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1,088 results on '"Schnittger, S"'

202. Genetic defects in PRC2 components other than EZH2 are not common in myeloid malignancies

Author

Kroeze, L., Nikoloski, G., da Silva-Coelho, P., van Hoogen, P., Stevens-Linders, E., Kuiper, R.P., Schnittger, S., Haferlach, T., Pahl, H.L., van der Reijden, B.A., Jansen, J.H., Kroeze, L., Nikoloski, G., da Silva-Coelho, P., van Hoogen, P., Stevens-Linders, E., Kuiper, R.P., Schnittger, S., Haferlach, T., Pahl, H.L., van der Reijden, B.A., and Jansen, J.H.

Abstract

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Published
2012

203. A variant allele of Growth Factor Independence 1 (GFI1) is associated with acute myeloid leukemia.

Author

Khandanpour, C., Thiede, C., Valk, P.J., Sharif-Askari, E., Nuckel, H., Lohmann, D., Horsthemke, B., Siffert, W., Neubauer, A., Grzeschik, K.H., Bloomfield, C.D., Marcucci, G., Maharry, K., Slovak, M.L., Reijden, B.A. van der, Jansen, J.H., Schackert, H.K., Afshar, K., Schnittger, S., Peeters, J.K., Kroschinsky, F., Ehninger, G., Lowenberg, B., Duhrsen, U., Moroy, T., Khandanpour, C., Thiede, C., Valk, P.J., Sharif-Askari, E., Nuckel, H., Lohmann, D., Horsthemke, B., Siffert, W., Neubauer, A., Grzeschik, K.H., Bloomfield, C.D., Marcucci, G., Maharry, K., Slovak, M.L., Reijden, B.A. van der, Jansen, J.H., Schackert, H.K., Afshar, K., Schnittger, S., Peeters, J.K., Kroschinsky, F., Ehninger, G., Lowenberg, B., Duhrsen, U., and Moroy, T.

Abstract

Item does not contain fulltext, The GFI1 gene encodes a transcriptional repressor, which regulates myeloid differentiation. In the mouse, Gfi1 deficiency causes neutropenia and an accumulation of granulomonocytic precursor cells that is reminiscent of a myelodysplastic syndrome. We report here that a variant allele of GFI1 (GFI1(36N)) is associated with acute myeloid leukemia (AML) in white subjects with an odds ratio of 1.6 (P < 8 x 10(-5)). The GFI1(36N) variant occurred in 1806 AML patients with an allele frequency of 0.055 compared with 0.035 in 1691 healthy control patients in 2 independent cohorts. We observed that both GFI1 variants maintain the same activity as transcriptional repressors but differ in their regulation by the AML1/ETO (RUNX1/RUNX1T1) fusion protein produced in AML patients with a t(8;21) translocation. AML1/ETO interacts and colocalizes with the more common GFI1(36S) form in the nucleus and inhibits its repressor activity. However, the variant GFI1(36N) protein has a different subnuclear localization than GFI1(36S). As a consequence, AML1/ETO does not colocalize with GFI1(36N) and is unable to inhibit its repressor activity. We conclude that both variants of GFI1 differ in their ability to be regulated by interacting proteins and that the GFI1(36N) variant form exhibits distinct biochemical features that may confer a predisposition to AML.

Published
2010

204. Real-time quantitative polymerase chain reaction detection of minimal residual disease by standardized WT1 assay to enhance risk stratification in acute myeloid leukemia: a European LeukemiaNet study.

Author

Cilloni, D., Renneville, A., Hermitte, F., Hills, R.K., Daly, S., Jovanovic, J.V., Gottardi, E., Fava, M., Schnittger, S., Weiss, T., Izzo, B., Nomdedeu, J., Heijden, A. van der, Reijden, B.A. van der, Jansen, J.H., Velden, V.H. van der, Ommen, H., Preudhomme, C., Saglio, G., Grimwade, D., Cilloni, D., Renneville, A., Hermitte, F., Hills, R.K., Daly, S., Jovanovic, J.V., Gottardi, E., Fava, M., Schnittger, S., Weiss, T., Izzo, B., Nomdedeu, J., Heijden, A. van der, Reijden, B.A. van der, Jansen, J.H., Velden, V.H. van der, Ommen, H., Preudhomme, C., Saglio, G., and Grimwade, D.

Abstract

Item does not contain fulltext, PURPOSE: Risk stratification in acute myeloid leukemia (AML) is currently based on pretreatment characteristics. It remains to be established whether relapse risk can be better predicted through assessment of minimal residual disease (MRD). One proposed marker is the Wilms tumor gene WT1, which is overexpressed in most patients with AML, thus providing a putative target for immunotherapy, although in the absence of a standardized assay, its utility for MRD monitoring remains controversial. PATIENTS AND METHODS: Nine published and in-house real-time quantitative polymerase chain reaction WT1 assays were systematically evaluated within the European LeukemiaNet; the best-performing assay was applied to diagnostic AML samples (n = 620), follow-up samples from 129 patients treated with intensive combination chemotherapy, and 204 normal peripheral blood (PB) and bone marrow (BM) controls. RESULTS: Considering relative levels of expression detected in normal PB and BM, WT1 was sufficiently overexpressed to discriminate > or = 2-log reduction in transcripts in 46% and 13% of AML patients, according to the respective follow-up sample source. In this informative group, greater WT1 transcript reduction after induction predicted reduced relapse risk (hazard ratio, 0.54 per log reduction; 95% CI, 0.36 to 0.83; P = .004) that remained significant when adjusted for age, WBC count, and cytogenetics. Failure to reduce WT1 transcripts below the threshold limits defined in normal controls by the end of consolidation also predicted increased relapse risk (P = .004). CONCLUSION: Application of a standardized WT1 assay provides independent prognostic information in AML, lending support to incorporation of early assessment of MRD to develop more robust risk scores, to enhance risk stratification, and to identify patients who may benefit from allogeneic transplantation.

Published
2009

205. A one-mutation mathematical model can explain the age incidence of acute myeloid leukemia with mutated nucleophosmin (NPM1)

Author

Liso, A. (Arcangelo), Castiglione, F. (Filippo), Cappuccio, A. (Antonio), Stracci, F. (Fabrizio), Schlenk, R.F. (Richard), Amadori, S. (Sergio), Thiede, C. (Christian), Schnittger, S. (Susanne), Valk, P.J.M. (Peter), Döhner, K. (Konstanze), Martelli, M.F. (Massimo F.), Schaich, M. (Markus), Krauter, J., Ganser, A. (Arnold), Bolli, N. (Niccolò), Löwenberg, B. (Bob), Haferlach, T. (Torsten), Ehninger, G. (Gerhard), Mandelli, F. (Franco), Michor, F. (Franziska), Falini, B., Liso, A. (Arcangelo), Castiglione, F. (Filippo), Cappuccio, A. (Antonio), Stracci, F. (Fabrizio), Schlenk, R.F. (Richard), Amadori, S. (Sergio), Thiede, C. (Christian), Schnittger, S. (Susanne), Valk, P.J.M. (Peter), Döhner, K. (Konstanze), Martelli, M.F. (Massimo F.), Schaich, M. (Markus), Krauter, J., Ganser, A. (Arnold), Bolli, N. (Niccolò), Löwenberg, B. (Bob), Haferlach, T. (Torsten), Ehninger, G. (Gerhard), Mandelli, F. (Franco), Michor, F. (Franziska), and Falini, B.

Abstract

Acute myeloid leukemia with mutated NPM1 gene and aberrant cytoplasmic expression of nucleophosmin (NPMc+acute myeloid leukemia) shows distinctive biological and clinical features. Experimental evidence of the oncogenic potential of the nucleophosmin mutant is, however, still lacking, and it is unclear whether other genetic lesion(s), e.g. FLT3 internal tandem duplication, cooperate with NPM1 mutations in acute myeloid leukemia development. An analysis of age-specific incidence, together with mathematical modeling of acute myeloid leukemia epidemiology, can help to uncover the number of genetic events needed to cause leukemia. We collected data on age at diagnosis of acute myeloid leukemia patients from five European Centers in Germany, The Netherlands and Italy, and determined the age-specific incidence of AML with mutated NPM1 (a total of 1,444 cases) for each country. Linear regression of the curves representing age-specific rates of diagnosis per year showed similar slopes of about 4 on a double logarithmic scale. We then adapted a previously designed mathematical model of hematopoietic tumorigenesis to analyze the age incidence of acute myeloid leukemia with mutated NPM1 and found that a one-mutation model can explain the incidence curve of this leukemia entity. This model fits with the hypothesis that NPMc+acute myeloid leukemia arises from an NPM1 mutation with haploinsufficiency of the wild-type NPM1 allele.

Published
2008
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206. A one-mutation mathematical model can explain the age incidence of acute myeloid leukemia with mutated nucleophosmin (NPM1)

Author

Liso, A, Castiglione, F, Cappuccio, A, Stracci, F, Schlenk, RF, Amadori, S, Thiede, C, Schnittger, S, Valk, Peter, Dohner, K, Martelli, MF, Schaich, M, Krauter, J, Ganser, A, Martelli, MP, Bolli, N, Löwenberg, Bob, Haferlach, T, Ehninger, G, Mandelli, F, Dohner, H, Michor, F, Falini, B, Liso, A, Castiglione, F, Cappuccio, A, Stracci, F, Schlenk, RF, Amadori, S, Thiede, C, Schnittger, S, Valk, Peter, Dohner, K, Martelli, MF, Schaich, M, Krauter, J, Ganser, A, Martelli, MP, Bolli, N, Löwenberg, Bob, Haferlach, T, Ehninger, G, Mandelli, F, Dohner, H, Michor, F, and Falini, B

Abstract

Acute myeloid leukemia with mutated NPM1 gene and aberrant cytoplasmic expression of nucleophosmin (NPMc(+) acute myeloid leukemia) shows distinctive biological and clinical features. Experimental evidence of the oncogenic potential of the nucleophosmin mutant is, however, still lacking, and it is unclear whether other genetic lesion(s), e.g. FLT3 internal tandem duplication, cooperate with NPM1 mutations in acute myeloid leukemia development. An analysis of age-specific incidence, together with mathematical modeling of acute myeloid leukemia epidemiology, can help to uncover the number of genetic events needed to cause leukemia. We collected data on age at diagnosis of acute myeloid leukemia patients from five European Centers in Germany, The Netherlands and Italy, and determined the age-specific incidence of AML with mutated NPM1 (a total of 1,444 cases) for each country. Linear regression of the curves representing age-specific rates of diagnosis per year showed similar slopes of about 4 on a double logarithmic scale. We then adapted a previously designed mathematical model of hematopoietic tumorigenesis to analyze the age incidence of acute myeloid leukemia with mutated NPM1 and found that a one-mutation model can explain the incidence curve of this leukemia entity. This model fits with the hypothesis that NPMc(+) acute myeloid leukemia arises from an NPM1 mutation with haploinsufficiency of the wild-type NPM1 allele.

Published
2008

207. The role of different genetic subtypes of CEBPA mutated AML

Author

Fasan, A, primary, Haferlach, C, additional, Alpermann, T, additional, Jeromin, S, additional, Grossmann, V, additional, Eder, C, additional, Weissmann, S, additional, Dicker, F, additional, Kohlmann, A, additional, Schindela, S, additional, Kern, W, additional, Haferlach, T, additional, and Schnittger, S, additional

Published
2013
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210. The Association of Mutations in RUNX1 and CSF3R with the Development of Leukemia in Severe Congenital Neutropenia: A unique pathway in leukemogenesis

Author

Skokowa, J, primary, Steinemann, D, additional, Zeidler, C, additional, Makaryan, V, additional, Beekman, R, additional, Klimiankou, M, additional, Ünalan, M, additional, Kandabarau, S, additional, Schnittger, S, additional, Kohlmann, A, additional, Valkhof, MG, additional, Hoogenboezem, R, additional, Göhring, G, additional, Schlegelberger, B, additional, Stanulla, M, additional, Vandenberghe, P, additional, Donadieu, J, additional, Touw, IP, additional, Dale, DC, additional, and Welte, K, additional

Published
2013
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214. P-027 Recurrent SETBP1 mutations in atypical chronic myeloid leukemia

Author

Piazza, R., primary, Valletta, S., additional, Winkelmann, N., additional, Redaelli, S., additional, Spinelli, R., additional, Pirola, A., additional, Antolini, L., additional, Mologni, L., additional, Donadoni, C., additional, Papaemmanuil, E., additional, Schnittger, S., additional, Kim, D.W., additional, Boultwood, J., additional, Rossi, F., additional, Gaipa, G., additional, De Martini, G.P., additional, Di Celle, P.F., additional, Jang, H.G., additional, Fantin, V., additional, Bignell, G.R., additional, Magistroni, V., additional, Haferlach, T., additional, Pogliani, E.M., additional, Campbell, P.J., additional, Chase, A.J., additional, Tapper, W.J., additional, Cross, N.C., additional, and Gambacorti-Passerini, C., additional

Published
2013
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217. Characterization, mapping and partial cDNA sequence of the 57-kD intracellular Ki-1 antigen

Author

Jörg Kobarg, Schnittger S, Fonatsch C, Lemke H, Ma, Bowen, Buck F, and Hp, Hansen

Subjects
Mice, Inbred BALB C, DNA, Complementary, Base Sequence, Molecular Sequence Data, Restriction Mapping, Ki-1 Antigen, Spodoptera, Cell Line, Chromosome Banding, Molecular Weight, Mice, Animals, Humans, Amino Acid Sequence, Cloning, Molecular, Chromosomes, Human, Pair 9, Baculoviridae, In Situ Hybridization, Fluorescence
Abstract

A novel antigen was identified by the cross-reactivity of the anti-CD30 antibody Ki-1. This 57-kD intracellular Ki-1 antigen (Ki-1/57) is induced upon activation of leukocytes and is transported to the nuclear compartment. We describe the partial cloning and sequencing of the Ki-1/57 cDNA from a lambda gt 11-cDNA library derived from the Hodgkin-analogous cell line L540. New monoclonal antibodies were produced against the recombinant Ki-1/57 protein fragment which were used to confirm that the Ki-1/57 antigen is associated with kinase activity and is expressed in a variety of tumor cell lines and in activated but not resting leukocytes. The Ki-1/57 gene was mapped to the bands 9q22.3-31 of human chromosome 9. This is an area which appears to be associated with secondary chromosomal aberrations in acute myeloid leukemias.

Published
1997

220. Both carboxy-terminus NES motif and mutated tryptophan(s) are crucial for aberrant nuclear export of nucleophosmin leukemic mutants in NPMc+ AML

Author

Falini, B, Bolli, N, Shan, J, Martelli, M, Liso, A, Pucciarini, A, Bigerna, B, Pasqualucci, L, Mannucci, R, Rosati, R, Gorello, P, Diverio, D, Roti, G, Tiacci, E, Cazzaniga, G, Biondi, A, Schnittger, S, Haferlach, T, Hiddemann, W, Gu, W, Mecucci, C, Nicoletti, I, Martelli, MP, Martelli, MF, Nicoletti, I., BIONDI, ANDREA, Falini, B, Bolli, N, Shan, J, Martelli, M, Liso, A, Pucciarini, A, Bigerna, B, Pasqualucci, L, Mannucci, R, Rosati, R, Gorello, P, Diverio, D, Roti, G, Tiacci, E, Cazzaniga, G, Biondi, A, Schnittger, S, Haferlach, T, Hiddemann, W, Gu, W, Mecucci, C, Nicoletti, I, Martelli, MP, Martelli, MF, Nicoletti, I., and BIONDI, ANDREA

Abstract

We recently identified aberrant cytoplasmic expression of nucleophosmin (NPM) as the immunohistochemical marker of a large subgroup of acute myeloid leukemia (AML) (about one-third of adult AML) that is characterized by normal karyotype and mutations occurring at the exon-12 of the NPM gene. In this paper, we have elucidated the molecular mechanism underlying the abnormal cytoplasmic localization of NPM. All 29 AML-associated mutated NPM alleles so far identified encode abnormal proteins which have acquired at the C-terminus a nuclear export signal (NES) motif and lost both tryptophan residues 288 and 290 (or only the residue 290) which determine nucleolar localization. We show for the first time that both alterations are crucial for NPM mutant export from nucleus to cytoplasm. In fact, the cytoplasmic accumulation of NPM is blocked by leptomycin-B and ratjadones, specific exportin-1/Crm1-inhibitors, and by reinsertion of tryptophan residues 288 and 290, which respectively relocate NPM mutants in the nucleoplasm and nucleoli. NPM leukemic mutants in turn recruit the wild-type NPM from nucleoli to nucleoplasm and cytoplasm. These findings indicate that potential therapeutic strategies aimed to retarget NPM to its physiological sites will have to overcome 2 obstacles, the new NES motif and the mutated tryptophan(s) at the NPM mutant C-terminus.

Published
2006

221. The MLL recombinome of acute leukemias

Author

Meyer, C, Schneider, B, Jakob, S, Strehl, S, Attarbaschi, A, Schnittger, S, Schoch, C, Jansen, M, Dongen, J, Boer, M, Pieters, R, Ennas, M, Angelucci, E, Koehl, U, Greil, J, Griesinger, F, zur Stadt, U, Eckert, C, Szczepanski, T, Niggli, F, Schafer, B, Kempski, H, Brady, H, Zuna, J, Trka, J, Nigro, L, Biondi, A, Delabesse, E, Macintyre, E, Stanulla, M, Schrappe, M, Haas, O, Burmeister, T, Dingermann, T, Klingebiel, T, Marschalek, R, Jansen, MWJC, Dongen, JJM, Boer, ML, Ennas, MG, Niggli, FK, Schafer, BW, Brady, HJM, Nigro, LL, Haas, OA, Marschalek, R., BIONDI, ANDREA, Meyer, C, Schneider, B, Jakob, S, Strehl, S, Attarbaschi, A, Schnittger, S, Schoch, C, Jansen, M, Dongen, J, Boer, M, Pieters, R, Ennas, M, Angelucci, E, Koehl, U, Greil, J, Griesinger, F, zur Stadt, U, Eckert, C, Szczepanski, T, Niggli, F, Schafer, B, Kempski, H, Brady, H, Zuna, J, Trka, J, Nigro, L, Biondi, A, Delabesse, E, Macintyre, E, Stanulla, M, Schrappe, M, Haas, O, Burmeister, T, Dingermann, T, Klingebiel, T, Marschalek, R, Jansen, MWJC, Dongen, JJM, Boer, ML, Ennas, MG, Niggli, FK, Schafer, BW, Brady, HJM, Nigro, LL, Haas, OA, Marschalek, R., and BIONDI, ANDREA

Abstract

Chromosomal rearrangements of the human MLL gene are a hallmark for aggressive (high-risk) pediatric, adult and therapy-associated acute leukemias. These patients need to be identified in order to subject these patients to appropriate therapy regimen. A recently developed long-distance inverse PCR method was applied to genomic DNA isolated from individual acute leukemia patients in order to identify chromosomal rearrangements of the human MLL gene. We present data of the molecular characterization of 414 samples obtained from 272 pediatric and 142 adult leukemia patients. The precise localization of genomic breakpoints within the MLL gene and the involved translocation partner genes (TPGs) was determined and several new TPGs were identified. The combined data of our study and published data revealed a total of 87 different MLL rearrangements of which 51 TPGs are now characterized at the molecular level. Interestingly, the four most frequently found TPGs (AF4, AF9, ENL and AF10) encode nuclear proteins that are part of a protein network involved in histone H3K79 methylation. Thus, translocations of the MLL gene, by itself coding for a histone H3K4 methyltransferase, are presumably not randomly chosen, rather functionally selected.

Published
2006

222. Diagnostik akuter Leukämien

Author

Bacher, U., primary, Haferlach, C., additional, Schnittger, S., additional, Kern, W., additional, Ott, M.M., additional, and Haferlach, T., additional

Published
2012
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223. Influence of molecular subgroups on outcome of acute myeloid leukemia with normal karyotype in 141 patients undergoing salvage allogeneic stem cell transplantation in primary induction failure or beyond first relapse

Author

Pfeiffer, T., primary, Schleuning, M., additional, Mayer, J., additional, Haude, K.-H., additional, Tischer, J., additional, Buchholz, S., additional, Bunjes, D., additional, Bug, G., additional, Holler, E., additional, Meyer, R. G., additional, Greinix, H., additional, Scheid, C., additional, Christopeit, M., additional, Schnittger, S., additional, Braess, J., additional, Schlimok, G., additional, Spiekermann, K., additional, Ganser, A., additional, Kolb, H.-J., additional, and Schmid, C., additional

Published
2012
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224. ASXL1 exon 12 mutations are frequent in AML with intermediate risk karyotype and are independently associated with an adverse outcome

Author

Schnittger, S, primary, Eder, C, additional, Jeromin, S, additional, Alpermann, T, additional, Fasan, A, additional, Grossmann, V, additional, Kohlmann, A, additional, Illig, T, additional, Klopp, N, additional, Wichmann, H-E, additional, Kreuzer, K-A, additional, Schmid, C, additional, Staib, P, additional, Peceny, R, additional, Schmitz, N, additional, Kern, W, additional, Haferlach, C, additional, and Haferlach, T, additional

Published
2012
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232. Use of CBL exon 8 and 9 mutations in diagnosis of myeloproliferative neoplasms and myelodysplastic/myeloproliferative disorders: an analysis of 636 cases

Author

Schnittger, S., primary, Bacher, U., additional, Alpermann, T., additional, Reiter, A., additional, Ulke, M., additional, Dicker, F., additional, Eder, C., additional, Kohlmann, A., additional, Grossmann, V., additional, Kowarsch, A., additional, Kern, W., additional, Haferlach, C., additional, and Haferlach, T., additional

Published
2012
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233. Clinical features and course of refractory anemia with ring sideroblasts associated with marked thrombocytosis

Author

Broseus, J., primary, Florensa, L., additional, Zipperer, E., additional, Schnittger, S., additional, Malcovati, L., additional, Richebourg, S., additional, Lippert, E., additional, Cermak, J., additional, Evans, J., additional, Mounier, M., additional, Raya, J. M., additional, Bailly, F., additional, Gattermann, N., additional, Haferlach, T., additional, Garand, R., additional, Allou, K., additional, Besses, C., additional, Germing, U., additional, Haferlach, C., additional, Travaglino, E., additional, Luno, E., additional, Pinan, M. A., additional, Arenillas, L., additional, Rozman, M., additional, Perez Sirvent, M. L., additional, Favre, B., additional, Guy, J., additional, Alonso, E., additional, Ahwij, N., additional, Jerez, A., additional, Hermouet, S., additional, Maynadie, M., additional, Cazzola, M., additional, and Girodon, F., additional

Published
2012
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235. Subtype-specific patterns of molecular mutations in acute myeloid leukemia

Author

Rose, D, Haferlach, T, Schnittger, S, Perglerová, K, Kern, W, and Haferlach, C

Abstract

Acute myeloid leukemia (AML) can be grouped into morphologically or genetically defined subtypes. Today, the AML phenotype–genotype associations, that is, FAB/WHO (French–American–British/World Health Organization) definitions and recurrent molecular mutations, are not fully understood. Therefore, we evaluated the impact of molecular mutations on the AML differentiation stage by molecular profiling of 4373 adult de novoAML patients in 7 cytomorphological subtypes. We investigated mutations in 20 genes, including myeloid transcription factors (CEBPA, RUNX1), tumor suppressors (TP53, WT1), DNA modifiers (DNMT3A, IDH1/2, TET2), chromatin modifiers (ASXL1, MLL), signal transduction genes (FLT3, KRAS, NRAS) and NPM1. The most frequently mutated genes per cytomorphological subtype were RUNX1in M0 (43%), NPM1in M1 (42%), DNMT3Ain M2 (26%), NPM1in M4 (57%), M5a (49%) and M5b (70%) and TP53in M6 (36%). Although some gene mutations were frequent in several cytomorphological subtypes, a series of associations of co-occurring mutations with distinct phenotypes were identified for molecularly defined subcohorts. FLT3, NPM1and WT1mutations were associated with an immature phenotype in myeloblastic AML, whereas other combinations involving ASXL1, RUNX1, MLL-PTD, CEBPAor KRASwere more frequent in myeloblastic AML with maturation. Within the NPM1mutated subcohort, ASXL1mutations were significantly associated with a monoblastic differentiation and DNMT3Amutations with a monocytic phenotype.

Published
2017
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236. Landscape of TET2 mutations in acute myeloid leukemia

Author

Weissmann, S, primary, Alpermann, T, additional, Grossmann, V, additional, Kowarsch, A, additional, Nadarajah, N, additional, Eder, C, additional, Dicker, F, additional, Fasan, A, additional, Haferlach, C, additional, Haferlach, T, additional, Kern, W, additional, Schnittger, S, additional, and Kohlmann, A, additional

Published
2011
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244. Development of standardized approaches to reporting of minimal residual disease data using a reporting software package designed within the European LeukemiaNet

Author

Østergaard, M, primary, Nyvold, C G, additional, Jovanovic, J V, additional, Andersen, M T, additional, Kairisto, V, additional, Morgan, Y G, additional, Tobal, K, additional, Pallisgaard, N, additional, Özbek, U, additional, Pfeifer, H, additional, Schnittger, S, additional, Grubach, L, additional, Larsen, J K, additional, Grimwade, D, additional, and Hokland, P, additional

Published
2011
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