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5 results on '"Ganmore, Ithamar"'

1. Acute lymphoblastic leukemia in children with Down syndrome: a retrospective analysis from the Ponte di Legno study group

Author

Buitenkamp, Trudy D., Izraeli, Shai, Zimmermann, Martin, Forestier, Erik, Heerema, Nyla A., van den Heuvel-Eibrink, Marry M., Pieters, Rob, Korbijn, Carin M., Silverman, Lewis B., Schmiegelow, Kjeld, Liang, Der-Cheng, Horibe, Keizo, Arico, Maurizio, Biondi, Andrea, Basso, Giuseppe, Rabin, Karin R., Schrappe, Martin, Cario, Gunnar, Mann, Georg, Morak, Maria, Panzer-Grümayer, Renate, Mondelaers, Veerle, Lammens, Tim, Cavé, Hélène, Stark, Batia, Ganmore, Ithamar, Moorman, Anthony V., Vora, Ajay, Hunger, Stephen P., Pui, Ching-Hon, Mullighan, Charles G., Manabe, Atsushi, Escherich, Gabriele, Kowalczyk, Jerzy R., Whitlock, James A., and Zwaan, C. Michel

Published
2014
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2. Down syndrome acute lymphoblastic leukemia, a highly heterogeneous disease in which aberrant expression of CRLF2 is associated with mutated JAK2: a report from the International BFM Study Group

Author

Hertzberg, Libi, Vendramini, Elena, Ganmore, Ithamar, Cazzaniga, Gianni, Schmitz, Maike, Chalker, Jane, Shiloh, Ruth, Iacobucci, Ilaria, Shochat, Chen, Zeligson, Sharon, Cario, Gunnar, Stanulla, Martin, Strehl, Sabine, Russell, Lisa J., Harrison, Christine J., Bornhauser, Beat, Yoda, Akinori, Rechavi, Gideon, Bercovich, Dani, Borkhardt, Arndt, Kempski, Helena, te Kronnie, Geertruy, Bourquin, Jean-Pierre, Domany, Eytan, and Izraeli, Shai

Published
2010
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3. DOWN'S Syndrome Acute Lymphoblastic LEUKEMIA: A HIGHLY Heterogeneous DISEASE DRIVEN by an Aberrant CRLF2/JAK2 Cooperation – A REPORT FROM the Ibfm-STUDY GROUP.

Author

Hertzberg, Libi, primary, Vendramini, Elena, additional, Ganmore, Ithamar, additional, Cazzaniga, Giovanni, additional, Schmitz, Maike, additional, Shiloh, Ruth, additional, Chalker, Jane, additional, Iacobucci, Ilaria, additional, Shochat, Chen, additional, Zeligson, Sharon, additional, Cario, Gunnar, additional, Stanulla, Martin, additional, Strehl, Sabine, additional, Russel, Lisa J, additional, Harrison, Christine, additional, Bornhauser, Beat, additional, Yoda, Akinori, additional, Rechavi, Gideon, additional, Bercovich, Dani, additional, Borkardt, Arndt, additional, Kempski, Helena, additional, Kronnie, Geertruy te, additional, Bourquin, Jean-Pierre, additional, Domany, Eytan, additional, and Izraeli, Shai, additional

Published
2009
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4. Collaboration between Activating Mutations in JAK2 and Trisomy 21 in the Acute Lymphoblastic Leukemias of Down Syndrome (DS).

Author

Ganmore, Ithamar, primary, Bercovich, Dan, additional, Scott, Linda M., additional, Green, Anthony R., additional, Cazzaniga, Giovanni, additional, Biondi, Andrea, additional, Basso, Giuseppe, additional, Cario, Gunnar, additional, Schrappe, Martin, additional, Stanulla, Martin, additional, Strehl, Sabine, additional, Haas, Oskar A., additional, Binder, Vera, additional, Borkhardt, Arndt, additional, Trka, Jan, additional, Bielorei, Bella, additional, Avigad, Smadar, additional, Stark, Batia, additional, Bourquin, Jean-Pierre, additional, Smith, Owen, additional, Kempski, Helena, additional, and Izraeli, Shai, additional

Published
2007
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5. Down syndrome acute lymphoblastic leukemia, a highly heterogeneous disease in which aberrant expression of CRLF2is associated with mutated JAK2: a report from the International BFM Study Group

Author

Hertzberg, Libi, Vendramini, Elena, Ganmore, Ithamar, Cazzaniga, Gianni, Schmitz, Maike, Chalker, Jane, Shiloh, Ruth, Iacobucci, Ilaria, Shochat, Chen, Zeligson, Sharon, Cario, Gunnar, Stanulla, Martin, Strehl, Sabine, Russell, Lisa J., Harrison, Christine J., Bornhauser, Beat, Yoda, Akinori, Rechavi, Gideon, Bercovich, Dani, Borkhardt, Arndt, Kempski, Helena, te Kronnie, Geertruy, Bourquin, Jean-Pierre, Domany, Eytan, and Izraeli, Shai

Abstract

We report gene expression and other analyses to elucidate the molecular characteristics of acute lymphoblastic leukemia (ALL) in children with Down syndrome (DS). We find that by gene expression DS-ALL is a highly heterogeneous disease not definable as a unique entity. Nevertheless, 62% (33/53) of the DS-ALL samples analyzed were characterized by high expression of the type I cytokine receptor CRLF2caused by either immunoglobulin heavy locus (IgH@) translocations or by interstitial deletions creating chimeric transcripts P2RY8-CRLF2. In 3 of these 33 patients, a novel activating somatic mutation, F232C in CRLF2, was identified. Consistent with our previous research, mutations in R683 of JAK2were identified in 10 specimens (19% of the patients) and, interestingly, all 10 had high CRLF2expression. Cytokine receptor-like factor 2 (CRLF2) and mutated Janus kinase 2 (Jak2) cooperated in conferring cytokine-independent growth to BaF3 pro-B cells. Intriguingly, the gene expression signature of DS-ALL is enriched with DNA damage and BCL6responsive genes, suggesting the possibility of B-cell lymphocytic genomic instability. Thus, DS confers increased risk for genetically highly diverse ALLs with frequent overexpression of CRLF2, associated with activating mutations in the receptor itself or in JAK2. Our data also suggest that the majority of DS children with ALL may benefit from therapy blocking the CRLF2/JAK2 pathways.

Published
2010
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