Volume 30, No. 5/2011(September/October)
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 Clinical Neuropathology
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Editorial
Clinical Neuropathology, Vol. 30 – No. 5/2011
J.A. Hainfellner
Abstract
Clinical Neuropathology, Vol. 30 – No. 5/2011 (213-216)
Clinical Neuropathology, Vol. 30 – No. 5/2011
J.A. Hainfellner
Original
IDH testing in diagnostic neuropathology: review and practical guideline article invited by the Euro-CNS research committee
M. Preusser, D. Capper and C. Hartmann
Abstract
Clinical Neuropathology, Vol. 30 – No. 5/2011 (217-230)
IDH testing in diagnostic neuropathology: review and practical guideline article invited by the Euro-CNS research committee
M. Preusser1, D. Capper2,3 and C. Hartmann2,3
1Department of Medicine I, Institute of Neurology and Comprehensive Cancer Center – CNS Unit (CCC-CNS), Medical University of Vienna, Vienna, Austria, and 2Department of Neuropathology, Institute of Pathology, Ruprecht-Karls-Universität Heidelberg, and 3Clinical Cooperation Unit Neuropathology, German Cancer Research Center, Heidelberg, Germany
Isocitrate dehydrogenase 1 (IDH1) gene mutations, primarily of the R132H type, occur in approximately 60 – 90% of diffuse and anaplastic gliomas and secondary glioblastomas. IDH mutations in gliomas are associated with several clinically relevant parameters including patient age, histopathological diagnosis, combined 1p/19q deletion, TP53 mutation, MGMT promoter hypermethylation and patient survival. Therefore, testing of the IDH status is relevant for diagnostic and prognostic considerations in primary brain tumors. IDH status can be assessed by immunohistochemistry or DNA-based methods including gene sequencing in the routine setting. Here, we review the relevance of IDH testing in diffuse gliomas and present practical instructions including detailed descriptions of procedures and protocols for diagnostic IDH testing using immunohistochemistry (for both automated and manual staining) and gene sequencing. Our article may provide guidance for laboratories aiming at establishing IDH testing for diagnostic evaluation of primary brain tumors.Correspondence to:
M. Preusser, MD
Department of Medicine I and
Comprehensive Cancer Center – CNS Unit (CCC-CNS)
Medical University of Vienna
Waehringer Guertel 18 – 20
1090 Vienna, Austria
Email: Matthias.preusser@meduniwien.ac.at
Original
Diagnostic utility of IDH1- and p53-mutation analysis in secondary gliosarcoma
B.F.M. Romeike, Y. Chen, J. Walter and I. Petersen
Abstract
Clinical Neuropathology, Vol. 30 – No. 5/2011 (231-234)
Diagnostic utility of IDH1- and p53-mutation analysis in secondary gliosarcoma
B.F.M. Romeike1, Y. Chen1, J. Walter2 and I. Petersen1
1Institute of Pathology, Friedrich-Schiller University, and 2Department of Neurosurgery, Friedrich-Schiller University, Jena, Germany
We report on a 47-year-old woman in whom an anaplastic astrocytoma was resected in 2006. Postoperative radiation had to be interrupted because of a wound infection necessitating explantation of the infected bone flap and implantation of a titanium mesh. Subsequently, radiation therapy was completed and temozolomide was administered for 45 cycles. In the beginning of 2010 a new contrast enhancing mass was seen in the former tumor region. The mass was subtotally excised and showed no histomorphological similarity to the first lesion but represented a highly pleomorphic and mainly sarcomatoid differentiated malignant tumor. The lack of expression of GFAP or MAP-2 raised the question of a secondary malignancy, however, molecular genetic analysis of IDH1 and p53 revealed the same mutations in the anaplastic astrocytoma from 2006 as in the sarcomatoid tumor operated in 2010. Furthermore, accumulation of mutated IDH1 and TP53 protein could be demonstrated immunohistochemically. Thus, the second tumor represented the rare instance of recurrence of an anaplastic astrocytoma as a secondary gliosarcoma and a second malignant neoplasm was ruled out. The postoperative therapy and the inflammation might have contributed to the severe change in morphological phenotype of the glioma.Correspondence to:
Priv.-Doz. Dr. med. B.F.M. Romeike
Department of Neuropathology
Institute of Pathology
Friedrich-Schiller University
Erlanger Allee 101
07747 Jena, Germany
Email: bernd.romeike@med.uni-jena.de
Original
Distinctive multicystic hemispheric lesions suggesting a novel variant of infantile astrocytoma
M. Santi, T. Feygin, M.J. Dougherty, J.A. Biegel and B. Harding
Abstract
Clinical Neuropathology, Vol. 30 – No. 5/2011 (235-241)
Distinctive multicystic hemispheric lesions suggesting a novel variant of infantile astrocytoma
M. Santi1, T. Feygin2, M.J. Dougherty1, J.A. Biegel1,3 and B. Harding1
1Department of Pathology and Lab. Medicine, 3Department of Pediatrics, The Children’s Hospital of Philadelphia and the University of Pennsylvania School of Medicine, and 2Department of Radiology, The Children’s Hospital of Philadelphia, Philadelphia, PA, USA
Two unrelated female infants presented at 9 days and 2 months, respectively, with apneic episodes in the former and gaze preference in the latter. MRI revealed enlargement of almost the entire right hemisphere, apparently smooth cortex, simplification of the gyral pattern, and expanded white matter with abnormal signal intensity containing multiple intraparenchymal cysts. Histologic examination of both cases revealed white matter infiltration by a hypocellular lesion composed of uniform, fibrillary astrocytes in a microcystic background. Multilocular tumor cysts were prominent, but Rosenthal fibers and eosinophilic granular bodies were absent. Very rare mitoses were seen in the absence of necrosis or vascular change. There was no convincing cortical infiltration, but the subpial zone was diffusely expanded by a band of astrocytes set in a dense fibrillar feltwork which opened out into numerous cystic spaces. No desmoplastic changes or associated atypical ganglion cells were identified. There was no evidence for a BRAFKIAA1549 fusion or BRAF mutation in one case tested. In conclusion, both lesions are not desmoplastic infantile astrocytoma/ganglioglioma, fibrillary astrocytoma, or typical for pilocytic astrocytoma. Such extreme subpial spread with cysts is most unusual and may suggest a novel variant of infantile astrocytoma.Correspondence to:
B. Harding, DPhil, FRCPath
Department of Pathology and Lab. Medicine
Childrens Hospital of Philadelphia
Main, 5NW-26, 324 South 34th Street
Philadelphia, PA 19104, USA
Email: hardingb@email.chop.edu
Original
PET response and tumor stabilization under erlotinib and bevacizumab treatment of an intracranial lesion non-invasively diagnosed as likely chordoma
T. Asklund, T. Danfors and R. Henriksson
Abstract
Clinical Neuropathology, Vol. 30 – No. 5/2011 (242-246)
PET response and tumor stabilization under erlotinib and bevacizumab treatment of an intracranial lesion non-invasively diagnosed as likely chordoma
T. Asklund1, T. Danfors2 and R. Henriksson3
1Department of Radiation Sciences and Oncology, Norrlands University Hospital, Umeå, and 2Department of Neuroscience, Neurology, Uppsala University Hospital, Uppsala, and 3Department of Oncology, Radiumhemmet, Karolinska Hospital and Institute, Stockholm, Sweden
Introduction: Chordoma is a rare and a slow-growing tumor originating from the notochord and commonly localized in the skull base. Surgery and occasionally radiotherapy have emerged as the treatments of choice. In the relapsed situations available treatment options are strictly limited; however, recently molecularly targeted agents have been proposed to be of potential beneficial value. The case: A 63-year-old male presenting with seizures and an extradural mass in the left brain hemisphere. An attempt to resect the tumor was followed by severe bradycardia when manipulating with the dura and therefore discontinued. It was considered too hazardous even to take a biopsy specimen. The tumor was considered radiologically and macroscopically as a chordoma. As the tumor progressed after radiotherapy, chemotherapy with erlotinib in combination with cetuximab was initiated. This treatment was interrupted due to progressive disease and toxicity. However, combination treatment with erlotinib and bevacizumab normalized the uptake of [11C]methionine PET signal and resulted in a slight tumor shrinkage on MRI. The patient is still (March 2011) free of symptoms, without cranial nerve deficits or seizures. Discussion: This report shows that erlotinib and bevacizumab in combination may completely quench the transport of the essential amino acid methionine to a treatment refractory intracranial tumor bearing radiological and clinical characteristics of a chordoma. Further studies are necessary to establish this strategy as a treatment option for this indication.Correspondence to:
T. Asklund, MD, PhD
Umeå University Hospital
901 87 Umeå, Sweden
Email: thomas.asklund@onkologi.umu.se
Abstracts
56th Annual Meeting of the German Society for Neuropathology and Neuroanatomy, Tübingen, Germany, September 21 – 24, 2011
Conference Chair: Prof. Dr. Richard Meyermann (Tübingen); Programme Committee: Prof. Dr. Hans Lassmann (Vienna/AT), Prof. Dr. Manuela Neumann (Zurich/CH), Prof. Dr. Guido Reifenberger (Düsseldorf), Prof. Dr. Joachim Weis (Aachen)
Abstract
Clinical Neuropathology, Vol. 30 – No. 5/2011 (247-282)
56th Annual Meeting of the German Society for Neuropathology and Neuroanatomy, Tübingen, Germany, September 21 – 24, 2011
Conference Chair: Prof. Dr. Richard Meyermann (Tübingen); Programme Committee: Prof. Dr. Hans Lassmann (Vienna/AT), Prof. Dr. Manuela Neumann (Zurich/CH), Prof. Dr. Guido Reifenberger (Düsseldorf), Prof. Dr. Joachim Weis (Aachen)
Euro-CNS News
Society News of the European Confederation of Neuropathological Societies
Abstract
Society News of the European Confederation of Neuropathological Societies
