11 results on '"Pietsch, T."'
Search Results
2. Meningioma as second malignant neoplasm after oncological treatment during childhood
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Müller, H.L., Gebhardt, U., Warmuth-Metz, M., Pietsch, T., Sörensen, N., Kortmann, R.-D., and on behalf of the study committee of HIT Endo
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- 2012
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3. Hirntumoren bei Kindern und Jugendlichen: Leitsymptome und diagnostische Standards
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Rutkowski, S., Fleischhack, G., Gnekow, A., Kramm, C., Müller, H., Calaminus, G., Wrede, B., Frühwald, M., Krauss, J., Faldum, A., Kortmann, R., Pietsch, T., and Warmuth-Metz, M.
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- 2008
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4. Hirntumoren bei Kindern und Jugendlichen: Standards und neue Entwicklungen in Diagnostik und Therapie
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Rutkowski, S., Gnekow, A., Fleischhack, G., Wagner, S., Calaminus, G., Wolff, J., Müller, H., Sörensen, N., Faldum, A., Tatagiba, M., Pietsch, T., Warmuth-Metz, M., and Kortmann, R.
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- 2006
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5. Hirntumoren im Kindesalter: Diagnostik und interdisziplinäre Therapiekonzepte
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Rutkowski, S., Warmuth-Metz, M., Sörensen, N., Faldum, A., Pietsch, T., Müller, H., Gnekow, A., Göbel, U., Wolff, J., Fleischhack, G., and Kortmann, R.
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- 2005
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6. International society of neuropathology-haarlem consensus guidelines for nervous system tumor classification and grading
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Louis D. N., Perry A., Burger P., Ellison D. W., Reifenberger G., von Deimling A., Aldape K., Brat D., Collins V. P., Eberhart C., Figarella-Branger D., Fuller G. N., Giangaspero F., Giannini C., Hawkins C., Kleihues P., Korshunov A., Kros J. M., Beatriz Lopes M., Ng H. -K., Ohgaki H., Paulus W., Pietsch T., Rosenblum M., Rushing E., Soylemezoglu F., Wiestler O., Wesseling P., University of Zurich, Pathology, CCA - Disease profiling, Louis D.N., Perry A., Burger P., Ellison D.W., Reifenberger G., von Deimling A., Aldape K., Brat D., Collins V.P., Eberhart C., Figarella-Branger D., Fuller G.N., Giangaspero F., Giannini C., Hawkins C., Kleihues P., Korshunov A., Kros J.M., Beatriz Lopes M., Ng H.-K., Ohgaki H., Paulus W., Pietsch T., Rosenblum M., Rushing E., Soylemezoglu F., Wiestler O., and Wesseling P.
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Molecular Diagnostic Technique ,Oligodendroglioma ,Nervous System Neoplasms ,10208 Institute of Neuropathology ,610 Medicine & health ,Astrocytoma ,Rare cancers Radboud Institute for Molecular Life Sciences [Radboudumc 9] ,World Health Organization ,Brain tumors ,Severity of Illness Index ,Humans ,Letter to the Editor ,Atypical teratoid rhabdoid tumor ,Classification ,Glioblastoma ,Glioma ,Grading ,Medulloblastoma ,Molecular Diagnostic Techniques ,Neuroscience (all) ,2734 ,Neurology (clinical) ,Nervous System Neoplasm ,2800 General Neuroscience ,Miscellaneous ,2734 Pathology and Forensic Medicine ,2728 Neurology (clinical) ,570 Life sciences ,biology ,brain tumor ,Human - Abstract
Item does not contain fulltext Major discoveries in the biology of nervous system tumors have raised the question of how non-histological data such as molecular information can be incorporated into the next World Health Organization (WHO) classification of central nervous system tumors. To address this question, a meeting of neuropathologists with expertise in molecular diagnosis was held in Haarlem, the Netherlands, under the sponsorship of the International Society of Neuropathology (ISN). Prior to the meeting, participants solicited input from clinical colleagues in diverse neuro-oncological specialties. The present "white paper" catalogs the recommendations of the meeting, at which a consensus was reached that incorporation of molecular information into the next WHO classification should follow a set of provided "ISN-Haarlem" guidelines. Salient recommendations include that (i) diagnostic entities should be defined as narrowly as possible to optimize interobserver reproducibility, clinicopathological predictions and therapeutic planning; (ii) diagnoses should be "layered" with histologic classification, WHO grade and molecular information listed below an "integrated diagnosis"; (iii) determinations should be made for each tumor entity as to whether molecular information is required, suggested or not needed for its definition; (iv) some pediatric entities should be separated from their adult counterparts; (v) input for guiding decisions regarding tumor classification should be solicited from experts in complementary disciplines of neuro-oncology; and (iv) entity-specific molecular testing and reporting formats should be followed in diagnostic reports. It is hoped that these guidelines will facilitate the forthcoming update of the fourth edition of the WHO classification of central nervous system tumors.
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- 2014
7. Secondary dissemination in children with high-grade malignant gliomas and diffuse intrinsic pontine gliomas.
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Wagner, S., Benesch, M., Berthold, F., Gnekow, A. K., Rutkowski, S., Sträter, R., Warmuth-Metz, M., Kortmann, R.-D., Pietsch, T., Wolff, J. E. A., and Sträter, R
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GLIOMAS ,CANCER treatment ,CANCER invasiveness ,TUMORS in children ,CEREBROSPINAL fluid ,METASTASIS ,GLIOMA treatment ,BRAIN tumor treatment ,CANCER diagnosis ,THERAPEUTIC use of antineoplastic agents ,BRAIN tumor diagnosis ,ETOPOSIDE ,RESEARCH ,CANCER cells ,RESEARCH methodology ,RETROSPECTIVE studies ,MEDICAL cooperation ,EVALUATION research ,BRAIN tumors ,CANCER ,TREATMENT effectiveness ,COMPARATIVE studies ,MENINGES ,KAPLAN-Meier estimator ,CYCLOPHOSPHAMIDE ,RADIOTHERAPY ,COMBINED modality therapy ,BRAIN stem ,VINCRISTINE - Abstract
In children, treatment regimen for high-grade gliomas (HGG) and diffuse intrinsic pontine gliomas (DIPG) are generally not stratified according to disease stage. The hypothesis was that secondary disseminating disease (SDD) in children with HGG is related to an even worse outcome. Description of SDD pattern was performed. In total, 270 children with newly diagnosed HGG or DIPG were eligible for retrospective analysis of SDD. Medical and computer records of these patients were reviewed for demographic characteristics, sites of dissemination, prognostic variables. Forty-six (17%) of the 270 patients had developed SDD. The median time to SDD was 8.2 months. The median overall survival (OS) after dissemination was 3.2 months. The SDD was located parenchymal in the supratentorial (34.8%), infratentorial (6.5%), supratentorial and infratentorial (19.6%), spinal (10.9%), spinal and cerebral (6.5%) regions of the CNS, or leptomeningeal (21.7%). For HGG patients, the median OS was shorter among patients with SDD than among patients without SDD (1.02 vs 1.41 years, P=0.0495). In the group of patients with SDD, patients with cerebrospinal fluid dissemination had a worse outcome compared with patients with parenchymal metastases. Summarising, SDD is a negative prognostic factor for patients with HGG outside the pons. Treatment stratification should be considered. [ABSTRACT FROM AUTHOR]
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- 2006
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8. DNA methylation and allelic losses on chromosome arm 14q in oligodendroglial tumours.
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Felsberg, J., Yan, P. S., Huang, T. H.-M., Milde, U., Schramm, J., Wiestler, O. D., Reifenberger, G., Pietsch, T., and Waha, A.
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CHROMOSOMES ,DNA ,METHYLATION ,ALKYLATION ,BRAIN tumors ,GLIOMAS - Abstract
Cytogenetic and molecular genetic studies have shown frequent losses on the long arm of chromosome 14 in different types of human gliomas. Using differential methylation hybridization as a genome-wide screening approach to determine DNA methylation patterns in gliomas, we recently identified two DNA fragments in 14q23.1 (CGI-clone ♯396) and 14q32.12 (CGI-clone ♯519) that were differentially methylated between astrocytic gliomas and mixed oligoastrocytomas. To validate this observation, we examined these 14q32.12 locus for methylation in an extended series of 43 astrocytic and oligodendroglial gliomas. All tumours were additionally investigated for loss of heterozygosity (LOH). Microsatellite analysis showed LOH in seven of 28 (25%) oligodendroglial tumours and three of 15 (20%) astrocytic tumours. Seven tumours demonstrated LOH at all informative 14q loci whereas three tumours carried partial deletions defining a commonly deleted region at 14q22.3–q32.1 between the microsatellite markers D14S282 and D14S995. Methylation-specific PCR analysis of the 14q32.12 locus revealed hypermethylation in 12 of 43 gliomas (28%). Hypermethylation was restricted to tumours with oligodendroglial differentiation (12 of 28 tumours, 43%). However, none of the hypermethylated tumours demonstrated LOH on 14q and vice versa. In total, 19 of 28 oligodendroglial tumours (68%) showed either hypermethylation at the 14q32.12 locus or LOH at 14q22.3–q32.2. Taken together, our data lend further support for the location of one or more yet to be identified glioma-associated tumour suppressor gene(s) on 14q. In addition, the restriction of 14q32.12 methylation to oligodendroglial tumours suggests a role for epigenetic DNA modifications in these particular gliomas. [ABSTRACT FROM AUTHOR]
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- 2006
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9. Hirntumoren im Kindesalter.
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Rutkowski, S., Warmuth-Metz, M., Sörensen, N., Faldum, A., Pietsch, T., Müller, H., Gnekow, A., Göbel, U., Wolff, J., Fleischhack, G., and Kortmann, R.
- Abstract
Copyright of Der Onkologe is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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- 2005
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10. Molecular genetic analysis of the TP53 ,PTEN ,CDKN2A ,EGFR ,CDK4 andMDM2 tumour-associated genes in supratentorial primitive neuroectodermal tumours and glioblastomas of childhood.
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Kraus, J. A., Felsberg, J., Tonn, J. C., Reifenberger, G., and Pietsch, T.
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BRAIN tumors ,MOLECULAR genetics ,TUMOR markers - Abstract
Supratentorial primitive neuroectodermal tumours (sPNETs) are malignant central nervous system tumours of childhood which are histologically characterized by poorly differentiated neuroepithelial cells with the capacity for divergent differentiation into glial, neuronal, myogenic or melanotic lines. The histological differential diagnosis between sPNET and glioblastoma multiforme (GBM) may be difficult, particularly as GBMs can sometimes demonstrate a poorly differentiated PNET-like phenotype. To identify molecular genetic markers that may distinguish sPNET and GBM, we investigated 12 cerebral sPNETs and six GBMs from paediatric patients for genetic alterations of the TP53, PTEN, CDKN2A, EGFR, CDK4 and MDM2 genes, as well as for allelic loss on chromosome arms l0q and 17p. Mutations of the TP53 tumour suppressor gene were found in one of 12 sPNE% (8%) and two of six GBMs (33 %). None of the sPNETs but two of six GBMs (33%, including one GBM with a TP53 mutation) showed allelic losses on chromosome arm 17p. PTEN mutations were detected in one of 12 sPNET (8%) and one of six GBMs (17%). None of the sPNETs and GBMs carried a homozygous deletion involving the CDKN2A tumour suppressor gene. No amplification of the EGFR, CDK4 or MDM2 proto-oncogenes was detected. Taken together, our results indicate that paediatric GBMs differ from sPNETs by a higher incidence of allelic losses on 17p and TP53 mutations. In addition, the patterns of genetic alterations in sPNETs and paediatric GBMs appear to be distinct from those in cerebellar medulloblastomas and adult GBMs, respectively. [ABSTRACT FROM AUTHOR]
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- 2002
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11. cIMPACT‐NOW update 6: new entity and diagnostic principle recommendations of the cIMPACT‐Utrecht meeting on future CNS tumor classification and grading
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Uri Tabori, Torsten Pietsch, Cynthia Hawkins, Arie Perry, David N. Louis, Valerie A. White, Guido Reifenberger, Dominique Figarella-Branger, Christine Haberler, Chitra Sarkar, Johan M. Kros, David Capper, Brent A. Orr, Sung Hye Park, Pieter Wesseling, Felix Sahm, Brian Rous, Caterina Giannini, David A. Solomon, Maryam Fouladi, Daniel J. Brat, Werner Paulus, Marc K. Rosenblum, Ian A. Cree, Michael Weller, Kenneth Aldape, Ho Keung Ng, Takashi Komori, Andreas von Deimling, Martin J. van den Bent, Gregory N. Fuller, Charles G. Eberhart, David Ellison, Institut de neurophysiopathologie (INP), Aix Marseille Université (AMU)-Centre National de la Recherche Scientifique (CNRS), Laboratoire d'Anatomie Pathologique-Neuropathologique [AP-HM Hôpital La Timone], Hôpital de la Timone [CHU - APHM] (TIMONE), CCA - Imaging and biomarkers, Pathology, Louis D.N., Wesseling P., Aldape K., Brat D.J., Capper D., Cree I.A., Eberhart C., Figarella-Branger D., Fouladi M., Fuller G.N., Giannini C., Haberler C., Hawkins C., Komori T., Kros J.M., Ng H.K., Orr B.A., Park S.-H., Paulus W., Perry A., Pietsch T., Reifenberger G., Rosenblum M., Rous B., Sahm F., Sarkar C., Solomon D.A., Tabori U., van den Bent M.J., von Deimling A., Weller M., White V.A., Ellison D.W., and Neurology
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0301 basic medicine ,medicine.medical_specialty ,[SDV]Life Sciences [q-bio] ,Clinical Sciences ,neoplasms ,World health ,Pathology and Forensic Medicine ,Central Nervous System Neoplasms ,03 medical and health sciences ,0302 clinical medicine ,Rare Diseases ,Medicine ,Humans ,Medical physics ,CNS TUMORS ,Grading (tumors) ,Cancer ,Neurology & Neurosurgery ,business.industry ,General Neuroscience ,Neurosciences ,central nervous system ,3. Good health ,030104 developmental biology ,Cns neoplasms ,classification ,brain tumors ,Neurology (clinical) ,Neoplasm Grading ,business ,030217 neurology & neurosurgery ,brain tumor - Abstract
International audience; cIMPACT-NOW (the Consortium to Inform Molecular and Practical Approaches to CNS Tumor Taxonomy) was established to evaluate and make practical recommendations on recent advances in the field of CNS tumor classification, particularly in light of the rapid progress in molecular insights into these neoplasms. For Round 2 of its deliberations, cIMPACT-NOW Working Committee 3 was reconstituted and convened in Utrecht, The Netherlands, for a meeting designed to review putative new CNS tumor types in advance of any future World Health Organization meeting on CNS tumor classification. In preparatory activities for the meeting and at the actual meeting, a list of possible entities was assembled and each type and subtype debated. Working Committee 3 recommended that a substantial number of newly recognized types and subtypes should be considered for inclusion in future CNS tumor classifications. In addition, the group endorsed a number of principles-relating to classification categories, approaches to classification, nomenclature, and grading-that the group hopes will also inform the future classification of CNS neoplasms.
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- 2020
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