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1. The rare cases of co-occurrences of Down Syndrome Disease and Juvenile Myelomonocytic Leukemia

Author

Buldini, Barbara, primary, Tumino, Manuela, additional, Varotto, Elena, additional, Francescato, Samuela, additional, Peloso, Alberto, additional, Meglio, Annamaria Di, additional, Leszl, Anna, additional, Gabelli, Maria, additional, Cani, Alice, additional, Masetti, Riccardo, additional, Biffi, Alessandra, additional, Sainati, Laura, additional, and Bresolin, Silvia, additional

Published
2023
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2. Donor Cell Acute Myeloid Leukemia after Hematopoietic Stem Cell Transplantation for Chronic Granulomatous Disease: A Case Report and Literature Review

Author

Micheloni, Giovanni, primary, Frattini, Annalisa, additional, Donini, Marta, additional, Dusi, Stefano, additional, Leszl, Anna, additional, Di Meglio, Annamaria, additional, Pigazzi, Martina, additional, Musio, Antonio, additional, Zecca, Marco, additional, Mina, Tommaso, additional, Rabusin, Marco, additional, Roccia, Pamela, additional, Bernasconi, Paolo, additional, Dambruoso, Irene, additional, Minelli, Antonella, additional, Montalbano, Giuseppe, additional, Acquati, Francesco, additional, Porta, Giovanni, additional, Valli, Roberto, additional, and Pasquali, Francesco, additional

Published
2023
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4. Prognostic significance of additional cytogenetic aberrations in 733 de novo pediatric 11q23/MLL-rearranged AML patients: results of an international study

Author

Coenen, Eva A., Raimondi, Susana C., Harbott, Jochen, Zimmermann, Martin, Alonzo, Todd A., Auvrignon, Anne, Beverloo, H. Berna, Chang, Myron, Creutzig, Ursula, Dworzak, Michael N., Forestier, Erik, Gibson, Brenda, Hasle, Henrik, Harrison, Christine J., Heerema, Nyla A., Kaspers, Gertjan J.L., Leszl, Anna, Litvinko, Nathalia, Lo Nigro, Luca, Morimoto, Akira, Perot, Christine, Reinhardt, Dirk, Rubnitz, Jeffrey E., Smith, Franklin O., Stary, Jan, Stasevich, Irina, Strehl, Sabine, Taga, Takashi, Tomizawa, Daisuke, Webb, David, Zemanova, Zuzana, Pieters, Rob, Zwaan, C. Michel, and van den Heuvel-Eibrink, Marry M.

Published
2011
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5. Novel prognostic subgroups in childhood 11q23/MLL-rearranged acute myeloid leukemia: results of an international retrospective study

Author

Balgobind, Brian V., Raimondi, Susana C., Harbott, Jochen, Zimmermann, Martin, Alonzo, Todd A., Auvrignon, Anne, Beverloo, H. Berna, Chang, Myron, Creutzig, Ursula, Dworzak, Michael N., Forestier, Erik, Gibson, Brenda, Hasle, Henrik, Harrison, Christine J., Heerema, Nyla A., Kaspers, Gertjan J.L., Leszl, Anna, Litvinko, Nathalia, Nigro, Luca Lo, Morimoto, Akira, Perot, Christine, Pieters, Rob, Reinhardt, Dirk, Rubnitz, Jeffrey E., Smith, Franklin O., Stary, Jan, Stasevich, Irina, Strehl, Sabine, Taga, Takashi, Tomizawa, Daisuke, Webb, David, Zemanova, Zuzana, Zwaan, C. Michel, and van den Heuvel-Eibrink, Marry M.

Published
2009
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7. Targeting mesenchymal stromal cells plasticity to reroute acute myeloid leukemia course

Author

Borella, Giulia, primary, Da Ros, Ambra, additional, Borile, Giulia, additional, Porcù, Elena, additional, Tregnago, Claudia, additional, Benetton, Maddalena, additional, Marchetti, Anna, additional, Bisio, Valeria, additional, Montini, Barbara, additional, Michielotto, Barbara, additional, Cani, Alice, additional, Leszl, Anna, additional, Campodoni, Elisabetta, additional, Sandri, Monica, additional, Montesi, Monica, additional, Bresolin, Silvia, additional, Cairo, Stefano, additional, Buldini, Barbara, additional, Locatelli, Franco, additional, and Pigazzi, Martina, additional

Published
2021
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8. Bone marrow ectopic expression of a non-coding RNA in childhood T-cell acute lymphoblastic leukemia with a novel t(2;11)(q11.2;p15.1) translocation

Author

Leszl Anna, Panagopoulos Ioannis, Vasta Isabella, Caruso Sebastiano, D'Addabbo Pietro, Albano Francesco, Impera Luciana, Lonoce Angelo, Guastadisegni Maria, Basso Giuseppe, Rocchi Mariano, and Storlazzi Clelia

Subjects
Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Abstract

Abstract Chromosomal translocations play a crucial role in tumorigenesis, often resulting in the formation of chimeric genes or in gene deregulation through position effects. T-cell acute lymphoblastic leukemia (T-ALL) is associated with a large number of such rearrangements. We report the ectopic expression of the 3' portion of EST DA926692 in the bone marrow of a childhood T-ALL case showing a t(2;11)(q11.2;p15.1) translocation as the sole chromosome abnormality. The breakpoints, defined at the sequence level, mapped within HPS5 (Hermansky Pudlak syndrome 5) intron 1 at 11p15.1, and DA926692 exon 2 at 2q11.2. The translocation was accompanied by a submicroscopic inversion that brought the two genes into the same transcriptional orientation. No chimeric trancript was detected. Interestingly, Real-Time Quantitative (RQ)-PCR detected, in the patient's bone marrow, expression of a 173 bp product corresponding to the 3' portion of DA926692. Samples from four T-ALL cases with a normal karyotype and normal bone marrow used as controls were negative. It might be speculated that the juxtaposition of this genomic segment to the CpG island located upstream HPS5 activated DA92669 expression. RQ-PCR analysis showed expression positivity in 6 of 23 human tissues examined. Bioinformatic analysis excluded that this small non-coding RNA is a precursor of micro-RNA, although it is conceivable that it has a different, yet unknown, functional role. To the best of our knowledge, this is the first report, in cancer, of the activation of a small non-coding RNA as a result of a chromosomal translocation.

Published
2008
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9. Targeting the plasticity of mesenchymal stromal cells to reroute the course of acute myeloid leukemia

Author

Borella, Giulia, Da Ros, Ambra, Borile, Giulia, Porcù, Elena, Tregnago, Claudia, Benetton, Maddalena, Marchetti, Anna, Bisio, Valeria, Montini, Barbara, Michielotto, Barbara, Cani, Alice, Leszl, Anna, Campodoni, Elisabetta, Sandri, Monica, Montesi, Monica, Bresolin, Silvia, Cairo, Stefano, Buldini, Barbara, Locatelli, Franco, and Pigazzi, Martina

Abstract

Bone marrow (BM) microenvironment contributes to the regulation of normal hematopoiesis through a finely tuned balance of self-renewal and differentiation processes, cell–cell interaction, and secretion of cytokines that during leukemogenesis are altered and favor tumor cell growth. In pediatric acute myeloid leukemia (AML), chemotherapy is the standard of care, but >30% of patients still relapse. The need to accelerate the evaluation of innovative medicines prompted us to investigate the role of mesenchymal stromal cells (MSCs) in the leukemic niche to define its contribution to the mechanism of leukemia drug escape. We generated a humanized 3-dimensional (3D) niche with AML cells and MSCs derived from either patients (AML-MSCs) or healthy donors. We observed that AML cells establish physical connections with MSCs, mediating a reprogrammed transcriptome inducing aberrant cell proliferation and differentiation and severely compromising their immunomodulatory capability. We confirmed that AML cells modulate h-MSCs transcriptional profile promoting functions similar to the AML-MSCs when cocultured in vitro, thus facilitating leukemia progression. Conversely, MSCs derived from BM of patients at time of disease remission showed recovered healthy features at transcriptional and functional levels, including the secretome. We proved that AML blasts alter MSCs activities in the BM niche, favoring disease development and progression. We discovered that a novel AML-MSC selective CaV1.2 channel blocker drug, lercanidipine, is able to impair leukemia progression in 3D both in vitro and when implanted in vivo if used in combination with chemotherapy, supporting the hypothesis that synergistic effects can be obtained by dual targeting approaches.

Published
2021
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12. Management of Chronic Myeloid Leukemia in Children and Adolescents According to Local Guidelines.the Italian Experience

Author

Giona, Fiorina, primary, Santopietro, Michelina, additional, Menna, Giuseppe, additional, Putti, Maria Caterina, additional, Micalizzi, Concetta, additional, Santoro, Nicola, additional, Ziino, Ottavio, additional, Mura, Rosamaria, additional, Ladogana, Saverio, additional, Iaria, Grazia, additional, Sau, Antonella, additional, Burnelli, Roberta, additional, Vacca, Nadia, additional, Nardi, Margherita, additional, Consarino, Caterina, additional, Moleti, Maria Luisa, additional, Nanni, Mauro, additional, Diverio, Daniela, additional, Leszl, Anna, additional, Biondi, Andrea, additional, Locatelli, Franco, additional, Saglio, Giuseppe, additional, and Foà, Robin, additional

Published
2016
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13. Genetic profile of T-cell acute lymphoblastic leukemias with MYC translocations

Author

La Starza, R, Borga, C, Barba, G, Pierini, V, Schwab, C, Matteucci, C, Lema Fernandez, A, Leszl, A, Cazzaniga, G, Chiaretti, S, Basso, G, Harrison, C, Te Kronnie, G, Mecucci, C, La Starza, Roberta, Borga, Chiara, Barba, Gianluca, Pierini, Valentina, Schwab, Claire, Matteucci, Caterina, Lema Fernandez, Anair G., Leszl, Anna, Cazzaniga, Giovanni, Chiaretti, Sabina, Basso, Giuseppe, Harrison, Christine J., Te Kronnie, Geertruy, Mecucci, Cristina, La Starza, R, Borga, C, Barba, G, Pierini, V, Schwab, C, Matteucci, C, Lema Fernandez, A, Leszl, A, Cazzaniga, G, Chiaretti, S, Basso, G, Harrison, C, Te Kronnie, G, Mecucci, C, La Starza, Roberta, Borga, Chiara, Barba, Gianluca, Pierini, Valentina, Schwab, Claire, Matteucci, Caterina, Lema Fernandez, Anair G., Leszl, Anna, Cazzaniga, Giovanni, Chiaretti, Sabina, Basso, Giuseppe, Harrison, Christine J., Te Kronnie, Geertruy, and Mecucci, Cristina

Abstract

MYC translocations represent a genetic subtype of T-lineage acute lymphoblastic leukemia (T-ALL), which occurs at an incidence of ∼6%, assessed within a cohort of 196 T-ALL patients (64 adults and 132 children). The translocations were of 2 types; those rearranged with the T-cell receptor loci and those with other partners. MYCtranslocations were significantly associated with the TAL/LMO subtype of T-ALL (P 5 .018) and trisomies 6 (P < .001) and 7 (P < .001). Within the TAL/LMO subtype, gene expression profiling identified 148 differentially expressed genes between patients with and without MYC translocations; specifically, 77 were upregulated and 71 downregulated in those with MYC translocations. The poor prognostic marker, CD44, was among the upregulated genes. MYC translocations occurred as secondary abnormalities, present in subclones in one-half of the cases. Longitudinal studies indicated an association with induction failure and relapse.

Published
2014

14. Prognostic significance of additional cytogenetic aberrations in 733 de novo pediatric 11q23/MLL-rearranged AML patients : results of an international study

Author

Coenen, Eva A, Raimondi, Susana C, Harbott, Jochen, Zimmermann, Martin, Alonzo, Todd A, Auvrignon, Anne, Beverloo, H Berna, Chang, Myron, Creutzig, Ursula, Dworzak, Michael N, Forestier, Erik, Gibson, Brenda, Hasle, Henrik, Harrison, Christine J, Heerema, Nyla A, Kaspers, Gertjan J L, Leszl, Anna, Litvinko, Nathalia, Lo Nigro, Luca, Morimoto, Akira, Perot, Christine, Reinhardt, Dirk, Rubnitz, Jeffrey E, Smith, Franklin O, Stary, Jan, Stasevich, Irina, Strehl, Sabine, Taga, Takashi, Tomizawa, Daisuke, Webb, David, Zemanova, Zuzana, Pieters, Rob, Zwaan, C Michel, van den Heuvel-Eibrink, Marry M, Coenen, Eva A, Raimondi, Susana C, Harbott, Jochen, Zimmermann, Martin, Alonzo, Todd A, Auvrignon, Anne, Beverloo, H Berna, Chang, Myron, Creutzig, Ursula, Dworzak, Michael N, Forestier, Erik, Gibson, Brenda, Hasle, Henrik, Harrison, Christine J, Heerema, Nyla A, Kaspers, Gertjan J L, Leszl, Anna, Litvinko, Nathalia, Lo Nigro, Luca, Morimoto, Akira, Perot, Christine, Reinhardt, Dirk, Rubnitz, Jeffrey E, Smith, Franklin O, Stary, Jan, Stasevich, Irina, Strehl, Sabine, Taga, Takashi, Tomizawa, Daisuke, Webb, David, Zemanova, Zuzana, Pieters, Rob, Zwaan, C Michel, and van den Heuvel-Eibrink, Marry M

Abstract

We previously demonstrated that outcome of pediatric 11q23/MLL-rearranged AML depends on the translocation partner (TP). In this multicenter international study on 733 children with 11q23/MLL-rearranged AML, we further analyzed which additional cytogenetic aberrations (ACA) had prognostic significance. ACAs occurred in 344 (47%) of 733 and were associated with unfavorable outcome (5-year overall survival [OS] 47% vs 62%, P < .001). Trisomy 8, the most frequent specific ACA (n = 130/344, 38%), independently predicted favorable outcome within the ACAs group (OS 61% vs 39%, P = .003; Cox model for OS hazard ratio (HR) 0.54, P = .03), on the basis of reduced relapse rate (26% vs 49%, P < .001). Trisomy 19 (n = 37/344, 11%) independently predicted poor prognosis in ACAs cases, which was partly caused by refractory disease (remission rate 74% vs 89%, P = .04; OS 24% vs 50%, P < .001; HR 1.77, P = .01). Structural ACAs had independent adverse prognostic value for event-free survival (HR 1.36, P = .01). Complex karyotype, defined as ≥ 3 abnormalities, was present in 26% (n = 192/733) and showed worse outcome than those without complex karyotype (OS 45% vs 59%, P = .003) in univariate analysis only. In conclusion, like TP, specific ACAs have independent prognostic significance in pediatric 11q23/MLL-rearranged AML, and the mechanism underlying these prognostic differences should be studied.

Published
2011
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15. Novel prognostic subgroups in childhood 11q23/MLL-rearranged acute myeloid leukemia : results of an international retrospective study.

Author

Balgobind, Brian V, Raimondi, Susana C, Harbott, Jochen, Zimmermann, Martin, Alonzo, Todd A, Auvrignon, Anne, Beverloo, H Berna, Chang, Myron, Creutzig, Ursula, Dworzak, Michael N, Forestier, Erik, Gibson, Brenda, Hasle, Henrik, Harrison, Christine J, Heerema, Nyla A, Kaspers, Gertjan J L, Leszl, Anna, Litvinko, Nathalia, Nigro, Luca Lo, Morimoto, Akira, Perot, Christine, Pieters, Rob, Reinhardt, Dirk, Rubnitz, Jeffrey E, Smith, Franklin O, Stary, Jan, Stasevich, Irina, Strehl, Sabine, Taga, Takashi, Tomizawa, Daisuke, Webb, David, Zemanova, Zuzana, Zwaan, C Michel, van den Heuvel-Eibrink, Marry M, Balgobind, Brian V, Raimondi, Susana C, Harbott, Jochen, Zimmermann, Martin, Alonzo, Todd A, Auvrignon, Anne, Beverloo, H Berna, Chang, Myron, Creutzig, Ursula, Dworzak, Michael N, Forestier, Erik, Gibson, Brenda, Hasle, Henrik, Harrison, Christine J, Heerema, Nyla A, Kaspers, Gertjan J L, Leszl, Anna, Litvinko, Nathalia, Nigro, Luca Lo, Morimoto, Akira, Perot, Christine, Pieters, Rob, Reinhardt, Dirk, Rubnitz, Jeffrey E, Smith, Franklin O, Stary, Jan, Stasevich, Irina, Strehl, Sabine, Taga, Takashi, Tomizawa, Daisuke, Webb, David, Zemanova, Zuzana, Zwaan, C Michel, and van den Heuvel-Eibrink, Marry M

Abstract

Translocations involving chromosome 11q23 frequently occur in pediatric acute myeloid leukemia (AML) and are associated with poor prognosis. In most cases, the MLL gene is involved, and more than 50 translocation partners have been described. Clinical outcome data of the 11q23-rearranged subgroups are scarce because most 11q23 series are too small for meaningful analysis of subgroups, although some studies suggest that patients with t(9;11)(p22;q23) have a more favorable prognosis. We retrospectively collected outcome data of 756 children with 11q23- or MLL-rearranged AML from 11 collaborative groups to identify differences in outcome based on translocation partners. All karyotypes were centrally reviewed before assigning patients to subgroups. The event-free survival of 11q23/MLL-rearranged pediatric AML at 5 years from diagnosis was 44% (+/- 5%), with large differences across subgroups (11% +/- 5% to 92% +/- 5%). Multivariate analysis identified the following subgroups as independent prognostic predictors: t(1;11)(q21;q23) (hazard ratio [HR] = 0.1, P = .004); t(6;11)(q27;q23) (HR = 2.2, P < .001); t(10;11)(p12;q23) (HR = 1.5, P = .005); and t(10;11)(p11.2;q23) (HR = 2.5, P = .005). We could not confirm the favorable prognosis of the t(9;11)(p22;q23) subgroup. We identified large differences in outcome within 11q23/MLL-rearranged pediatric AML and novel subgroups based on translocation partners that independently predict clinical outcome. Screening for these translocation partners is needed for accurate treatment stratification at diagnosis.

Published
2009
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16. Novel Chimeric Transcripts Involving PAX5 in B-Cell Precursor ALL

Author

Fazio, Grazia, primary, Storlazzi, Clelia Tiziana, additional, Severgnini, Marco, additional, Cazzaniga, Valeria, additional, Impera, Luciana, additional, Daniele, Giulia, additional, Iacobucci, Ilaria, additional, Galbiati, Marta, additional, Leszl, Anna, additional, Bungaro, Silvia, additional, Cifola, Ingrid, additional, De Bellis, Gianluca, additional, Martinelli, Giovanni, additional, Basso, Giuseppe, additional, Biondi, Andrea, additional, and Cazzaniga, Giovanni, additional

Published
2013
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17. CI-FISH, GEP, and SNPs Correlate Genomic Categories with Risk Stratification in Children with T-ALL.

Author

la Starza, Roberta, primary, Lettieri, Antonella, additional, Pierini, Valentina, additional, Matteucci, Caterina, additional, Nofrini, Valeria, additional, Gorello, Paolo, additional, Songia, Simona, additional, Crescenzi, Barbara, additional, te Kronnie, Geertruy, additional, Giordan, Marco, additional, Leszl, Anna, additional, Valsecchi, Maria Grazia, additional, Aversa, Franco, additional, Basso, Giuseppe, additional, Biondi, Andrea, additional, Conter, Valentino, additional, Cazzaniga, Giovanni, additional, and Mecucci, Cristina, additional

Published
2012
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18. Familial platelet disorder with propensity to acute myelogenous leukemia: genetic heterogeneity and progression to leukemia via acquisition of clonal chromosome anomalies

Author

Minelli, Antonella, Maserati, Emanuela, Rossi, Gabriele, Bernardo, Maria Ester, De Stefano, Piero, Cecchini, Maria Paola, Valli, Roberto, Albano, Veronica, Pierani, Paolo, Leszl, Anna, Sainati, Laura, Lo Curto, Francesco, Danesino, Cesare, Locatelli, Franco, Pasquali, Francesco, Locatelli, Franco (ORCID:0000-0002-7976-3654), Minelli, Antonella, Maserati, Emanuela, Rossi, Gabriele, Bernardo, Maria Ester, De Stefano, Piero, Cecchini, Maria Paola, Valli, Roberto, Albano, Veronica, Pierani, Paolo, Leszl, Anna, Sainati, Laura, Lo Curto, Francesco, Danesino, Cesare, Locatelli, Franco, Pasquali, Francesco, and Locatelli, Franco (ORCID:0000-0002-7976-3654)

Abstract

Familial platelet disorder with propensity to acute myelogenous leukemia, or FPD/AML (OMIM #601399), is a rare autosomal dominant condition, with only 12 families reported. It is characterized by qualitative and quantitative platelet defects and predisposition to the development of myeloid malignancies. Causal mutations have been identified in the RUNX1 gene (also known as AML1, CBFA2) in the 11 families so far analyzed. RUNX1 is a gene frequently involved in the pathogenesis of sporadic leukemia and myelodysplastic syndromes, through acquired chromosome rearrangements and point mutations. We report an Italian family with three members affected with FPD/AML, two sibs and their father, who developed myelodysplastic syndromes (which in one subsequently evolved into AML). Direct sequencing and polymorphisms haplotype analysis of the region of chromosome 21 where RUNX1 is mapped demonstrated that FPD/AML in this family was not caused by any mutation of the RUNX1 gene, thus providing evidence for the genetic heterogeneity of this disorder. Cytogenetic studies showed monosomy 7 in the marrow of all the three affected subjects, as well as an independent clone with trisomy 8 in the father. The importance of mucator effects in the pathogenesis of familial myeloid malignancies characterized by relevant chromosome changes, in the presence or absence of an underlying Mendelian disorder, has already been suggested. Our results and a review of the cytogenetic literature led us to postulate that mutations also causing FPD/AML may have a mutator effect that could give origin to myelodysplastic syndromes and acute myeloid leukemias through acquired chromosome changes. (C) 2004 Wiley-Liss, Inc.

Published
2004

19. Clinical Impact of Additional Cytogenetic Aberrations and Complex Karyotype In Pediatric 11q23/MLL-Rearranged AML: Results from an International Retrospective Study

Author

Coenen, Eva A, primary, Raimondi, Susana C., additional, Harbott, Jochen, additional, Martin, Zimmermann, additional, Balgobind, Brian V, additional, Alonzo, Todd A., additional, Auvrignon, Anne, additional, Beverloo, Berna, additional, Chang, Myron, additional, Creutzig, Ursula, additional, Dworzak, Michael, additional, Forestier, Erik, additional, Gibson, Brenda, additional, Hasle, Henrik, additional, Harrison, Christine J, additional, Heerema, Nyla A., additional, Kaspers, Gertjan J., additional, Leszl, Anna, additional, Litvinko, Nathalia, additional, Nigro, Luca lo, additional, Morimoto, Akira, additional, Perot, Christine, additional, Reinhardt, Dirk, additional, Rubnitz, Jeffrey, additional, Smith, Franklin O., additional, Stary, Jan, additional, Stasevich, Irina, additional, Strehl, Sabine, additional, Taga, Takashi, additional, Tomizawa, Daisuke, additional, Webb, David, additional, Zemanova, Zuzana, additional, Pieters, Rob, additional, Zwaan, C. Michel, additional, and Heuvel-Eibrink, Marry van den, additional

Published
2010
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20. Biological Features and Prognostic Impact of CRLF2 Overexpression In Childhood ALL

Author

Cazzaniga, Giovanni, primary, Vendramini, Elena, additional, Palmi, Chiara, additional, Silvestri, Daniela, additional, Frison, Daniela, additional, Longinotti, Giulia, additional, Leszl, Anna, additional, Fazio, Grazia, additional, Giarin, Emanuela, additional, Rossi, Vincenzo, additional, Bungaro, Silvia, additional, Basso, Giuseppe, additional, Biondi, Andrea, additional, Valsecchi, Maria Grazia, additional, Conter, Valentino, additional, and Kronnie, Truus te, additional

Published
2010
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21. Trisomy of Chromosome 7: a Novel Cytogenetic Abnormality in a Paediatric Case of Mixed Acute Leukemia.

Author

Parasole, Rosanna, primary, Vicari, Laura, additional, Petruzziello, Fara, additional, Leszl, Anna, additional, Menna, Giuseppe, additional, Tarsitano, M., additional, Del Vecchio, Luigi, additional, Scalia, Giulia, additional, Maisto, Giovanna, additional, Basso, Giuseppe, additional, Poggi, Vincenzo, additional, and Marra, Nicoletta, additional

Published
2009
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22. Imatinib Mesylate Induces High Complete Cytogenetic and Molecular Response Rates in Children and Adolescents with Philadelphia Chromosome-Positive (Ph+) Chronic Myelogenous Leukemia (CML) in Chronic Phase (CP)

Author

Giona, Fiorina, primary, Putti, Maria Caterina, primary, Moleti, Maria Luisa, primary, Nanni, Mauro, primary, Testi, Anna Maria, primary, Varotto, Stefania, primary, Gottardi, Enrico Marco, primary, De Vellis, Annalisa, primary, Nunes, Vittorio, primary, Diverio, Daniela, primary, Leszl, Anna, primary, Saglio, Giuseppe, primary, and Foà, Robert, primary

Published
2008
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23. Bone marrow ectopic expression of a non-coding RNA in childhood T-cell acute lymphoblastic leukemia with a novel t(2;11)(q11.2;p15.1) translocation

Author

Guastadisegni, Maria Corsignano, primary, Lonoce, Angelo, additional, Impera, Luciana, additional, Albano, Francesco, additional, D'Addabbo, Pietro, additional, Caruso, Sebastiano, additional, Vasta, Isabella, additional, Panagopoulos, Ioannis, additional, Leszl, Anna, additional, Basso, Giuseppe, additional, Rocchi, Mariano, additional, and Storlazzi, Clelia Tiziana, additional

Published
2008
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24. Identification of New Genomic Lesions in Childhood ALL without Known Genetic Aberrations: A Microarray Study of Gene Expression and Genotype Data.

Author

Bungaro, Silvia, primary, Dell’Orto, Marta Campo, additional, Basso, Dario, additional, Gorletta, Tatiana A., additional, Raghavan, Manoj, additional, Leszl, Anna, additional, Young, Bryan D., additional, Basso, Giuseppe, additional, te Kronnie, Gertruy, additional, Bicciato, Silvio, additional, Biondi, Andrea, additional, and Cazzaniga, Giovanni, additional

Published
2006
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26. Novel Chimeric Transcripts Involving PAX5in B-Cell Precursor ALL

Author

Fazio, Grazia, Storlazzi, Clelia Tiziana, Severgnini, Marco, Cazzaniga, Valeria, Impera, Luciana, Daniele, Giulia, Iacobucci, Ilaria, Galbiati, Marta, Leszl, Anna, Bungaro, Silvia, Cifola, Ingrid, De Bellis, Gianluca, Martinelli, Giovanni, Basso, Giuseppe, Biondi, Andrea, and Cazzaniga, Giovanni

Abstract

PAX5, located on 9p13, belongs to the PAXgene family and encodes for a transcription factor essential for B lymphoid cell commitment. It functions both as a transcriptional activator and repressor of different target genes involved in lineages development. PAX5has been recently reported to be target of aberrancies (including point mutation, deletions, and gene fusions), in approximately 30% of pediatric patients affected by BCP-ALL, the most frequent leukemia subset in children. Translocations are estimated to occur at an incidence of 2-3%, with a variety of partner genes, encoding for transcription factors (TEL, PML, FOXP1), kinases (JAK2), structural proteins (ELN, POM121) or molecules of unknown function (C20orf112, AUTS2).

Published
2013
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28. Three novel fusion transcripts of the paired box 5 gene in B-cell precursor acute lymphoblastic leukemia

Author

Ilaria Iacobucci, Giulia Daniele, Marta Galbiati, Paola Bresciani, Giovanni Martinelli, Clelia Tiziana Storlazzi, Ingrid Cifola, Grazia Fazio, Luciana Impera, Giovanni Cazzaniga, Valeria Cazzaniga, Giuseppe Basso, Andrea Biondi, Marco Severgnini, Anna Leszl, Gianluca De Bellis, Fazio, G, Daniele, G, Cazzaniga, V, Impera, L, Severgnini, M, Iacobucci, I, Galbiati, M, Leszl, A, Cifola, I, De Bellis, G, Bresciani, P, Martinelli, G, Basso, G, Biondi, A, Storlazzi, C, Cazzaniga, G, Fazio, Grazia, Daniele, Giulia, Cazzaniga, Valeria, Impera, Luciana, Severgnini, Marco, Iacobucci, Ilaria, Galbiati, Marta, Leszl, Anna, Cifola, Ingrid, Bellis, Gianluca De, Bresciani, Paola, Martinelli, Giovanni, Basso, Giuseppe, Biondi, Andrea, Storlazzi, Clelia Tiziana, and Cazzaniga, Giovanni

Subjects
B-cell precursor ALL, PAX5, CHFR, fusion gene, Oncogene Proteins, Fusion, B-cell precursor ALL, Prognosi, Ubiquitin-Protein Ligases, Cell, Cell Cycle Proteins, CHFR, Biology, B-Cell-Specific Activator Protein, Fusion gene, Chromosome Aberration, Translocation, Genetic, Neoplasm Protein, immune system diseases, Precursor B-Cell Lymphoblastic Leukemia-Lymphoma, hemic and lymphatic diseases, Cell Cycle Protein, medicine, Humans, Chromosomes, Human, Online Only Articles, Poly-ADP-Ribose Binding Proteins, Gene, Transcription factor, In Situ Hybridization, Fluorescence, B cell, Nuclear Protein, Chromosome Aberrations, PAX5, Protein, Medicine (all), PAX5 Transcription Factor, Nuclear Proteins, Proteins, Hematology, Prognosis, Molecular biology, Neoplasm Proteins, Cytoskeletal Proteins, ETV6, medicine.anatomical_structure, Cancer research, Transcription Factors, Human
Abstract

PAX5 encodes for a transcription factor essential for B-lymphoid cell commitment and is rearranged in 30% of B-cell precursor acute lymphoblastic leukemia pediatric patients (BCP-ALL). Since the first characterization of PAX5/ETV6, an increasing number of PAX5 fusion genes have been described in both adult and pediatric BCP-ALL patients. As reported in our recent review, PAX5 fusion partners encode a variety of proteins involved in cell structure (ELN, POM121), transcriptional regulation (ETV6, PML, FOXP1, MLLT3), phosphorylation (JAK2), and unknown functions (C20orf112,7AUTS2). Here we report the characterization of three new PAX5 partner genes in BCP-ALL: CHFR (a novel transcript isoform), SOX5 and POM121C. Moreover, we report cases displaying PAX5/AUTS2 and PAX5/MLLT3 fusions.

Published
2015
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29. Three novel fusion transcripts of the paired box 5 gene in B-cell precursor acute lymphoblastic leukemia.

Author

Fazio G, Daniele G, Cazzaniga V, Impera L, Severgnini M, Iacobucci I, Galbiati M, Leszl A, Cifola I, De Bellis G, Bresciani P, Martinelli G, Basso G, Biondi A, Storlazzi CT, and Cazzaniga G

Subjects
Chromosome Aberrations, Cytoskeletal Proteins, Humans, In Situ Hybridization, Fluorescence, Poly-ADP-Ribose Binding Proteins, Precursor B-Cell Lymphoblastic Leukemia-Lymphoma, Prognosis, Transcription Factors, Translocation, Genetic genetics, Ubiquitin-Protein Ligases, Cell Cycle Proteins genetics, Chromosomes, Human genetics, Neoplasm Proteins genetics, Nuclear Proteins genetics, Oncogene Proteins, Fusion genetics, PAX5 Transcription Factor genetics, Proteins genetics
Published
2015
Full Text
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