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13 results on '"Zamecnik, Josef"'

1. Correction to: Amplification of the PLAG-family genes—PLAGL1 and PLAGL2—is a key feature of the novel tumor type CNS embryonal tumor with PLAGL amplification (Acta Neuropathologica, (2023), 145, 1, (49-69), 10.1007/s00401-022-02516-2)

Author

Keck, Michaela-Kristina, Sill, Martin, Wittmann, Andrea, Joshi, Piyush, Stichel, Damian, Beck, Pengbo, Okonechnikow, Konstantin, Sievers, Philipp, Wefers, Annika K, Roncaroli, Federico, Avula, Shivaram, McCabe, Martin G, Hayden, James T, Wesseling, Pieter, Øra, Ingrid, Nistér, Monica, Kranendonk, Mariëtte E G, Tops, Bastiaan B J, Zapotocky, Michal, Zamecnik, Josef, Vasiljevic, Alexandre, Fenouil, Tanguy, Meyronet, David, von Hoff, Katja, Schüller, Ulrich, Loiseau, Hugues, Figarella-Branger, Dominique, Kramm, Christof M, Sturm, Dominik, Scheie, David, Rauramaa, Tuomas, Pesola, Jouni, Gojo, Johannes, Haberler, Christine, Brandner, Sebastian, Jacques, Tom, Sexton Oates, Alexandra, Saffery, Richard, Koscielniak, Ewa, Baker, Suzanne J, Yip, Stephen, Snuderl, Matija, Ud Din, Nasir, Samuel, David, Schramm, Kathrin, Blattner-Johnson, Mirjam, Selt, Florian, Ecker, Jonas, Milde, Till, von Deimling, Andreas, Korshunov, Andrey, Perry, Arie, Pfister, Stefan M, Sahm, Felix, and Solomon, David A

Subjects
Manchester Cancer Research Centre, ResearchInstitutes_Networks_Beacons/mcrc
Abstract

In the original publication, incorrect version of Fig. 6 was published and the correct version (Fig. 6) is given below. The original article has been corrected.

Published
2023
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2. Correction to: Amplification of the PLAG-family genes—PLAGL1 and PLAGL2—is a key feature of the novel tumor type CNS embryonal tumor with PLAGL amplification (Acta Neuropathologica, (2023), 145, 1, (49-69), 10.1007/s00401-022-02516-2)

Author

Keck, Michaela-Kristina, Sill, Martin, Wittmann, Andrea, Joshi, Piyush, Stichel, Damian, Beck, Pengbo, Okonechnikow, Konstantin, Sievers, Philipp, Wefers, Annika K., Roncaroli, Federico, Avula, Shivaram, McCabe, Martin G., Hayden, James T., Wesseling, Pieter, Øra, Ingrid, Nistér, Monica, Kranendonk, Mariëtte E. G., Tops, Bastiaan B. J., Zapotocky, Michal, Zamecnik, Josef, Vasiljevic, Alexandre, Fenouil, Tanguy, Meyronet, David, von Hoff, Katja, Schüller, Ulrich, Loiseau, Hugues, Figarella-Branger, Dominique, Kramm, Christof M., Sturm, Dominik, Scheie, David, Rauramaa, Tuomas, Pesola, Jouni, Gojo, Johannes, Haberler, Christine, Brandner, Sebastian, Jacques, Tom, Sexton Oates, Alexandra, Saffery, Richard, Koscielniak, Ewa, Baker, Suzanne J., Yip, Stephen, Snuderl, Matija, Ud Din, Nasir, Samuel, David, Schramm, Kathrin, Blattner-Johnson, Mirjam, Selt, Florian, Ecker, Jonas, Milde, Till, von Deimling, Andreas, Korshunov, Andrey, Perry, Arie, Pfister, Stefan M., Sahm, Felix, Solomon, David A., Jones, David T. W., Pathology, AII - Cancer immunology, CCA - Cancer biology and immunology, and CCA - Imaging and biomarkers

Abstract

In the original publication, incorrect version of Fig. 6 was published and the correct version (Fig. 6) is given below. The original article has been corrected.

Published
2023
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3. Amplification of the PLAG-family genes-PLAGL1 and PLAGL2-is a key feature of the novel tumor type CNS embryonal tumor with PLAGL amplification

Author

Keck, Michaela-Kristina, Sill, Martin, Wittmann, Andrea, Joshi, Piyush, Stichel, Damian, Beck, Pengbo, Okonechnikow, Konstantin, Sievers, Philipp, Wefers, Annika K, Roncaroli, Federico, Avula, Shivaram, McCabe, Martin G, Hayden, James T, Wesseling, Pieter, Øra, Ingrid, Nistér, Monica, Kranendonk, Mariëtte EG, Tops, Bastiaan BJ, Zapotocky, Michal, Zamecnik, Josef, Vasiljevic, Alexandre, Fenouil, Tanguy, Meyronet, David, von Hoff, Katja, Schüller, Ulrich, Loiseau, Hugues, Figarella-Branger, Dominique, Kramm, Christof M, Sturm, Dominik, Scheie, David, Rauramaa, Tuomas, Pesola, Jouni, Gojo, Johannes, Haberler, Christine, Brandner, Sebastian, Jacques, Tom, Sexton Oates, Alexandra, Saffery, Richard, Koscielniak, Ewa, Baker, Suzanne J, Yip, Stephen, Snuderl, Matija, Ud Din, Nasir, Samuel, David, Schramm, Kathrin, Blattner-Johnson, Mirjam, Selt, Florian, Ecker, Jonas, Milde, Till, von Deimling, Andreas, Korshunov, Andrey, Perry, Arie, Pfister, Stefan M, Sahm, Felix, Solomon, David A, and Jones, David TW

Subjects
Male, Pediatric Research Initiative, Pediatric cancer, Pediatric Cancer, Clinical Sciences, Neuroectodermal Tumors, Cell Cycle Proteins, Central Nervous System Neoplasms, Rare Diseases, Primitive, Genetics, Humans, Child, Preschool, Wnt Signaling Pathway, Cancer, Pediatric, Neurology & Neurosurgery, Tumor Suppressor Proteins, Neurosciences, RNA-Binding Proteins, Infant, DNA Methylation, Brain Disorders, DNA-Binding Proteins, Brain Cancer, PLAGL1, Female, PLAGL2, Transcription Factors, Molecular neuro-oncology
Abstract

Pediatric central nervous system (CNS) tumors represent the most common cause of cancer-related death in children aged 0-14years. They differ from their adult counterparts, showing extensive clinical and molecular heterogeneity as well as a challenging histopathological spectrum that often impairs accurate diagnosis. Here, we use DNA methylation-based CNS tumor classification in combination with copy number, RNA-seq, and ChIP-seq analysis to characterize a newly identified CNS tumor type. In addition, we report histology, patient characteristics, and survival data in this tumor type. We describe a biologically distinct pediatric CNS tumor type (n = 31 cases) that is characterized by focal high-level amplification and resultant overexpression of either PLAGL1 or PLAGL2, and an absence of recurrent genetic alterations characteristic of other pediatric CNS tumor types. Both genes act as transcription factors for a regulatory subset of imprinted genes (IGs), components of the Wnt/β-Catenin pathway, and the potential drug targets RET and CYP2W1, which are also specifically overexpressed in this tumor type. A derived PLAGL-specific gene expression signature indicates dysregulation of imprinting control and differentiation/development. These tumors occurred throughout the neuroaxis including the cerebral hemispheres, cerebellum, and brainstem, and were predominantly composed of primitive embryonal-like cells lacking robust expression of markers of glial or neuronal differentiation (e.g., GFAP, OLIG2, and synaptophysin). Tumors with PLAGL1 amplification were typically diagnosed during adolescence (median age 10.5years), whereas those with PLAGL2 amplification were diagnosed during early childhood (median age 2years). The 10-year overall survival was 66% for PLAGL1-amplified tumors, 25% for PLAGL2-amplified tumors, 18% for male patients, and 82% for female patients. In summary, we describe a new type of biologically distinct CNS tumor characterized by PLAGL1/2 amplification that occurs predominantly in infants and toddlers (PLAGL2) or adolescents (PLAGL1) which we consider best classified as a CNS embryonal tumor and which is associated with intermediate survival. The cell of origin and optimal treatment strategies remain to be defined.

Published
2023

4. Author Correction:Coding and small non-coding transcriptional landscape of tuberous sclerosis complex cortical tubers: implications for pathophysiology and treatment (Scientific Reports, (2017), 7, 1, (8089), 10.1038/s41598-017-06145-8)

Author

Mills, James D., Iyer, Anand M., van Scheppingen, Jackelien, Bongaarts, Anika, Anink, Jasper J., Janssen, Bart, Zimmer, Till S., Spliet, Wim G., van Rijen, Peter C., Jansen, Floor E., Feucht, Martha, Hainfellner, Johannes A., Krsek, Pavel, Zamecnik, Josef, Kotulska, Katarzyna, Jozwiak, Sergiusz, Jansen, Anna, Lagae, Lieven, Curatolo, Paolo, Kwiatkowski, David J., Pasterkamp, R. Jeroen, Senthilkumar, Ketharini, von Oerthel, Lars, Hoekman, Marco F., Gorter, Jan A., Crino, Peter B., Mühlebner, Angelika, Scicluna, Brendon P., Aronica, Eleonora, Pathology, APH - Aging & Later Life, APH - Mental Health, Amsterdam Neuroscience - Cellular & Molecular Mechanisms, Center of Experimental and Molecular Medicine, AII - Infectious diseases, and AII - Inflammatory diseases

Abstract

This Article contains an error in the Acknowledgements section. “This work was supported by European Union’s Seventh Framework Programme (FP7/2007-2013) under the grant agreement no. 602391 (project acronym EPISTOP; A.I., J.v.S., A.M., E.A., F.I., K.K., S.K., A.J., L.L., P.C., D.K.); Epilepsiefonds (WAR 15-05; RJP); European Union’s Horizon 2020 research and innovation programme under the Marie Sklodowska-Curie grant agreement No 642881 (ECMED; A.E., J.G.). None of the authors has any conflict of interest to disclose. We confirm that we have read the Journal’s position on issues involved in ethical publication and affirm that this report is consistent with those guidelines.” should read: “This work was supported by European Union’s Seventh Framework Programme (FP7/2007-2013) under the Grant Agreement no. 602391 (project acronym EPISTOP; A.I., J.v.S., A.M., E.A., F.I., K.K., S.J., A.J., L.L., P.C., D.K.) and partially supported by the Polish Ministerial funds for science (years 2013–2019) for the implementation of international co-financed project (K.K, S.J.); Epilepsiefonds (WAR 15-05; RJP); European Union’s Horizon 2020 research and innovation programme under the Marie Sklodowska-Curie grant agreement No 642881 (ECMED; A.E., J.G.). None of the authors has any conflict of interest to disclose. We confirm that we have read the Journal’s position on issues involved in ethical publication and affirm that this report is consistent with those guidelines.”.

Published
2022
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5. Additional file 2 of Integrated genomic analysis reveals actionable targets in pediatric spinal cord low-grade gliomas

Author

Misove, Adela, Vicha, Ales, Broz, Petr, Vanova, Katerina, Sumerauer, David, Stolova, Lucie, Sramkova, Lucie, Koblizek, Miroslav, Zamecnik, Josef, Kyncl, Martin, Holubova, Zuzana, Liby, Petr, Taborsky, Jakub, Benes, Vladimir, Pernikova, Ivana, Jones, David T. W., Sill, Martin, Stancokova, Terezia, Krskova, Lenka, and Zapotocky, Michal

Abstract

Additional file 2: Table S2. Table showing the complete sLGGs cohort emphasizing the original histology before molecular pathology reevaluation, anatomical location, and molecular-biology data.

Published
2022
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6. Additional file 2 of Down-regulation of the brain-specific cell-adhesion molecule contactin-3 in tuberous sclerosis complex during the early postnatal period

Author

Korotkov, Anatoly, Luinenburg, Mark J., Romagnolo, Alessia, Zimmer, Till S., van Scheppingen, Jackelien, Bongaarts, Anika, Broekaart, Diede W. M., Anink, Jasper J., Mijnsbergen, Caroline, Jansen, Floor E., van Hecke, Wim, Spliet, Wim G., van Rijen, Peter C., Feucht, Martha, Hainfellner, Johannes A., Krsek, Pavel, Zamecnik, Josef, Crino, Peter B., Kotulska, Katarzyna, Lagae, Lieven, Jansen, Anna C., Kwiatkowski, David J., Jozwiak, Sergiusz, Curatolo, Paolo, M��hlebner, Angelika, van Vliet, Erwin A., Mills, James D., and Aronica, Eleonora

Subjects
Data_FILES
Abstract

Additional file 2.

Published
2022
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13. Pattern of Relapse and Treatment Response in WNT- Activated Medulloblastoma

Author

Tara McKeown, Eric Bouffet, Seung-Ki Kim, Amulya A. Nageswara Rao, Liana Nobre, Andrew S. Moore, Joshua B. Rubin, Toshihiro Kumabe, Maura Massimino, James M. Olson, Sara Khan, Rajeev Vibhakar, Ales Vicha, Ho Keung Ng, Lenka Krskova, Wiesława Grajkowska, Jason E. Cain, Joanna Trubicka, Enrique López-Aguilar, Shayna Zelcer, Marie Lise van Veelen-Vincent, Ji Yeoun Lee, Alexandre Vasiljevic, Young Shin Ra, Ian F. Pollack, Massimo Zollo, Kohei Fukuoka, Boleslaw Lach, Carlos Gilberto Carlotti, Claudia C. Faria, Jordan R. Hansford, Shin Jung, David Sumerauer, Paul A. Northcott, Roger E. McLendon, Kay Ka Wai Li, Michal Zapotocky, Annie Huang, Peter Hauser, William A. Weiss, Lola B. Chambless, Josef Zamecnik, Ronald L. Hamilton, Cécile Faure-Conter, Sarah Leary, Vijay Ramaswamy, Helen Wheeler, Jaume Mora, Pim J. French, Erwin G. Van Meir, Ute Bartels, Adriana Fonseca, Luca Massimi, Stephen Yip, Jaroslav Sterba, Caterina Giannini, Michael D. Taylor, Nalin Gupta, Uri Tabori, Cynthia Hawkins, Veronica Ferruci, Nobre, Liana, Zapotocky, Michal, Khan, Sara, Fukuoka, Kohei, Fonseca, Adriana, Mckeown, Tara, Sumerauer, David, Vicha, Ale, Grajkowska, Wieslawa A., Trubicka, Joanna, Ka Wai Li, Kay, Ng, Ho-Keung, Massimi, Luca, Yeoun Lee, Ji, Kim, Seung-Ki, Zelcer, Shayna, Vasiljevic, Alexandre, ́ cile Faure-Conter, Ce, Hauser, Peter, Lach, Boleslaw, van Veelen-Vincent, Marie-Lise, French, Pim J., Van Meir, Erwin G., Weiss, William A., Pollack, Nalin Gupta Ian F., Hamilton, Ronald L., Nageswara Rao, Amulya A., Giannini, Caterina, Rubin, Joshua B., Moore, Andrew S., Chambless, Lola B., Vibhakar, Rajeev, Shin Ra, Young, Massimino, Maura, Mclendon, Roger E., Wheeler, Helen, Zollo, Massimo, Ferrucci, Veronica, Kumabe, Toshihiro, Faria, Claudia C., Sterba, Jaroslav, Jung, Shin, ́ pez-Aguilar, Enrique Lo, Mora, Jaume, Carlotti, Carlos G., Olson, James M., Leary, Sarah, Cain, Jason, Krskova, Lenka, Zamecnik, Josef, Hawkins, Cynthia E., Tabori, Uri, Huang, Annie, Bartels, Ute, Northcott, Paul A., Taylor, Michael D., Yip, Stephen, Hansford, Jordan R., Bouffet, Eric, Vijay Ramaswamy, And, McKeown, Tara, Grajkowska, Wieslawa A, Li, Kay Ka Wai, Lee, Ji Yeoun, Faure-Conter, Cécile, French, Pim J, Van Meir, Erwin G, Weiss, William A, Gupta, Nalin, Pollack, Ian F, Hamilton, Ronald L, Nageswara Rao, Amulya A, Rubin, Joshua B, Moore, Andrew S, Chambless, Lola B, Ra, Young Shin, McLendon, Roger E, Ferruci, Veronica, Faria, Claudia C, López-Aguilar, Enrique, Carlotti, Carlos G, Olson, James M, Hawkins, Cynthia E, Northcott, Paul A, Taylor, Michael D, Hansford, Jordan R, Ramaswamy, Vijay, Neurosurgery, and Neurology

Subjects
Oncology, Male, medicine.medical_treatment, chemotherapy, Lateral ventricles, 0302 clinical medicine, Antineoplastic Combined Chemotherapy Protocols, Child, Cancer, lcsh:R5-920, Tumor, Wnt signaling pathway, Middle Aged, Chemotherapy regimen, Progression-Free Survival, 3. Good health, Local, 5.1 Pharmaceuticals, RECIDIVA LOCAL DE NEOPLASIA, 6.1 Pharmaceuticals, 030220 oncology & carcinogenesis, Cohort, Female, Development of treatments and therapeutic interventions, lcsh:Medicine (General), medicine.drug, Human, medicine.medical_specialty, Treatment response, Cyclophosphamide, Adolescent, medulloblastoma, survival, Article, General Biochemistry, Genetics and Molecular Biology, WNT, 03 medical and health sciences, Clinical Research, Internal medicine, genomics, medicine, Biomarkers, Tumor, Humans, Ifosfamide, Cerebellar Neoplasms, Medulloblastoma, Chemotherapy, Antineoplastic Combined Chemotherapy Protocol, business.industry, subgroup, Cerebellar Neoplasm, Evaluation of treatments and therapeutic interventions, medicine.disease, radiation, Neoplasm Recurrence, wingless, prognosis, Neoplasm Recurrence, Local, business, Biomarkers, 030217 neurology & neurosurgery
Abstract

SUMMARY Over the past decade, wingless-activated (WNT) medulloblastoma has been identified as a candidate for therapy de-escalation based on excellent survival; however, a paucity of relapses has precluded additional analyses of markers of relapse. To address this gap in knowledge, an international cohort of 93 molecularly confirmed WNT MB was assembled, where 5-year progression-free survival is 0.84 (95%, 0.763–0.925) with 15 relapsed individuals identified. Maintenance chemotherapy is identified as a strong predictor of relapse, with individuals receiving high doses of cyclophosphamide or ifosphamide having only one very late molecularly confirmed relapse (p = 0.032). The anatomical location of recurrence is metastatic in 12 of 15 relapses, with 8 of 12 metastatic relapses in the lateral ventricles. Maintenance chemotherapy, specifically cumulative cyclophosphamide doses, is a significant predictor of relapse across WNT MB. Future efforts to de-escalate therapy need to carefully consider not only the radiation dose but also the chemotherapy regimen and the propensity for metastatic relapses., Graphical Abstract, In Brief Nobre et al. analyze a clinically annotated cohort of 93 WNT-activated medulloblastoma using an integrated genomic approach. A maintenance chemotherapy regimen is the strongest predictor of relapse, and cumulative cyclophosphamide doses confer a reduced risk of relapse. Unlike other medulloblastoma subgroups, WNT-activated medulloblastoma recurs most frequently in the lateral ventricles.

Published
2020

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