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451 results on '"Zemanova, Zuzana"'

6. Experience with luspatercept therapy in patients with transfusion-dependent low-risk myelodysplastic syndromes in real-world clinical practice: exploring the positive effect of combination with erythropoietin alfa.

Author

Jonasova, Anna, Sotakova, Slavka, Belohlavkova, Petra, Minarik, Lubomir, Stopka, Tomas, Jonas, Jan Jakub, Aghova, Tatiana, and Zemanova, Zuzana

Subjects
TRANSFORMING growth factors-beta, MYELODYSPLASTIC syndromes, ERYTHROPOIETIN
Abstract

Background: Luspatercept, an inhibitor of the transforming growth factor beta (TGF-β) pathway, is a novel treatment for anemic patients with lower-risk myelodysplastic syndromes (MDS) with transfusion dependence (TD) who do not respond to erythropoiesis-stimulating agents (ESA) therapy or are not suitable candidates for this treatment. We present real-world experience with luspatercept therapy from two hematology centers in the Czech Republic. Methods: By January 2024, 54 MDS patients (33 men, 21 women) with a median age of 74 years (range, 55–95) were treated with luspatercept ± ESA at two Charles University hematology centers in Prague and Hradec Králové. According to the WHO 2016 classification, the cohort included 32 MDS-RS-MLD, seven MDS-MLD, two patients with 5q- + ring sideroblasts (RS), 12 RARS-T, and 1 patient with CMML-0 + RS. SF3B1 mutation data were available for 45 patients. All patients were in the IPSS-R and IPSS-M lower-risk groups (except four IPSS-M high). The median follow-up was 17 months (range, 1–54). All patients were transfusion-dependent. Thirty-five (64.8%) patients had a high transfusion burden (HTB) with ≥ 4 transfusion units (TU)/8 weeks, and 19 (35.2%) had a low transfusion burden (LTB) (< 4 TU/8 weeks). The median time between diagnosis and initiation of luspatercept was 27 months (range, 4–156). ESA were used prior to luspatercept in 45 patients, and luspatercept was used as first-line treatment in nine patients. Thirty-one (61%) patients were treated simultaneously with ESA. Results: Only patients who received luspatercept for ≥ 8 weeks (51 patients) were assessed. We evaluated the achievement of transfusion independence (TI) lasting 8, 12, 16, and 24 weeks. Thirty-two (62.7%) patients achieved TI for ≥ 8 weeks, 31 (60.7%) for ≥ 12 weeks, 29 (56.8%) for ≥ 16 weeks, and 25 (49%) for ≥ 24 weeks. Hematologic improvement (HI) without TI was achieved in six patients (11.7%). Overall, HI + TI was achieved in 38 patients (74.5%). Epoetin alfa was used simultaneously in 31 patients (60.7%). In 21 (55.2%) of all responding patients, concomitant therapy with epoetin alfa led to an improved response, with 16 reaching TI. Thirteen (25.5%) patients were nonresponders. Eight (21%) patients experienced therapy failure and became transfusion-dependent again. Optimal response required a gradual increase in the luspatercept dose to 1.75 mg/kg in up to 35 patients, with 23 responders (TI + HI). Response rates varied by transfusion burden: 79% in LTB and 50% in HTB reached TI. Of RS+ patients, 70% reached TI, while only one out of five RS− patients achieved TI. Among 39 SF3B1 -positive patients, 61.6% achieved TI. In the low and very low IPSS-M groups, 86% of patients responded (TI + HI), compared to 62% in the moderate-low group. Luspatercept was well-tolerated, with no adverse events higher than grade II toxicity. Conclusion: We have demonstrated in real-world clinical practice that luspatercept is a very effective agent, even in an unselected, pretreated, significantly TD MDS population. The effect was particularly high in the IPSS-M low and very low groups. We believe that the relatively high response rate in our patients was influenced by the frequent use of a higher dose (1.75 mg/kg) and especially by adding ESA to luspatercept in poorly responding patients. [ABSTRACT FROM AUTHOR]

Published
2024
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7. Impact of PIK3CAgain and PTEN loss on mantle cell lymphoma biology and sensitivity to targeted therapies

Author

Bettazova, Nardjas, Senavova, Jana, Kupcova, Kristyna, Sovilj, Dana, Rajmonova, Anezka, Andera, Ladislav, Svobodova, Karla, Berkova, Adela, Zemanova, Zuzana, Daumova, Lenka, Herman, Vaclav, Dolníkova, Alexandra, Davis, R. Eric, Trneny, Marek, Klener, Pavel, and Havranek, Ondrej

Abstract

•PIK3CAgain and PTENloss decrease the dependence of MCL cells on BCR signaling and antiapoptotic BCL2.•PIK3CAgain and PTENloss lead to complex metabolic rewiring and increased survival of MCL cells under hypoxia.

Published
2024
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8. International cooperative study identifies treatment strategy in childhood ambiguous lineage leukemia

Author

Hrusak, Ondrej, de Haas, Valerie, Stancikova, Jitka, Vakrmanova, Barbora, Janotova, Iveta, Mejstrikova, Ester, Capek, Vaclav, Trka, Jan, Zaliova, Marketa, Luks, Ales, Bleckmann, Kirsten, Möricke, Anja, Irving, Julie, Konatkowska, Benigna, Alexander, Thomas B., Inaba, Hiroto, Schmiegelow, Kjeld, Stokley, Simone, Zemanova, Zuzana, Moorman, Anthony V., Rossi, Jorge Gabriel, Felice, Maria Sara, Dalla-Pozza, Luciano, Morales, Jessa, Dworzak, Michael, Buldini, Barbara, Basso, Giuseppe, Campbell, Myriam, Cabrera, Maria Elena, Marinov, Neda, Elitzur, Sarah, Izraeli, Shai, Luria, Drorit, Feuerstein, Tamar, Kolenova, Alexandra, Svec, Peter, Kreminska, Olena, Rabin, Karen R., Polychronopoulou, Sophia, da Costa, Elaine, Marquart, Hanne Vibeke, Kattamis, Antonis, Ratei, Richard, Reinhardt, Dirk, Choi, John K., Schrappe, Martin, and Stary, Jan

Published
2018
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12. Copy number neutral loss of heterozygosity at 17p and homozygous mutations of TP53 are associated with complex chromosomal aberrations in patients newly diagnosed with myelodysplastic syndromes

Author

Svobodova, Karla, Zemanova, Zuzana, Lhotska, Halka, Novakova, Milena, Podskalska, Lucie, Belickova, Monika, Brezinova, Jana, Sarova, Iveta, Izakova, Silvia, Lizcova, Libuse, Berkova, Adela, Siskova, Magda, Jonasova, Anna, Cermak, Jaroslav, and Michalova, Kyra

Published
2016
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14. Supplementary Data from Cotargeting of BCL2 with Venetoclax and MCL1 with S63845 Is Synthetically Lethal In Vivo in Relapsed Mantle Cell Lymphoma

Author

Prukova, Dana, primary, Andera, Ladislav, primary, Nahacka, Zuzana, primary, Karolova, Jana, primary, Svaton, Michael, primary, Klanova, Magdalena, primary, Havranek, Ondrej, primary, Soukup, Jan, primary, Svobodova, Karla, primary, Zemanova, Zuzana, primary, Tuskova, Diana, primary, Pokorna, Eva, primary, Helman, Karel, primary, Forsterova, Kristina, primary, Pacheco-Blanco, Mariana, primary, Vockova, Petra, primary, Berkova, Adela, primary, Fronkova, Eva, primary, Trneny, Marek, primary, and Klener, Pavel, primary

Published
2023
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15. Involvement of deleted chromosome 5 in complex chromosomal aberrations in newly diagnosed myelodysplastic syndromes (MDS) is correlated with extremely adverse prognosis

Author

Zemanova, Zuzana, Michalova, Kyra, Buryova, Halka, Brezinova, Jana, Kostylkova, Karla, Bystricka, Dagmar, Novakova, Milena, Sarova, Iveta, Izakova, Silvia, Lizcova, Libuse, Ransdorfova, Sarka, Krejcik, Zdenek, Merkerova, Michaela Dostalova, Dohnalova, Alena, Siskova, Magda, Jonasova, Anna, Neuwirtova, Radana, and Cermak, Jaroslav

Published
2014
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20. 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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21. Association of unbalanced translocation der(1;7) with germline GATA2 mutations

Author

Kozyra, Emilia J., Göhring, Gudrun, Hickstein, Dennis D., Calvo, Katherine R., DiNardo, Courtney D., Dworzak, Michael, de Haas, Valerie, Starý, Jan, Hasle, Henrik, Shimamura, Akiko, Fleming, Mark D., Inaba, Hiroto, Lewis, Sara, Hsu, Amy P., Holland, Steven M., Arnold, Danielle E., Mecucci, Cristina, Keel, Siobán B., Bertuch, Alison A., Tawana, Kiran, Barzilai, Shlomit, Hirabayashi, Shinsuke, Onozawa, Masahiro, Lei, Shaohua, Alaiz, Helena, Andrikovics, Hajnalka, Betts, David, Beverloo, Berna H., Buechner, Jochen, Čermák, Martin, Cervera, José, Haus, Olga, Jahnukainen, Kirsi, Manola, Kalliopi N., Nebral, Karin, Pasquali, Francesco, Tchinda, Joelle, Turkiewicz, Dominik, Van Roy, Nadine, Zemanova, Zuzana, Pastor, Victor B., Strahm, Brigitte, Noellke, Peter, Niemeyer, Charlotte M., Schlegelberger, Brigitte, Yoshimi, Ayami, and Wlodarski, Marcin W.

Published
2021
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24. 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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26. Fibroblast Activation Protein Expressing Mesenchymal Cells Promote Glioblastoma Angiogenesis

Author

Balaziova, Eva, Vymola, Petr, Hrabal, Petr, Mateu, Rosana, Zubal, Michal, Tomas, Robert, Netuka, David, Kramar, Filip, Zemanova, Zuzana, Svobodova, Karla, Brabec, Marek, Sedo, Aleksi, and Busek, Petr

Subjects
fibroblast activation protein, congenital, hereditary, and neonatal diseases and abnormalities, angiogenesis, seprase, angiopoietin, vessel destabilisation, glioblastoma, Neoplasms. Tumors. Oncology. Including cancer and carcinogens, neoplasms, microenvironment, Article, RC254-282, digestive system diseases
Abstract

Simple Summary The perivascular niche in glioblastoma is crucial for maintaining a tumour- permissive microenvironment. In various extracranial cancers, mesenchymal cells that express fibroblast activation protein (FAP) are an important stromal component and a potential therapeutic target. In this study, we examine their functions in the glioblastoma microenvironment where their role is so far largely unexplored. Glioblastoma-associated FAP+ mesenchymal cells are localised around activated endothelial cells and their presence positively correlates with vascular density. They represent a subpopulation of stromal, non-tumorigenic cells which mostly lack the chromosomal aberrations characteristic of glioma cells. By soluble factors they induce angiogenic sprouting, chemotaxis of endothelial cells, contribute to destabilisation of blood vessels, and increase the migration and growth of glioma cells. Taken together, we identified a subpopulation of FAP+ mesenchymal cells in the perivascular niche in glioblastoma that may contribute to tumour progression by promoting angiogenesis and supporting dissemination of transformed cells into the surrounding tissue. Abstract Fibroblast activation protein (FAP) is a membrane-bound protease that is upregulated in a wide range of tumours and viewed as a marker of tumour-promoting stroma. Previously, we demonstrated increased FAP expression in glioblastomas and described its localisation in cancer and stromal cells. In this study, we show that FAP+ stromal cells are mostly localised in the vicinity of activated CD105+ endothelial cells and their quantity positively correlates with glioblastoma vascularisation. FAP+ mesenchymal cells derived from human glioblastomas are non-tumorigenic and mostly lack the cytogenetic aberrations characteristic of glioblastomas. Conditioned media from these cells induce angiogenic sprouting and chemotaxis of endothelial cells and promote migration and growth of glioma cells. In a chorioallantoic membrane assay, co-application of FAP+ mesenchymal cells with glioma cells was associated with enhanced abnormal angiogenesis, as evidenced by an increased number of erythrocytes in vessel-like structures and higher occurrence of haemorrhages. FAP+ mesenchymal cells express proangiogenic factors, but in comparison to normal pericytes exhibit decreased levels of antiangiogenic molecules and an increased Angiopoietin 2/1 ratio. Our results show that FAP+ mesenchymal cells promote angiogenesis and glioma cell migration and growth by paracrine communication and in this manner, they may thus contribute to glioblastoma progression.

Published
2021
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27. Development of treatment and clinical results in childhood acute myeloid leukemia in the Czech Republic

Author

Sramkova, Lucie, Sterba, Jaroslav, Hrstkova, Hana, Mihal, Vladimir, Blazek, Bohumir, Timr, Pavel, Cerna, Zdena, Prochazkova, Daniela, Hak, Jiri, Sedlacek, Petr, Janotova, Iveta, Vodickova, Elena, Zemanova, Zuzana, Jarosova, Marie, Oltova, Alexandra, Zdrahalova, Katerina, Hrusak, Ondrej, Mejstrikova, Ester, Schwarz, Jiri, Zuna, Jan, Trka, Jan, and Stary, Jan

Published
2013
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29. Publisher Correction : Clinical evolution, genetic landscape and trajectories of clonal hematopoiesis in SAMD9/SAMD9L syndromes (Nature Medicine, (2021), 27, 10, (1806-1817), )

Author

Sahoo, Sushree S., Pastor, Victor B., Goodings, Charnise, Voss, Rebecca K., Kozyra, Emilia J., Szvetnik, Amina, Noellke, Peter, Dworzak, Michael, Starý, Jan, Locatelli, Franco, Masetti, Riccardo, Schmugge, Markus, De Moerloose, Barbara, Catala, Albert, Kállay, Krisztián, Turkiewicz, Dominik, Hasle, Henrik, Buechner, Jochen, Jahnukainen, Kirsi, Ussowicz, Marek, Polychronopoulou, Sophia, Smith, Owen P., Fabri, Oksana, Barzilai, Shlomit, de Haas, Valerie, Baumann, Irith, Schwarz-Furlan, Stephan, Moerloose, Barbara De, Kallay, Krisztián, Smith, Owen, Haas, Valérie De, Gohring, Gudrun, Niemeyer, Charlotte, Nebral, Karin, Simonitsch-Kluppp, Ingrid, Paepe, Pascale De, Van Roy, Nadine, Campr, Vit, Zemanova, Zuzana, Clasen-Linde, Erik, Plesner, Tine, Schlegelberger, Brigitte, Rudelius, Martina, Manola, Kalliopi, Stefanaki, Kalliopi, Csomor, Judit, Andrikovics, Hajnalka, Betts, David, O’Sullivan, Maureen, Zohar, Yaniv, Jeison, Marta, Vito, Rita De, Pasquali, Francesco, Maldyk, Jadwiga, Haus, Olga, Alaiz, Helena, Kjollerstrom, Paula, Lemos, Luis Mascarenhas de, Bodova, Ivana, Čermák, Martin, Plank, Lukas, Gazic, Barbara, Kavcic, Marko, Podgornik, Helena, Ros, Margarita Llavador, Cervera, Jose, Gengler, Carole, Tchinda, Joelle, Beverloo, Berna, Leguit, Roos, Niewisch, Marena R., Sauer, Martin G., Burkhardt, Birgit, Lang, Peter, Bader, Peter, Beier, Rita, Müller, Ingo, Albert, Michael H., Meisel, Roland, Schulz, Ansgar, Cario, Gunnar, Panda, Pritam K., Wehrle, Julius, Hirabayashi, Shinsuke, Derecka, Marta, Durruthy-Durruthy, Robert, Göhring, Gudrun, Yoshimi-Noellke, Ayami, Ku, Manching, Lebrecht, Dirk, Erlacher, Miriam, Flotho, Christian, Strahm, Brigitte, Niemeyer, Charlotte M., and Wlodarski, Marcin W.

Subjects
Medizin
Abstract

Korrektur zu 10.1038/s41591-021-01511-6

Published
2021

36. A high TP53 mutation burden is a strong predictor of primary refractory mantle cell lymphoma

Author

Obr, Ales, primary, Klener, Pavel, additional, Furst, Tomas, additional, Kriegova, Eva, additional, Zemanova, Zuzana, additional, Urbankova, Helena, additional, Jirkuvova, Andrea, additional, Petrackova, Anna, additional, Malarikova, Diana, additional, Forsterova, Kristina, additional, Cudova, Barbora, additional, Sedlarikova, Lenka, additional, Berkova, Adela, additional, Kasalova, Nela, additional, Papajik, Tomas, additional, and Trneny, Marek, additional

Published
2020
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38. Concurrent TP53 and CDKN2A Gene Aberrations in Newly Diagnosed Mantle Cell Lymphoma Correlate with Chemoresistance and Call for Innovative Upfront Therapy

Author

Malarikova, Diana, primary, Berkova, Adela, additional, Obr, Ales, additional, Blahovcova, Petra, additional, Svaton, Michael, additional, Forsterova, Kristina, additional, Kriegova, Eva, additional, Prihodova, Eva, additional, Pavlistova, Lenka, additional, Petrackova, Anna, additional, Zemanova, Zuzana, additional, Trneny, Marek, additional, and Klener, Pavel, additional

Published
2020
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39. Cryptic aberrations may allow more accurate prognostic classification of patients with myelodysplastic syndromes and clonal evolution

Author

Svobodova, Karla, primary, Lhotska, Halka, additional, Hodanova, Lucie, additional, Pavlistova, Lenka, additional, Vesela, Denisa, additional, Belickova, Monika, additional, Vesela, Jitka, additional, Brezinova, Jana, additional, Sarova, Iveta, additional, Izakova, Silvia, additional, Lizcova, Libuse, additional, Siskova, Magda, additional, Jonasova, Anna, additional, Cermak, Jaroslav, additional, Michalova, Kyra, additional, and Zemanova, Zuzana, additional

Published
2020
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40. Somatic mutation dynamics in MDS patients treated with azacitidine indicate clonal selection in patients-responders

Author

Polgarova, Kamila, Vargova, Karina, Kulvait, Vojtech, Dusilkova, Nina, Minarik, Lubomir, Zemanova, Zuzana, Pesta, Michal, Jonasova, Anna, and Stopka, Tomas

Subjects
azacitidine, AML, NGS, MDS, somatic mutation, Research Paper
Abstract

Azacitidine (AZA) for higher risk MDS patients is a standard therapy with limited durability. To monitor mutation dynamics during AZA therapy we utilized massive parallel sequencing of 54 genes previously associated with MDS/AML pathogenesis. Serial sampling before and during AZA therapy of 38 patients (reaching median overall survival 24 months (Mo) with 60% clinical responses) identified 116 somatic pathogenic variants with allele frequency (VAF) exceeding 5%. High accuracy of data was achieved via duplicate libraries from myeloid cells and T-cell controls. We observed that nearly half of the variants were stable while other variants were highly dynamic. Patients with marked decrease of allelic burden upon AZA therapy achieved clinical responses. In contrast, early-progressing patients on AZA displayed minimal changes of the mutation pattern. We modeled the VAF dynamics on AZA and utilized a joint model for the overall survival and response duration. While the presence of certain variants associated with clinical outcomes, such as the mutations of CDKN2A were adverse predictors while KDM6A mutations yield lower risk of dying, the data also indicate that allelic burden volatility represents additional important prognostic variable. In addition, preceding 5q- syndrome represents strong positive predictor of longer overall survival and response duration in high risk MDS patients treated with AZA. In conclusion, variants dynamics detected via serial sampling represents another parameter to consider when evaluating AZA efficacy and predicting outcome.

Published
2017

44. Novel SAMD9 Mutation in a Patient With Immunodeficiency, Neutropenia, Impaired Anti-CMV Response, and Severe Gastrointestinal Involvement

Author

Formankova, Renata, Kanderova, Veronika, Rackova, Marketa, Svaton, Michael, Brdicka, Tomas, Riha, Petr, Keslova, Petra, Mejstrikova, Ester, Zaliova, Marketa, Freiberger, Tomas, Grombirikova, Hana, Zemanova, Zuzana, Vlkova, Marcela, Fencl, Filip, Copova, Ivana, Bronsky, Jiri, Jabandziev, Petr, Sedlacek, Petr, Soukalova, Jana, Zapletal, Ondrej, Stary, Jan, Trka, Jan, Kalina, Tomas, Skvarova Kramarzova, Karolina, Hlavackova, Eva, Litzman, Jiri, and Fronkova, Eva

Subjects
dysphagia, SAMD9, MIRAGE, Immunology, hematopoietic stem cell transplantation, gastrointestinal disorder, neutropenia, Case Report, cytomegalovirus infection, immunodeficiency
Abstract

Mutations in the Sterile alpha motif domain containing 9 (SAMD9) gene have been described in patients with severe multisystem disorder, MIRAGE syndrome, but also in patients with bone marrow (BM) failure in the absence of other systemic symptoms. The role of hematopoietic stem cell transplantation (HSCT) in the management of the disease is still unclear. Here, we present a patient with a novel mutation in SAMD9 (c.2471 G>A, p.R824Q), manifesting with prominent gastrointestinal tract involvement and immunodeficiency, but without any sign of adrenal insufficiency typical for MIRAGE syndrome. He suffered from severe CMV (cytomegalovirus) infection at 3 months of age, with a delayed development of T lymphocyte functional response against CMV, profound T cell activation, significantly reduced B lymphocyte counts and impaired lymphocyte proliferative response. Cultured T cells displayed slightly lower calcium flux and decreased survival. At the age of 6 months, he developed severe neutropenia requiring G-CSF administration, and despite only mild morphological and immunophenotypical disturbances in the BM, 78% of the BM cells showed monosomy 7 at the age of 18 months. Surprisingly, T cell proliferation after CD3 stimulation and apoptosis of the cells normalized during the follow-up, possibly reflecting the gradual development of monosomy 7. Among other prominent symptoms, he had difficulty swallowing, requiring percutaneous endoscopic gastrostomy (PEG), frequent gastrointestinal infections, and perianal erosions. He suffered from repeated infections and periodic recurring fevers with the elevation of inflammatory markers. At 26 months of age, he underwent HSCT that significantly improved hematological and immunological laboratory parameters. Nevertheless, he continued to suffer from other conditions, and subsequently, he died at day 440 post-transplant due to sepsis. Pathogenicity of this novel SAMD9 mutation was confirmed experimentally. Expression of mutant SAMD9 caused a significant decrease in proliferation and increase in cell death of the transfected cells. Conclusion: We describe a novel SAMD9 mutation in a patient with prominent gastrointestinal and immunological symptoms but without adrenal hypoplasia. Thus, SAMD9 mutations should be considered as cause of enteropathy in pediatric patients. The insufficient therapeutic outcome of transplantation further questions the role of HSCT in the management of patients with SAMD9 mutations and multisystem involvement.

Published
2019

47. Guidance for reporting the interpretation of cytogenomic test results in haematological neoplasms

Author

Rack, Katrina, primary, van den Berg, Eva, additional, Haferlach, Claudia, additional, Beverloo, Berna, additional, Espinet, Blanca, additional, Foot, Nicola, additional, Martin, Kate, additional, O'Connor, Sheila, additional, Schoumans, Jacqueline, additional, Talley, Polly, additional, Stioui, Sabine, additional, Zemanova, Zuzana, additional, Luquet, Isabelle, additional, and Hastings, Ros, additional

Published
2019
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48. RUNX1 Mutation Accompanied with Dysregulated Cellular Senescence in Lower-Risk Myelodysplastic Syndrome Patients Is Associated with Disease Progression

Author

Hruba, Monika, primary, Vesela, Jitka, additional, Votavova, Hana, additional, Dostalova Merkerova, Michaela, additional, Kundrat, David, additional, Szikszai, Katarina, additional, Lauermanova, Marie, additional, Zemanova, Zuzana, additional, Jonasova, Anna, additional, Cermak, Jaroslav, additional, and Belickova, Monika, additional

Published
2019
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50. High TP53 Mutation Load Predicts Primary Refractory Mantle Cell Lymphoma

Author

Obr, Aleš, primary, Klener, Pavel, additional, Kriegova, Eva, additional, Zemanova, Zuzana, additional, Urbankova, Helena, additional, Jirkuvova, Andrea, additional, Petrackova, Anna, additional, Cudova, Barbora, additional, Sedlarikova, Lenka, additional, Prochazka, VIT K, additional, Papajik, Tomas, additional, and Trneny, Marek, additional

Published
2019
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