F., Heuser M., Ganser A., Koren-Michowitz M., Kornblau S. M., Kantarjian H. M., Nowak D., Hofmann W. -K., Yang H., Stock W., Ghavamzadeh A., Alimoghaddam K., Haferlach T., Ogawa S., Shih L. -Y., Mathews V., and Koeffler H. P.

Abstract

Acute promyelocytic leukemia (APL) is a subtype of myeloid leukemia characterized by differentiation block at the promyelocyte stage. Besides the presence of chromosomal rearrangement t(15;17), leading to the formation of PML-RARA (promyelocytic leukemia-retinoic acid receptor alpha) fusion, other genetic alterations have also been implicated in APL. Here, we performed comprehensive mutational analysis of primary and relapse APL to identify somatic alterations, which cooperate with PML-RARA in the pathogenesis of APL. We explored the mutational landscape using whole-exome (n=12) and subsequent targeted sequencing of 398 genes in 153 primary and 69 relapse APL. Both primary and relapse APL harbored an average of eight non-silent somatic mutations per exome. We observed recurrent alterations of FLT3, WT1, NRAS and KRAS in the newly diagnosed APL, whereas mutations in other genes commonly mutated in myeloid leukemia were rarely detected. The molecular signature of APL relapse was characterized by emergence of frequent mutations in PML and RARA genes. Our sequencing data also demonstrates incidence of loss-of-function mutations in previously unidentified genes, ARID1B and ARID1A, both of which encode for key components of the SWI/SNF complex. We show that knockdown of ARID1B in APL cell line, NB4, results in large-scale activation of gene expression and reduced in vitro differentiation potential.

Published
2016

3. Comprehensive mutational analysis of primary and relapse acute promyelocytic leukemia

Author

Madan, V, Shyamsunder, P, Han, L, Mayakonda, A, Nagata, Y, Sundaresan, J, Kanojia, D, Yoshida, K, Ganesan, S, Hattori, N, Fulton, N, Tan, K, Alpermann, T, Kuo, M, Rostami, S, Matthews, J, Sanada, M, Liu, L, Shiraishi, Y, Miyano, S, Chendamarai, E, Hou, H, Malnassy, G, Ma, T, Garg, M, Ding, L, Sun, Q, Chien, W, Ikezoe, T, Lill, M, Biondi, A, Larson, R, Powell, B, Lubbert, M, Chng, W, Tien, H, Heuser, M, Ganser, A, Koren-Michowitz, M, Kornblau, S, Kantarjian, H, Nowak, D, Hofmann, W, Yang, H, Stock, W, Ghavamzadeh, A, Alimoghaddam, K, Haferlach, T, Ogawa, S, Shih, L, Mathews, V, Koeffler, H, Madan V., Shyamsunder P., Han L., Mayakonda A., Nagata Y., Sundaresan J., Kanojia D., Yoshida K., Ganesan S., Hattori N., Fulton N., Tan K. -T., Alpermann T., Kuo M. -C., Rostami S., Matthews J., Sanada M., Liu L. -Z., Shiraishi Y., Miyano S., Chendamarai E., Hou H. -A., Malnassy G., Ma T., Garg M., Ding L. -W., Sun Q. -Y., Chien W., Ikezoe T., Lill M., Biondi A., Larson R. A., Powell B. L., Lubbert M., Chng W. J., Tien H. -F., Heuser M., Ganser A., Koren-Michowitz M., Kornblau S. M., Kantarjian H. M., Nowak D., Hofmann W. -K., Yang H., Stock W., Ghavamzadeh A., Alimoghaddam K., Haferlach T., Ogawa S., Shih L. -Y., Mathews V., Koeffler H. P., Madan, V, Shyamsunder, P, Han, L, Mayakonda, A, Nagata, Y, Sundaresan, J, Kanojia, D, Yoshida, K, Ganesan, S, Hattori, N, Fulton, N, Tan, K, Alpermann, T, Kuo, M, Rostami, S, Matthews, J, Sanada, M, Liu, L, Shiraishi, Y, Miyano, S, Chendamarai, E, Hou, H, Malnassy, G, Ma, T, Garg, M, Ding, L, Sun, Q, Chien, W, Ikezoe, T, Lill, M, Biondi, A, Larson, R, Powell, B, Lubbert, M, Chng, W, Tien, H, Heuser, M, Ganser, A, Koren-Michowitz, M, Kornblau, S, Kantarjian, H, Nowak, D, Hofmann, W, Yang, H, Stock, W, Ghavamzadeh, A, Alimoghaddam, K, Haferlach, T, Ogawa, S, Shih, L, Mathews, V, Koeffler, H, Madan V., Shyamsunder P., Han L., Mayakonda A., Nagata Y., Sundaresan J., Kanojia D., Yoshida K., Ganesan S., Hattori N., Fulton N., Tan K. -T., Alpermann T., Kuo M. -C., Rostami S., Matthews J., Sanada M., Liu L. -Z., Shiraishi Y., Miyano S., Chendamarai E., Hou H. -A., Malnassy G., Ma T., Garg M., Ding L. -W., Sun Q. -Y., Chien W., Ikezoe T., Lill M., Biondi A., Larson R. A., Powell B. L., Lubbert M., Chng W. J., Tien H. -F., Heuser M., Ganser A., Koren-Michowitz M., Kornblau S. M., Kantarjian H. M., Nowak D., Hofmann W. -K., Yang H., Stock W., Ghavamzadeh A., Alimoghaddam K., Haferlach T., Ogawa S., Shih L. -Y., Mathews V., and Koeffler H. P.

Abstract

Acute promyelocytic leukemia (APL) is a subtype of myeloid leukemia characterized by differentiation block at the promyelocyte stage. Besides the presence of chromosomal rearrangement t(15;17), leading to the formation of PML-RARA (promyelocytic leukemia-retinoic acid receptor alpha) fusion, other genetic alterations have also been implicated in APL. Here, we performed comprehensive mutational analysis of primary and relapse APL to identify somatic alterations, which cooperate with PML-RARA in the pathogenesis of APL. We explored the mutational landscape using whole-exome (n=12) and subsequent targeted sequencing of 398 genes in 153 primary and 69 relapse APL. Both primary and relapse APL harbored an average of eight non-silent somatic mutations per exome. We observed recurrent alterations of FLT3, WT1, NRAS and KRAS in the newly diagnosed APL, whereas mutations in other genes commonly mutated in myeloid leukemia were rarely detected. The molecular signature of APL relapse was characterized by emergence of frequent mutations in PML and RARA genes. Our sequencing data also demonstrates incidence of loss-of-function mutations in previously unidentified genes, ARID1B and ARID1A, both of which encode for key components of the SWI/SNF complex. We show that knockdown of ARID1B in APL cell line, NB4, results in large-scale activation of gene expression and reduced in vitro differentiation potential.

Published
2016

4. RAS-pathway mutation patterns define epigenetic subclasses in juvenile myelomonocytic leukemia

Author

Lipka, D. B., Witte, T., Toth, R., Yang, J., Wiesenfarth, M., Nollke, P., Fischer, A., Brocks, D., Gu, Z., Park, J., Strahm, B., Wlodarski, M., Yoshimi, A., Claus, R., Lubbert, M., Busch, H., Boerries, M., Hartmann, M., Schonung, M., Kilik, U., Langstein, J., Wierzbinska, J. A., Pabst, C., Garg, S., Catala, A., De Moerloose, B., Dworzak, M., Hasle, H., Locatelli, Franco, Masetti, R., Schmugge, M., Smith, O., Stary, J., Ussowicz, M., Van Den Heuvel-Eibrink, M. M., Assenov, Y., Schlesner, M., Niemeyer, C., Flotho, C., Plass, C., Locatelli F. (ORCID:0000-0002-7976-3654), Lipka, D. B., Witte, T., Toth, R., Yang, J., Wiesenfarth, M., Nollke, P., Fischer, A., Brocks, D., Gu, Z., Park, J., Strahm, B., Wlodarski, M., Yoshimi, A., Claus, R., Lubbert, M., Busch, H., Boerries, M., Hartmann, M., Schonung, M., Kilik, U., Langstein, J., Wierzbinska, J. A., Pabst, C., Garg, S., Catala, A., De Moerloose, B., Dworzak, M., Hasle, H., Locatelli, Franco, Masetti, R., Schmugge, M., Smith, O., Stary, J., Ussowicz, M., Van Den Heuvel-Eibrink, M. M., Assenov, Y., Schlesner, M., Niemeyer, C., Flotho, C., Plass, C., and Locatelli F. (ORCID:0000-0002-7976-3654)

Abstract

Juvenile myelomonocytic leukemia (JMML) is an aggressive myeloproliferative disorder of early childhood characterized by mutations activating RAS signaling. Established clinical and genetic markers fail to fully recapitulate the clinical and biological heterogeneity of this disease. Here we report DNA methylome analysis and mutation profiling of 167 JMML samples. We identify three JMML subgroups with unique molecular and clinical characteristics. The high methylation group (HM) is characterized by somatic PTPN11 mutations and poor clinical outcome. The low methylation group is enriched for somatic NRAS and CBL mutations, as well as for Noonan patients, and has a good prognosis. The intermediate methylation group (IM) shows enrichment for monosomy 7 and somatic KRAS mutations. Hypermethylation is associated with repressed chromatin, genes regulated by RAS signaling, frequent co-occurrence of RAS pathway mutations and upregulation of DNMT1 and DNMT3B, suggesting a link between activation of the DNA methylation machinery and mutational patterns in JMML.

Published
2017

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