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835 results on '"Stary, J."'

51. The variable biological signature of refractory cytopenia of childhood (RCC), a retrospective EWOG-MDS study

Author

de Winter, D. T. C., Langerak, A. W., te Marvelde, J., Dworzak, M. N., De Moerloose, B., Stary, J., Locatelli, Franco, Hasle, H., de Vries, A. C. H., Schmugge, M., Niemeyer, C. M., van den Heuvel-Eibrink, M. M., van der Velden, V. H. J., Locatelli F. (ORCID:0000-0002-7976-3654), de Winter, D. T. C., Langerak, A. W., te Marvelde, J., Dworzak, M. N., De Moerloose, B., Stary, J., Locatelli, Franco, Hasle, H., de Vries, A. C. H., Schmugge, M., Niemeyer, C. M., van den Heuvel-Eibrink, M. M., van der Velden, V. H. J., and Locatelli F. (ORCID:0000-0002-7976-3654)

Abstract

NO ABSTRACT

Published
2021

52. The clinical and biological characteristics of NUP98-KDM5A pediatric acute myeloid leukemia

Author

Noort, S., Wander, P., Alonzo, T. A., Smith, J., Ries, R. E., Gerbing, R. B., Dolman, E. M. M., Locatelli, Franco, Reinhardt, D., Baruchel, A., Stary, J., Molenaar, J. J., Stam, R. W., van den Heuvel-Eibrink, M. M., Michel Zwaan, C., Meshinchi, S., Locatelli F. (ORCID:0000-0002-7976-3654), Noort, S., Wander, P., Alonzo, T. A., Smith, J., Ries, R. E., Gerbing, R. B., Dolman, E. M. M., Locatelli, Franco, Reinhardt, D., Baruchel, A., Stary, J., Molenaar, J. J., Stam, R. W., van den Heuvel-Eibrink, M. M., Michel Zwaan, C., Meshinchi, S., and Locatelli F. (ORCID:0000-0002-7976-3654)

Abstract

NO ABSTRACT

Published
2021

53. The clinical and biological characteristics of NUP98-KDM5A in pediatric acute myeloid leukemia

Author

Noort, Sanne, Wander, P, Alonzo, TA, Smith, J, Ries, RE, Gerbing, RB, Dolman, MEM, Locatelli, F (Franco), Reinhardt, D, Baruchel, A, Stary, J, Molenaar, JJ, Stam, RW, van den Heuvel-Eibrink, M, Zwaan, M, Meshinchi, S, Noort, Sanne, Wander, P, Alonzo, TA, Smith, J, Ries, RE, Gerbing, RB, Dolman, MEM, Locatelli, F (Franco), Reinhardt, D, Baruchel, A, Stary, J, Molenaar, JJ, Stam, RW, van den Heuvel-Eibrink, M, Zwaan, M, and Meshinchi, S

Published
2021

54. Clinical Implications of Minimal Residual Disease Detection in Infants With KMT2A-Rearranged Acute Lymphoblastic Leukemia Treated on the Interfant-06 Protocol

Author

Stutterheim, J, van der Sluis, I, de Lorenzo, P, Alten, J, Ancliffe, P, Attarbaschi, A, Brethon, B, Biondi, A, Campbell, M, Cazzaniga, G, Escherich, G, Ferster, A, Kotecha, R, Lausen, B, Li, C, Lo Nigro, L, Locatelli, F, Marschalek, R, Meyer, C, Schrappe, M, Stary, J, Vora, A, Zuna, J, van der Velden, V, Szczepanski, T, Valsecchi, M, Pieters, R, Stutterheim, Janine, van der Sluis, Inge M, de Lorenzo, Paola, Alten, Julia, Ancliffe, Philip, Attarbaschi, Andishe, Brethon, Benoit, Biondi, Andrea, Campbell, Myriam, Cazzaniga, Giovanni, Escherich, Gabriele, Ferster, Alina, Kotecha, Rishi S, Lausen, Birgitte, Li, Chi Kong, Lo Nigro, Luca, Locatelli, Franco, Marschalek, Rolf, Meyer, Claus, Schrappe, Martin, Stary, Jan, Vora, Ajay, Zuna, Jan, van der Velden, Vincent H J, Szczepanski, Tomasz, Valsecchi, Maria Grazia, Pieters, Rob, Stutterheim, J, van der Sluis, I, de Lorenzo, P, Alten, J, Ancliffe, P, Attarbaschi, A, Brethon, B, Biondi, A, Campbell, M, Cazzaniga, G, Escherich, G, Ferster, A, Kotecha, R, Lausen, B, Li, C, Lo Nigro, L, Locatelli, F, Marschalek, R, Meyer, C, Schrappe, M, Stary, J, Vora, A, Zuna, J, van der Velden, V, Szczepanski, T, Valsecchi, M, Pieters, R, Stutterheim, Janine, van der Sluis, Inge M, de Lorenzo, Paola, Alten, Julia, Ancliffe, Philip, Attarbaschi, Andishe, Brethon, Benoit, Biondi, Andrea, Campbell, Myriam, Cazzaniga, Giovanni, Escherich, Gabriele, Ferster, Alina, Kotecha, Rishi S, Lausen, Birgitte, Li, Chi Kong, Lo Nigro, Luca, Locatelli, Franco, Marschalek, Rolf, Meyer, Claus, Schrappe, Martin, Stary, Jan, Vora, Ajay, Zuna, Jan, van der Velden, Vincent H J, Szczepanski, Tomasz, Valsecchi, Maria Grazia, and Pieters, Rob

Abstract

Purpose: Infant acute lymphoblastic leukemia (ALL) is characterized by a high incidence of KMT2A gene rearrangements and poor outcome. We evaluated the value of minimal residual disease (MRD) in infants with KMT2A-rearranged ALL treated within the Interfant-06 protocol, which compared lymphoid-style consolidation (protocol IB) versus myeloid-style consolidation (araC, daunorubicin, etoposide/mitoxantrone, araC, etoposide). Materials and methods: MRD was measured in 249 infants by DNA-based polymerase chain reaction of rearranged KMT2A, immunoglobulin, and/or T-cell receptor genes, at the end of induction (EOI) and end of consolidation (EOC). MRD results were classified as negative, intermediate (< 5 × 10-4), and high (≥ 5 × 10-4). Results: EOI MRD levels predicted outcome with 6-year disease-free survival (DFS) of 60.2% (95% CI, 43.2 to 73.6), 45.0% (95% CI, 28.3 to 53.1), and 33.8% (95% CI, 23.8 to 44.1) for infants with negative, intermediate, and high EOI MRD levels, respectively (P = .0039). EOC MRD levels were also predictive of outcome, with 6-year DFS of 68.2% (95% CI, 55.2 to 78.1), 40.1% (95% CI, 28.1 to 51.9), and 11.9% (95% CI, 2.6 to 29.1) for infants with negative, intermediate, and high EOC MRD levels, respectively (P < .0001). Analysis of EOI MRD according to the type of consolidation treatment showed that infants treated with lymphoid-style consolidation had 6-year DFS of 78.2% (95% CI, 51.4 to 91.3), 47.2% (95% CI, 33.0 to 60.1), and 23.2% (95% CI, 12.1 to 36.4) for negative, intermediate, and high MRD levels, respectively (P < .0001), while for myeloid-style-treated patients the corresponding figures were 45.0% (95% CI, 23.9 to 64.1), 41.3% (95% CI, 23.2 to 58.5), and 45.9% (95% CI, 29.4 to 60.9). Conclusion: This study provides support for the idea that induction therapy selects patients for subsequent therapy; infants with high EOI MRD may benefit from AML-like consolidation (DFS 45.9% v 23.2%), whereas patients with low EOI MRD may bene

Published
2021

58. Standardized MRD quantification in European ALL trials: Proceedings of the Second International Symposium on MRD assessment in Kiel, Germany, 18–20 September 2008

Author

Brüggemann, M, Schrauder, A, Raff, T, Pfeifer, H, Dworzak, M, Ottmann, O G, Asnafi, V, Baruchel, A, Bassan, R, Benoit, Y, Biondi, A, Cavé, H, Dombret, H, Fielding, A K, Foà, R, Gökbuget, N, Goldstone, A H, Goulden, N, Henze, G, Hoelzer, D, Janka-Schaub, G E, Macintyre, E A, Pieters, R, Rambaldi, A, Ribera, J-M, Schmiegelow, K, Spinelli, O, Stary, J, von Stackelberg, A, Kneba, M, Schrappe, M, and van Dongen, J J M

Published
2010
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67. Childhood secondary ALL after ALL treatment

Author

Zuna, J, Cavé, H, Eckert, C, Szczepanski, T, Meyer, C, Mejstrikova, E, Fronkova, E, Muzikova, K, Clappier, E, Mendelova, D, Boutard, P, Schrauder, A, Sterba, J, Marschalek, R, van Dongen, J J M, Hrusak, O, Stary, J, and Trka, J

Published
2007
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71. Synonymous GATA2 mutations result in selective loss of mutated RNA and are common in patients with GATA2 deficiency

Author

Kozyra, E. J., Pastor, V. B., Lefkopoulos, S., Sahoo, S. S., Busch, H., Voss, R. K., Erlacher, M., Lebrecht, D., Szvetnik, E. A., Hirabayashi, S., Pasauliene, R., Pedace, L., Tartaglia, M., Klemann, C., Metzger, P., Boerries, M., Catala, A., Hasle, H., de Haas, V., Kallay, K., Masetti, R., De Moerloose, B., Dworzak, M., Schmugge, M., Smith, O., Stary, J., Mejstrikova, E., Ussowicz, M., Morris, E., Singh, P., Collin, M., Derecka, M., Gohring, G., Flotho, C., Strahm, B., Locatelli, Franco, Niemeyer, C. M., Trompouki, E., Wlodarski, M. W., Locatelli F. (ORCID:0000-0002-7976-3654), Kozyra, E. J., Pastor, V. B., Lefkopoulos, S., Sahoo, S. S., Busch, H., Voss, R. K., Erlacher, M., Lebrecht, D., Szvetnik, E. A., Hirabayashi, S., Pasauliene, R., Pedace, L., Tartaglia, M., Klemann, C., Metzger, P., Boerries, M., Catala, A., Hasle, H., de Haas, V., Kallay, K., Masetti, R., De Moerloose, B., Dworzak, M., Schmugge, M., Smith, O., Stary, J., Mejstrikova, E., Ussowicz, M., Morris, E., Singh, P., Collin, M., Derecka, M., Gohring, G., Flotho, C., Strahm, B., Locatelli, Franco, Niemeyer, C. M., Trompouki, E., Wlodarski, M. W., and Locatelli F. (ORCID:0000-0002-7976-3654)

Abstract

Deficiency of the transcription factor GATA2 is a highly penetrant genetic disorder predisposing to myelodysplastic syndromes (MDS) and immunodeficiency. It has been recognized as the most common cause underlying primary MDS in children. Triggered by the discovery of a recurrent synonymous GATA2 variant, we systematically investigated 911 patients with phenotype of pediatric MDS or cellular deficiencies for the presence of synonymous alterations in GATA2. In total, we identified nine individuals with five heterozygous synonymous mutations: c.351C>G, p.T117T (N = 4); c.649C>T, p.L217L; c.981G>A, p.G327G; c.1023C>T, p.A341A; and c.1416G>A, p.P472P (N = 2). They accounted for 8.2% (9/110) of cases with GATA2 deficiency in our cohort and resulted in selective loss of mutant RNA. While for the hotspot mutation (c.351C>G) a splicing error leading to RNA and protein reduction was identified, severe, likely late stage RNA loss without splicing disruption was found for other mutations. Finally, the synonymous mutations did not alter protein function or stability. In summary, synonymous GATA2 substitutions are a new common cause of GATA2 deficiency. These findings have broad implications for genetic counseling and pathogenic variant discovery in Mendelian disorders.

Published
2020

72. Therapeutic Drug Monitoring of Asparaginase: Intra-individual Variability and Predictivity in Children With Acute Lymphoblastic Leukemia Treated With PEG-Asparaginase in the AIEOP-BFM Acute Lymphoblastic Leukemia 2009 Study

Author

Würthwein, G, Lanverskaminsky, C, Gerss, J, Möricke, A, Zimmermann, M, Stary, J, Smisek, P, Attarbaschi, A, Nath, C, Zucchetti, M, Rizzari, C, Schrappe, M, Boos, J, LanversKaminsky, C, Stary, Jan, Würthwein, G, Lanverskaminsky, C, Gerss, J, Möricke, A, Zimmermann, M, Stary, J, Smisek, P, Attarbaschi, A, Nath, C, Zucchetti, M, Rizzari, C, Schrappe, M, Boos, J, LanversKaminsky, C, and Stary, Jan

Abstract

BACKGROUND: Therapeutic drug monitoring (TDM) can identify patients with subtherapeutic asparaginase (ASNase) activity [silent inactivation (SI)] and prospectively guide therapeutic adaptation. However, limited intra-individual variability is a precondition for targeted dosing and the diagnosis of SI. METHODS: In the AIEOP-BFM acute lymphoblastic leukemia (ALL) 2009 trial, 2771 children with ALL were included and underwent ASNase-TDM in a central laboratory in Münster. Two biweekly administrations of pegylated ASNase during induction and a third dose during reinduction or the high-risk block, which was administered several weeks later, were monitored. We calculated (1) the incidence of SI; and (2) the predictivity of SI for SI after the subsequent administration. ASNase activities monitored during induction were categorized into percentiles at the respective sampling time points. These percentiles were used to calculate the intra-individual range of percentiles as a surrogate for intrapatient variability and to evaluate the predictivity of ASNase activity for the subsequent administration. RESULTS: The overall incidence of SI was low (4.9%). The positive predictive value of SI identified by one sample was ≤21%. Confirmation of SI by a second sample indicated a high positive predictive value of 100% for biweekly administrations, but not for administration more than 17 weeks later. Sampling and/or documentation errors were risks for misdiagnosis of SI. High intra-individual variability in ASNase activities, with ranges of percentiles over more than 2 quartiles and low predictivity, was observed in approximately 25% of the patients. These patients were likely to fail dose individualization based on TDM data. CONCLUSIONS: To use TDM as a basis for clinical decisions, standardized clinical procedures are required and high intra-individual variability should be taken into account. Details of the treatment are available in the European Clinical Trials Database at https

Published
2020

85. Blastic plasmacytoid dendritic cell neoplasm: First retrospective study in the Czech Republic

Author

CERNAN, M., primary, SZOTKOWSKI, T., additional, HISEMOVA, M., additional, CETKOVSKY, P., additional, SRAMKOVA, L., additional, STARY, J., additional, RACIL, Z., additional, MAYER, J., additional, SRAMEK, J., additional, JINDRA, P., additional, VISEK, B., additional, ZAK, P., additional, NOVAK, J., additional, KOZAK, T., additional, FURST, T., additional, and PAPAJIK, T., additional

Published
2020
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86. Erratum: Outcome of relapsed infant acute lymphoblastic leukemia treated on the interfant-99 protocol (Leukemia (2016) 30 5 (1184-1187))

Author

Driessen E. M. C., Driessen, E, de Lorenzo, P, Campbell, M, Felice, M, Ferster, A, Hann, I, Vora, A, Hovi, L, Escherich, G, Li, C, Mann, G, Leblanc, T, Locatelli, F, Biondi, A, Rubnitz, J, Schrappe, M, Silverman, L, Stary, J, Suppiah, R, Szczepanski, T, Valsecchi, M, Pieters, R, Driessen E. M. C., de Lorenzo P., Campbell M., Felice M., Ferster A., Hann I., Vora A., Hovi L., Escherich G., Li C. K., Mann G., Leblanc T., Locatelli F., Biondi A., Rubnitz J., Schrappe M., Silverman L., Stary J., Suppiah R., Szczepanski T., Valsecchi M., Pieters R., Driessen E. M. C., Driessen, E, de Lorenzo, P, Campbell, M, Felice, M, Ferster, A, Hann, I, Vora, A, Hovi, L, Escherich, G, Li, C, Mann, G, Leblanc, T, Locatelli, F, Biondi, A, Rubnitz, J, Schrappe, M, Silverman, L, Stary, J, Suppiah, R, Szczepanski, T, Valsecchi, M, Pieters, R, Driessen E. M. C., de Lorenzo P., Campbell M., Felice M., Ferster A., Hann I., Vora A., Hovi L., Escherich G., Li C. K., Mann G., Leblanc T., Locatelli F., Biondi A., Rubnitz J., Schrappe M., Silverman L., Stary J., Suppiah R., Szczepanski T., Valsecchi M., and Pieters R.

Abstract

This corrects the article DOI: 10.1038/leu.2015.246.

Published
2017

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