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3. Comparative value of post-remission treatment in cytogenetically normal AML subclassified by NPM1 and FLT3-ITD allelic ratio

Author

Versluis, J, in ‘t Hout, F E M, Devillier, R, van Putten, W L J, Manz, M G, Vekemans, M -C, Legdeur, M -C, Passweg, J R, Maertens, J, Kuball, J, Biemond, B J, Valk, P J M, van der Reijden, B A, Meloni, G, Schouten, H C, Vellenga, E, Pabst, T, Willemze, R, Löwenberg, B, Ossenkoppele, G, Baron, F, Huls, G, and Cornelissen, J J

Published
2017
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8. Specific proteome changes in platelets from individuals with GATA1-, GFI1B-, and RUNX1-linked bleeding disorders

Author

Van Bergen, M G J M, Marneth, A E, Hoogendijk, A J, Van Alphen, F P J, Van den Akker, E, Laros-Van Gorkom, B A P, Hoeks, M, Simons, A, De Munnik, S A, Janssen, J J W M, Martens, J H A, Jansen, J H, Meijer, A B, Van der Reijden, B A, Afd Biomol.Mass Spect. and Proteomics, and Biomolecular Mass Spectrometry and Proteomics

Subjects
Blood Platelet Disorders/metabolism, Mutation/genetics, Repressor Proteins/metabolism, Core Binding Factor Alpha 2 Subunit/metabolism, Proteome/metabolism, Transcription Factors/genetics, Homeostasis, Humans, Blood Platelets/metabolism, Proto-Oncogene Proteins/metabolism, GATA1 Transcription Factor/metabolism, Signal Transduction
Abstract

Mutations in the transcription factors GATA binding factor 1 (GATA1), growth factor independence 1B (GFI1B), and Runt-related transcription factor 1 (RUNX1) cause familial platelet and bleeding disorders. Mutant platelets exhibit common abnormalities including an α-granule reduction resulting in a grayish appearance in blood smears. This suggests that similar pathways are deregulated by different transcription factor mutations. To identify common factors, full platelet proteomes from 11 individuals with mutant GATA1R216Q, GFI1BQ287*, RUNX1Q154Rfs, or RUNX1TD2-6 and 28 healthy controls were examined by label-free quantitative mass spectrometry. In total, 2875 platelet proteins were reliably quantified. Clustering analysis of more than 300 differentially expressed proteins revealed profound differences between cases and controls. Among cases, 44 of 143 significantly downregulated proteins were assigned to platelet function, hemostasis, and granule biology, in line with platelet dysfunction and bleedings. Remarkably, none of these proteins were significantly diminished in all affected cases. Similarly, no proteins were commonly overrepresented in all affected cases compared with controls. These data indicate that the studied transcription factor mutations alter platelet proteomes in distinct largely nonoverlapping manners. This work provides the quantitative landscape of proteins that affect platelet function when deregulated by mutated transcription factors in inherited bleeding disorders.

Published
2021

9. Specific proteome changes in platelets from individuals with GATA1-, GFI1B-, and RUNX1-linked bleeding disorders

Author

Afd Biomol.Mass Spect. and Proteomics, Biomolecular Mass Spectrometry and Proteomics, Van Bergen, M G J M, Marneth, A E, Hoogendijk, A J, Van Alphen, F P J, Van den Akker, E, Laros-Van Gorkom, B A P, Hoeks, M, Simons, A, De Munnik, S A, Janssen, J J W M, Martens, J H A, Jansen, J H, Meijer, A B, Van der Reijden, B A, Afd Biomol.Mass Spect. and Proteomics, Biomolecular Mass Spectrometry and Proteomics, Van Bergen, M G J M, Marneth, A E, Hoogendijk, A J, Van Alphen, F P J, Van den Akker, E, Laros-Van Gorkom, B A P, Hoeks, M, Simons, A, De Munnik, S A, Janssen, J J W M, Martens, J H A, Jansen, J H, Meijer, A B, and Van der Reijden, B A

Published
2021

14. Specific proteome changes in platelets from individuals with GATA1-, GFI1B-, and RUNX1-linked bleeding disorders

Author

Van Bergen, M. G. J. M., primary, Marneth, A. E., additional, Hoogendijk, A. J., additional, Van Alphen, F. P. J., additional, Van den Akker, E., additional, Laros-Van Gorkom, B. A. P., additional, Hoeks, M., additional, Simons, A., additional, De Munnik, S. A., additional, Janssen, J. J. W. M., additional, Martens, J. H. A., additional, Jansen, J. H., additional, Meijer, A. B., additional, and Van der Reijden, B. A., additional

Published
2021
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19. Establishing optimal quantitative-polymerase chain reaction assays for routine diagnosis and tracking of minimal residual disease in JAK2-V617F-associated myeloproliferative neoplasms: a joint European LeukemiaNet/MPN&MPNr-EuroNet (COST action BM0902) study

Author

Jovanovic, J V, Ivey, A, Vannucchi, A M, Lippert, E, Leibundgut, E Oppliger, Cassinat, B, Pallisgaard, N, Maroc, N, Hermouet, S, Nickless, G, Guglielmelli, P, van der Reijden, B A, Jansen, J H, Alpermann, T, Schnittger, S, Bench, A, Tobal, K, Wilkins, B, Cuthill, K, McLornan, D, Yeoman, K, Akiki, S, Bryon, J, Jeffries, S, Jones, A, Percy, M J, Schwemmers, S, Gruender, A, Kelley, T W, Reading, S, Pancrazzi, A, McMullin, M F, Pahl, H L, Cross, N CP, Harrison, C N, Prchal, J T, Chomienne, C, Kiladjian, J J, Barbui, T, and Grimwade, D

Published
2013
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24. Chromatin-Based Classification of Genetically Heterogeneous AMLs into Two Distinct Subtypes with Diverse Stemness Phenotypes

Author

Yi, G., Wierenga, A., Petraglia, F., Narang, P., Janssen-Megens, E., Mandoli, A., Merkel, A., Berentsen, K., Kim, B., Matarese, F., Singh, A., Habibi, E., Prange, K., Mulder, A., Jansen, J., Clarke, L., Heath, S., van der Reijden, B., Flicek, P., Yaspo, M., Gut, I., Bock, C., Schuringa, J., Altucci, L., Vellenga, E., Stunnenberg, H., Martens, J., H., A., Yi, Guoqiang, Wierenga, Albertus T. J., Petraglia, Francesca, Narang, Pankaj, Janssen-Megens, Eva M., Mandoli, Amit, Merkel, Angelika, Berentsen, Kim, Kim, Bowon, Matarese, Filomena, Singh, Abhishek A., Habibi, Ehsan, Prange, Koen H. M., Mulder, André B., Jansen, Joop H., Clarke, Laura, Heath, Simon, van der Reijden, Bert A., Flicek, Paul, Yaspo, Marie-Laure, Gut, Ivo, Bock, Christoph, Schuringa, Jan Jacob, Altucci, Lucia, Vellenga, Edo, Stunnenberg, Hendrik G., Martens, Joost H. A., Medical Biochemistry, ACS - Atherosclerosis & ischemic syndromes, Stem Cell Aging Leukemia and Lymphoma (SALL), and Guided Treatment in Optimal Selected Cancer Patients (GUTS)

Subjects
Spliceosome, NPM1, Oncogene Proteins, Fusion, chromatin state, Cancer development and immune defence Radboud Institute for Molecular Life Sciences [Radboudumc 2], DNA accessibility, epigenome, Biology, acute myeloid leukemia, Article, General Biochemistry, Genetics and Molecular Biology, stemness, 03 medical and health sciences, chemistry.chemical_compound, All institutes and research themes of the Radboud University Medical Center, 0302 clinical medicine, AML, hemic and lymphatic diseases, Humans, chromatin states, histone mark, Molecular Biology, 030304 developmental biology, Genetics, 0303 health sciences, Biochemistry, Genetics and Molecular Biology (all), histone marks, Nuclear Proteins, Myeloid leukemia, Epigenome, Phenotype, Chromatin, stemne, Leukemia, Myeloid, Acute, Histone, RUNX1, chemistry, 030220 oncology & carcinogenesis, Core Binding Factor Alpha 2 Subunit, Mutation, biology.protein, transcriptome, Nucleophosmin, human activities
Abstract

Summary Global investigation of histone marks in acute myeloid leukemia (AML) remains limited. Analyses of 38 AML samples through integrated transcriptional and chromatin mark analysis exposes 2 major subtypes. One subtype is dominated by patients with NPM1 mutations or MLL-fusion genes, shows activation of the regulatory pathways involving HOX-family genes as targets, and displays high self-renewal capacity and stemness. The second subtype is enriched for RUNX1 or spliceosome mutations, suggesting potential interplay between the 2 aberrations, and mainly depends on IRF family regulators. Cellular consequences in prognosis predict a relatively worse outcome for the first subtype. Our integrated profiling establishes a rich resource to probe AML subtypes on the basis of expression and chromatin data.

Published
2019

25. Richtlijn Acute promyelocytenleukemie (APL): richtlijnen voor diagnostiek en behandeling

Author

Huls, G, Löwenberg, Bob, van de Loosdrecht, AA, Janssen, JJWM, Jongen - Lavrencic, Mojca, Raaijmakers, Marc, Wouters, Bas, van den Borne, P, Kuball, J, Biemond, B, van Gelder, M, van der Velden, WJFM, de Weerdt, O, Marwijk Kooy, R, Klein, S, Ammatuna, Emanuele, Poel, M, van Rhenen, A, Jong, JJM, Valk, Peter, van der Reijden, B, Cornelissen, Jan, Vellenga, E, Ossenkoppele, G, and Hematology

Published
2019

27. GFI1(36N) as a therapeutic and prognostic marker for myelodysplastic syndrome

Author

Botezatu, L, Michel, LC, Makishima, H, Schroeder, T, Germing, U, Haas, R, van der Reijden, B, Marneth, AE, Bergevoet, SM, Jansen, JH, Przychodzen, B, Wlodarski, M, Niemeyer, C, Platzbecker, U, Ehninger, G, Unnikrishnan, A, Beck, D, Pimanda, J, Hellström-Lindberg, E, Cazzola, M, Malcovati, L, Boultwood, J, Pellagatti, A, Papaemmanuil, E, Le Coutre, P, Kaeda, J, Opalka, B, Möröy, T, Dührsen, U, Maciejewski, J, and Khandanpour, C

Subjects
Male, 0301 basic medicine, Oncology, Cancer Research, Myeloid, Pancytopenia, Cancer development and immune defence Radboud Institute for Molecular Life Sciences [Radboudumc 2], Medizin, Bioinformatics, Cohort Studies, 0302 clinical medicine, Gene Frequency, Bone Marrow, Genotype, 10. No inequality, Univariate analysis, Hematopoietic stem cell, Hematology, Middle Aged, Prognosis, 3. Good health, DNA-Binding Proteins, Phenotype, medicine.anatomical_structure, 030220 oncology & carcinogenesis, Cytogenetic Analysis, Female, Adult, medicine.medical_specialty, Malignant Hematopoiesis, Polymorphism, Single Nucleotide, 03 medical and health sciences, Internal medicine, Genetics, medicine, Humans, Allele, Molecular Biology, Allele frequency, Alleles, Survival analysis, Aged, business.industry, Myelodysplastic syndromes, Cell Biology, medicine.disease, Survival Analysis, 030104 developmental biology, Amino Acid Substitution, Myelodysplastic Syndromes, business, Biomarkers, Transcription Factors
Abstract

Inherited gene variants play an important role in malignant diseases. The transcriptional repressor growth factor independence 1 (GFI1) regulates hematopoietic stem cell (HSC) self-renewal and differentiation. A single-nucleotide polymorphism of GFI1 (rs34631763) generates a protein with an asparagine (N) instead of a serine (S) at position 36 (GFI136N) and has a prevalence of 3%–5% among Caucasians. Because GFI1 regulates myeloid development, we examined the role of GFI136N on the course of MDS disease. To this end, we determined allele frequencies of GFI136N in four independent MDS cohorts from the Netherlands and Belgium, Germany, the ICGC consortium, and the United States. The GFI136N allele frequency in the 723 MDS patients genotyped ranged between 9% and 12%. GFI136N was an independent adverse prognostic factor for overall survival, acute myeloid leukemia-free survival, and event-free survival in a univariate analysis. After adjustment for age, bone marrow blast percentage, IPSS score, mutational status, and cytogenetic findings, GFI136N remained an independent adverse prognostic marker. GFI136S homozygous patients exhibited a sustained response to treatment with hypomethylating agents, whereas GFI136N patients had a poor sustained response to this therapy. Because allele status of GFI136N is readily determined using basic molecular techniques, we propose inclusion of GFI136N status in future prospective studies for MDS patients to better predict prognosis and guide therapeutic decisions., Graphical abstract, Highlights • GFI136N is present in about 9%–12% of all Caucasian patients with myelodysplastic syndrome. • GFI136N is an independent, adverse prognostic factor for survival. • GFI136N patients with myelodysplastic syndrome respond poorly to hypomethylating agents.

Published
2016

29. Richtlijn Acute promyelocytenleukemie (APL): richtlijnen voor diagnostiek en behandeling

Author

Huls, Geert, Lowenberg, B., van de Loosdrecht, A.A., Janssen, J.J.W.M., Jongen-Lavrencic, M., Raaijmakers, M., Wouters, B., Von dem Borne, Peter A., Kuball, Jurgen, Biemond, Bart J., Van Gelder, Michel, van der Velden, W.J.F.M, de Weerdt, Okke, van Marwijk Kooy, Rien, Klein, Saskia, van der Poel, M., van Rhenen, A., Jong, J.J.M. de, Valk, P, van der Reijden, B., Cornelissen, J.J., Vellenga, Edo, Ossenkoppele, G., Stem Cell Aging Leukemia and Lymphoma, and Guided Treatment in Optimal Selected Cancer Patients

Abstract

Acute myeloïde leukemie (AML) is een heterogene ziekte die wordt gekenmerkt door (oligo)klonale maligne hematopoëse met een blokkade in de differentiatie en daardoor een excessieve toename van leukemische blasten. Acute promyelocytenleukemie (APL) is een zeldzame variant van AML die zich goed laat behandelen met ATRA-bevattende therapie. Vanwege complicaties van de ziekte (trombose, bloeding) is vroege herkenning en start van behandeling extreem belangrijk. Het is daarom belangrijk dat diagnostiek en behandeling van APL-patiënten in de dagelijkse praktijk zorgvuldig en gestructureerd plaatsvindt. Hieronder bespreken we de richtlijnen voor diagnostiek en behandeling zoals de HOVONLeukemiewerkgroep denkt dat die voor APL zou moeten plaatsvinden

Published
2018

33. Comparative value of post-remission treatment in cytogenetically normal AML subclassified by NPM1 and FLT3-ITD allelic ratio

Author

MS Hematologie, Infection & Immunity, Regenerative Medicine and Stem Cells, CTI Kuball, Cancer, Versluis, J, In 't Hout, F E M, Devillier, R, van Putten, W L J, Manz, M G, Vekemans, M-C, Passweg, J R, Maertens, J, Kuball, J, Biemond, B J, Valk, P J M, van der Reijden, B A, Meloni, G, Schouten, H C, Vellenga, E, Pabst, T, Willemze, R, Löwenberg, B, Ossenkoppele, G, Baron, F, Huls, G, Cornelissen, J J, MS Hematologie, Infection & Immunity, Regenerative Medicine and Stem Cells, CTI Kuball, Cancer, Versluis, J, In 't Hout, F E M, Devillier, R, van Putten, W L J, Manz, M G, Vekemans, M-C, Passweg, J R, Maertens, J, Kuball, J, Biemond, B J, Valk, P J M, van der Reijden, B A, Meloni, G, Schouten, H C, Vellenga, E, Pabst, T, Willemze, R, Löwenberg, B, Ossenkoppele, G, Baron, F, Huls, G, and Cornelissen, J J

Published
2017

34. C-terminal BRE overexpression in 11q23-rearranged and t(8;16) acute myeloid leukemia is caused by intragenic transcription initiation

Author

Marneth, A E, primary, Prange, K H M, additional, Al Hinai, A S A, additional, Bergevoet, S M, additional, Tesi, N, additional, Janssen-Megens, E M, additional, Kim, B, additional, Sharifi, N, additional, Yaspo, M L, additional, Kuster, J, additional, Sanders, M A, additional, Stoetman, E C G, additional, Knijnenburg, J, additional, Arentsen-Peters, T C J M, additional, Zwaan, C M, additional, Stunnenberg, H G, additional, van den Heuvel-Eibrink, M M, additional, Haferlach, T, additional, Fornerod, M, additional, Jansen, J H, additional, Valk, P J M, additional, van der Reijden, B A, additional, and Martens, J H A, additional

Published
2017
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36. Comparative value of post-remission treatment in cytogenetically normal AML subclassified by NPM1 and FLT3-ITD allelic ratio

Author

UCL - (SLuc) Service d'hématologie, Versluis, J, in ‘t Hout, F E M, Devillier, R, van Putten, W L J, Manz, M G, Vekemans, M -C, Legdeur, M -C, Passweg, J R, Maertens, J, Kuball, J, Biemond, B J, Valk, P J M, van der Reijden, B A, Meloni, G, Schouten, H C, Vellenga, E, Pabst, T, Willemze, R, Löwenberg, B, Ossenkoppele, G, Baron, F, Huls, G, Cornelissen, J J, UCL - (SLuc) Service d'hématologie, Versluis, J, in ‘t Hout, F E M, Devillier, R, van Putten, W L J, Manz, M G, Vekemans, M -C, Legdeur, M -C, Passweg, J R, Maertens, J, Kuball, J, Biemond, B J, Valk, P J M, van der Reijden, B A, Meloni, G, Schouten, H C, Vellenga, E, Pabst, T, Willemze, R, Löwenberg, B, Ossenkoppele, G, Baron, F, Huls, G, and Cornelissen, J J

Abstract

Post-remission treatment (PRT) in patients with cytogenetically normal (CN) acute myeloid leukemia (AML) in first complete remission (CR1) is debated. We studied 521 patients with CN-AML in CR1, for whom mutational status of NPM1 and FLT3-ITD was available, including the FLT3-ITD allelic ratio. PRT consisted of reduced intensity conditioning (RIC) allogeneic hematopoietic stem cell transplantation (alloHSCT) (n=68), myeloablative conditioning (MAC) alloHSCT (n=137), autologous hematopoietic stem cell transplantation (autoHSCT) (n=168) or chemotherapy (n=148). Favorable overall survival (OS) was found for patients with mutated NPM1 without FLT3-ITD (71±4%). Outcome in patients with a high FLT3-ITD allelic ratio appeared to be very poor with OS and relapse-free survival (RFS) of 23±8% and 12±6%, respectively. Patients with wild-type NPM1 without FLT3-ITD or with a low allelic burden of FLT3-ITD were considered as intermediate-risk group because of similar OS and RFS at 5 years, in which PRT by RIC alloHSCT resulted in better OS and RFS as compared with chemotherapy (hazard ratio (HR) 0.56, P=0.022 and HR 0.50, P=0.004, respectively) or autoHSCT (HR 0.60, P=0.046 and HR 0.60, P=0.043, respectively). The lowest cumulative incidence of relapse (23±4%) was observed following MAC alloHSCT. These results suggest that alloHSCT may be preferred in patients with molecularly intermediate-risk CN-AML, while the choice of conditioning type may be personalized according to risk for non-relapse mortality.

Published
2016

37. Comparative value of post-remission treatment in cytogenetically normal AML subclassified by NPM1 and FLT3-ITD allelic ratio

Author

Versluis, J, primary, in ‘t Hout, F E M, additional, Devillier, R, additional, van Putten, W L J, additional, Manz, M G, additional, Vekemans, M -C, additional, Legdeur, M -C, additional, Passweg, J R, additional, Maertens, J, additional, Kuball, J, additional, Biemond, B J, additional, Valk, P J M, additional, van der Reijden, B A, additional, Meloni, G, additional, Schouten, H C, additional, Vellenga, E, additional, Pabst, T, additional, Willemze, R, additional, Löwenberg, B, additional, Ossenkoppele, G, additional, Baron, F, additional, Huls, G, additional, and Cornelissen, J J, additional

Published
2016
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38. 72 PERSONALIZED TREATMENT APPROACH FOR GFI136N HETEROZYGOUS OR HOMOZYGOUS MDS PATIENTS

Author

Lacramioara, B., primary, Makishima, H., additional, Michel, L., additional, Hoenes, J., additional, Marneth, A., additional, van der Reijden, B., additional, Radiovoyevich, T., additional, Germing, U., additional, Haas, R., additional, Schroeder, T., additional, Vadnais, C., additional, Helness, A., additional, Pimanda, J., additional, Jansen, J., additional, Unnikrishnan, A., additional, Platzbecker, U., additional, Papaemmanuil, E., additional, Ehninger, G., additional, Moroy, T., additional, Duhrsen, U., additional, Maciejewski, J., additional, and Khandanpour, C., additional

Published
2015
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39. 62 MUTATIONS IN EPIGENETIC REGULATORS ARE SIGNIFICANTLY ASSOCIATED WITH ABERRANT EXPRESSION OF MYELOID DIFFERENTIATION ANTIGENS ON MYELOID PROGENITOR CELLS IN LOW/INTERMEDIATE RISK MDS

Author

Coelho, P. Silva, primary, Cremers, E.M.P., additional, Westers, T.M., additional, de Graaf, A.O., additional, Alhan, C., additional, Cali, C., additional, Visser-Wisselaar, H.A., additional, Chitu, D.A., additional, Vellenga, E., additional, Klein, S.K., additional, Wijermans, P.W., additional, de Greef, G.E., additional, Legdeur, M.C., additional, Muus, P., additional, Ossenkoppele, G.J., additional, Stevens-Kroef, M.J.P.L., additional, van der Reijden, B., additional, Jansen, J.H., additional, and van de Loosdrecht, A.A., additional

Published
2015
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42. C-terminal BRE overexpression in 11q23-rearranged and t(8;16) acute myeloid leukemia is caused by intragenic transcription initiation

Author

Marneth, A E, Prange, K H M, Al Hinai, A S A, Bergevoet, S M, Tesi, N, Janssen-Megens, E M, Kim, B, Sharifi, N, Yaspo, M L, Kuster, J, Sanders, M A, Stoetman, E C G, Knijnenburg, J, Arentsen-Peters, T C J M, Zwaan, C M, Stunnenberg, H G, van den Heuvel-Eibrink, M M, Haferlach, T, Fornerod, M, Jansen, J H, Valk, P J M, van der Reijden, B A, and Martens, J H A

Abstract

Overexpression of the BRE (brain and reproductive organ-expressed) gene defines a distinct pediatric and adult acute myeloid leukemia (AML) subgroup. Here we identify a promoter enriched for active chromatin marks in BRE intron 4 causing strong biallelic expression of a previously unknown C-terminal BRE transcript. This transcript starts with BRE intron 4 sequences spliced to exon 5 and downstream sequences, and if translated might code for an N terminally truncated BRE protein. Remarkably, the new BRE transcript was highly expressed in over 50% of 11q23/KMT2A (lysine methyl transferase 2A)-rearranged and t(8;16)/KAT6A-CREBBP cases, while it was virtually absent from other AML subsets and normal tissues. In gene reporter assays, the leukemia-specific fusion protein KMT2A-MLLT3 transactivated the intragenic BRE promoter. Further epigenome analyses revealed 97 additional intragenic promoter marks frequently bound by KMT2A in AML with C-terminal BRE expression. The corresponding genes may be part of a context-dependent KMT2A-MLLT3-driven oncogenic program, because they were higher expressed in this AML subtype compared with other groups. C-terminal BRE might be an important contributor to this program because in a case with relapsed AML, we observed an ins(11;2) fusing CHORDC1 to BRE at the region where intragenic transcription starts in KMT2A-rearranged and KAT6A-CREBBP AML.

Published
2018
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43. Comparative value of post-remission treatment in cytogenetically normal AML subclassified by NPM1and FLT3-ITD allelic ratio

Author

Versluis, J, in ‘t Hout, F E M, Devillier, R, van Putten, W L J, Manz, M G, Vekemans, M -C, Legdeur, M -C, Passweg, J R, Maertens, J, Kuball, J, Biemond, B J, Valk, P J M, van der Reijden, B A, Meloni, G, Schouten, H C, Vellenga, E, Pabst, T, Willemze, R, Löwenberg, B, Ossenkoppele, G, Baron, F, Huls, G, and Cornelissen, J J

Abstract

Post-remission treatment (PRT) in patients with cytogenetically normal (CN) acute myeloid leukemia (AML) in first complete remission (CR1) is debated. We studied 521 patients with CN-AML in CR1, for whom mutational status of NPM1and FLT3-ITD was available, including the FLT3-ITD allelic ratio. PRT consisted of reduced intensity conditioning (RIC) allogeneic hematopoietic stem cell transplantation (alloHSCT) (n=68), myeloablative conditioning (MAC) alloHSCT (n=137), autologous hematopoietic stem cell transplantation (autoHSCT) (n=168) or chemotherapy (n=148). Favorable overall survival (OS) was found for patients with mutated NPM1without FLT3-ITD (71±4%). Outcome in patients with a high FLT3-ITD allelic ratio appeared to be very poor with OS and relapse-free survival (RFS) of 23±8% and 12±6%, respectively. Patients with wild-type NPM1without FLT3-ITD or with a low allelic burden of FLT3-ITD were considered as intermediate-risk group because of similar OS and RFS at 5 years, in which PRT by RIC alloHSCT resulted in better OS and RFS as compared with chemotherapy (hazard ratio (HR) 0.56, P=0.022 and HR 0.50, P=0.004, respectively) or autoHSCT (HR 0.60, P=0.046 and HR 0.60, P=0.043, respectively). The lowest cumulative incidence of relapse (23±4%) was observed following MAC alloHSCT. These results suggest that alloHSCT may be preferred in patients with molecularly intermediate-risk CN-AML, while the choice of conditioning type may be personalized according to risk for non-relapse mortality.

Published
2017
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44. Systematic Evaluation of DNA-Based Quantitative-Polymerase Chain Reaction (Q-PCR) Assays to Track Treatment Response in Patients with JAK2-V617F Associated Myeloproliferative Neoplasms: A Joint European LeukemiaNet/ MPN&MPNr-EuroNet Study

Author

Jovanovic, J V, primary, Vannucchi, A M, additional, Lippert, E, additional, Leibundgut, E Oppliger, additional, Maroc, N, additional, Hermouet, S, additional, Nickless, G, additional, Cassinat, B, additional, Guglielmelli, P, additional, van der Reijden, B, additional, Bench, A, additional, Tobal, K, additional, Wilkins, B, additional, Cuthill, K, additional, Ivey, A, additional, Yeoman, K, additional, Percy, M J, additional, Schwemmers, S, additional, Gruender, A, additional, Kelley, T W, additional, Reading, S, additional, Pancrazzi, A, additional, McMullin, MF, additional, Pahl, H L, additional, Harrison, C N, additional, Prchal, J T, additional, Chomienne, C, additional, Kiladjian, JJ, additional, Barbui, T, additional, and Grimwade, D, additional

Published
2011
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47. Incidence and Clinical Impact of TET2 Mutations in Acute Myeloid Leukemia Patients Treated within the EORTC/GIMEMA AML-12/06991 AML Trial.

Author

Aslanyan, M. G, primary, Langemeijer, S. M.C., additional, Cilloni, D., additional, Saglio, G., additional, Marie, JP, additional, Tang, R., additional, Labar, B., additional, Zadro, R., additional, Batinic, D., additional, Amadori, S., additional, Lo Coco, F., additional, Scheele, T., additional, Kroeze, L., additional, Massop, M., additional, van Hoogen, P., additional, Stevens, E., additional, Muus, P., additional, Suciu, S., additional, Baila, L., additional, Marijt, E. W.A., additional, Willemze, R., additional, de Witte, T., additional, van der Reijden, B., additional, and Jansen, J. H., additional

Published
2009
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49. WT1 Promotes Myeloid Development and Inhibits Lymphoid Development.

Author

Menke, Aschwin L., primary, Knops, G.H. J., additional, Linssen, P.C. M., additional, Nikoloski, G., additional, Pennings, A., additional, Philippens, M., additional, Vierwinden, G., additional, Lemmers, B., additional, De Witte, T., additional, Van der Reijden, B. A., additional, and Jansen, J. H., additional

Published
2004
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50. Degradable dU-based DNA template as a standard in real-time PCR quantitation.

Author

Pennings, J L A, Van de Locht, L T F, Jansen, J H, Van der Reijden, B A, De Witte, T, Mensink, E J B M, Pennings, J L, Van De Locht, L T, and Mensink, E J

Subjects
DNA, URACIL
Abstract

Development of real-time quantitative PCR assays requires suitable positive controls. For assays with clinical applications, these controls may be difficult to obtain because some molecular aberrations are rare and patient material may be available in limited amounts. Because of the risk of introducing contaminations in the laboratory, cloned DNA is not a desirable alternative. We describe the use of dU-containing DNA as a positive control template in real-time quantitative PCR. dU-DNA constructs can be decontaminated by adding uracil N-glycosylase (UNG) to the reaction mixture. In addition, dU-DNA can be used for accurate quantification, because it allows quantification to be expressed in numbers of molecules. Since synthetic dU-DNA constructs can easily be quantitated spectroscopically, they provide a more accurate control than arbitrary cell line units. We applied this method for the detection of the E2A-Pbx1 gene fusion and show that UNG-containing reactions can be employed for diagnostics without loss of sensitivity, and that for positive and quantitative controls UNG negative reactions can be used. The use of dU-DNA provides a novel type of control template that can easily be integrated into existing PCR protocols. [ABSTRACT FROM AUTHOR]

Published
2001
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