R
Roland Berger
Researcher at Memorial Sloan Kettering Cancer Center
Publications - 54
Citations - 2918
Roland Berger is an academic researcher from Memorial Sloan Kettering Cancer Center. The author has contributed to research in topics: Chromosomal translocation & Leukemia. The author has an hindex of 27, co-authored 54 publications receiving 2870 citations.
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Journal ArticleDOI
Characterization of acute promyelocytic leukemia cases lacking the classic t(15;17): results of the European Working Party
David Grimwade,Andrea Biondi,M J Mozziconacci,Anne Hagemeijer,Roland Berger,M. Neat,Kathy Howe,Nicole Dastugue,Joop H. Jansen,Isabelle Radford-Weiss,F. Lo Coco,Michel Lessard,Jesús M. Hernández,Eric Delabesse,David R. Head,Vincenzo Liso,Danielle Sainty,G. Flandrin,Ellen Solomon,Françoise Birg,Marina Lafage-Pochitaloff +20 more
TL;DR: In this paper, the authors used morphologic, cytogenetic, and molecular analyses for optimal management of acute promyelocytic leukemia (APL) patients and better understanding of the pathogenesis of the disease.
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The BCMA gene, preferentially expressed during B lymphoid maturation, is bidirectionally transcribed
Yacine Laabi,Marie-Pierre Gras,Jean-Claude Brouet,Roland Berger,Christian-Jacques Larsen,Andreas Tsapis +5 more
TL;DR: It is shown that the BCMA gene is organized into three exons and its major initiation transcription site is located 69 nucleotides downstream of a TATA box, suggesting a role for this gene in the B-cell developmental process.
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Essential thrombocythemias: clinical evolutionary and biological data
Sylvia Bellucci,Maud Janvier,Gérard Tobelem,Georges Flandrin,Yves Charpak,Roland Berger,Michel Boiron +6 more
TL;DR: This retrospective study reviewed 94 patients with thrombocythemia, finding that therapeutic measures must be conservative: anti‐aggregating drugs in small doses, and chemotherapy beginning with nonalkylating agents, are needed.
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P53 Gene Mutations in Acute Myeloid Leukemia With 17p Monosomy
Pierre Fenaux,Philippe Jonveaux,I. Quiquandon,Jean Luc Laï,Jean Michel Pignon,Loucheux-Lefebvre Mh,Francis Bauters,Roland Berger,Jean Pierre Kerckaert +8 more
TL;DR: The fact that P53 gene mutations occurred more often in patients with 17p monosomy seems to support the "recessive" model of tumor suppressive activity of the P53 genes rather than the "dominant" model, in which alteration of only one allele is sufficient for the development of malignancy.
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Fusion of Huntingtin Interacting Protein 1 to Platelet-Derived Growth Factor β Receptor (PDGFβR) in Chronic Myelomonocytic Leukemia With t(5;7)(q33;q11.2)
TL;DR: The fusion of the Huntingtin interactin protein 1 (HIP1) gene to the platelet-derived growth factor betareceptor (PDGF betaR) gene in a patient with chronic myelomonocytic leukemia is reported, consistent with an alternative mechanism for activation of PDGFbetaR tyrosine kinase activity by fusion with HIP1, leading to transformation of hematopoietic cells.