Skeletal spread of an anaplastic astrocytoma (WHO grade III) and preservation of histopathological properties within metastases.

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Skeletal spread of an anaplastic astrocytoma (WHO grade III) and preservation of histopathological properties within metastases. / Martens, T; Matschke, J; Müller, Carolin; Riethdorf, S; Balabanov, S; Westphal, M; Heese, O.

in: CLIN NEUROL NEUROSUR, Jahrgang 115, Nr. 3, 3, 2013, S. 323-328.

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@article{084dc3a3fe6e46db87f0e88cbcd5f609,
title = "Skeletal spread of an anaplastic astrocytoma (WHO grade III) and preservation of histopathological properties within metastases.",
abstract = "BACKGROUND: The incidence of extraneural metastases of glioma is low. Metastases occur at different sites and, infrequently, as diffuse bone marrow infiltration. Direct contact of a glioma with extrameningeal tissues might be a reason for extraneural metastases. However, the role of haematogenous spread remains unclear.METHODS: We report on a young patient who suffered from a left frontal anaplastic WHO grade III astrocytoma, which was treated with gross total resection and irradiation (60 Gy). No local relapse occurred during the following course, but a diffuse infiltration of the bone marrow was diagnosed 12 months after the initial diagnosis. The patient died 6 months later, as a result of hypercalcaemia and pancytopenia. The histopathological properties of the tumour and its bone metastases were analysed, as well as the mutations of the isocitrate dehydrogenase 1 gene (IDH1). To study the route of tumour dissemination, the peripheral blood of the patient was analysed for circulating tumour cells (CTCs).RESULTS: This study describes a rare case of an extraneurally metastasised WHO grade III anaplastic astrocytoma. The occurrence of bone marrow infiltration coinciding with the finding of a stable intracranial tumour is a notably unusual situation. The properties of the primary tumour were maintained within the metastases in our patient. No CTCs were found in the peripheral blood at one random time point after the diagnosis of bone metastases.CONCLUSIONS: Despite young patient age, a stable intracranial course with a single location and mutations in the IDH1 gene, the patient's overall survival was short at 18 months after diagnosis. This finding illustrates the therapeutic dilemma in patients with bone marrow involvement complicating the use of alkylating agents, such as temozolomide. Repeated and systematic blood sampling in a large cohort of patients is needed for the detection of CTCs in glioma patients with systemic tumour spread. Future studies investigating how intrinsic factors in glioma cell biology cause rare metastases in these tumours are needed.",
keywords = "Adult, Astrocytoma, Biological Markers, Biopsy, Bone Marrow Neoplasms, Bone Neoplasms, Brain Neoplasms, C-Reactive Protein, DNA Modification Methylases, DNA Repair Enzymes, Fatal Outcome, Glial Fibrillary Acidic Protein, Humans, Hypercalcemia, Immunohistochemistry, Isocitrate Dehydrogenase, Magnetic Resonance Imaging, Male, Neoplastic Cells, Circulating, Neurosurgical Procedures, Polymerase Chain Reaction, Tomography, X-Ray Computed, Tumor Suppressor Proteins",
author = "T Martens and J Matschke and Carolin M{\"u}ller and S Riethdorf and S Balabanov and M Westphal and O Heese",
note = "Copyright {\textcopyright} 2012 Elsevier B.V. All rights reserved.",
year = "2013",
doi = "10.1016/j.clineuro.2012.05.025",
language = "English",
volume = "115",
pages = "323--328",
journal = "CLIN NEUROL NEUROSUR",
issn = "0303-8467",
publisher = "Elsevier",
number = "3",

}

RIS

TY - JOUR

T1 - Skeletal spread of an anaplastic astrocytoma (WHO grade III) and preservation of histopathological properties within metastases.

AU - Martens, T

AU - Matschke, J

AU - Müller, Carolin

AU - Riethdorf, S

AU - Balabanov, S

AU - Westphal, M

AU - Heese, O

N1 - Copyright © 2012 Elsevier B.V. All rights reserved.

PY - 2013

Y1 - 2013

N2 - BACKGROUND: The incidence of extraneural metastases of glioma is low. Metastases occur at different sites and, infrequently, as diffuse bone marrow infiltration. Direct contact of a glioma with extrameningeal tissues might be a reason for extraneural metastases. However, the role of haematogenous spread remains unclear.METHODS: We report on a young patient who suffered from a left frontal anaplastic WHO grade III astrocytoma, which was treated with gross total resection and irradiation (60 Gy). No local relapse occurred during the following course, but a diffuse infiltration of the bone marrow was diagnosed 12 months after the initial diagnosis. The patient died 6 months later, as a result of hypercalcaemia and pancytopenia. The histopathological properties of the tumour and its bone metastases were analysed, as well as the mutations of the isocitrate dehydrogenase 1 gene (IDH1). To study the route of tumour dissemination, the peripheral blood of the patient was analysed for circulating tumour cells (CTCs).RESULTS: This study describes a rare case of an extraneurally metastasised WHO grade III anaplastic astrocytoma. The occurrence of bone marrow infiltration coinciding with the finding of a stable intracranial tumour is a notably unusual situation. The properties of the primary tumour were maintained within the metastases in our patient. No CTCs were found in the peripheral blood at one random time point after the diagnosis of bone metastases.CONCLUSIONS: Despite young patient age, a stable intracranial course with a single location and mutations in the IDH1 gene, the patient's overall survival was short at 18 months after diagnosis. This finding illustrates the therapeutic dilemma in patients with bone marrow involvement complicating the use of alkylating agents, such as temozolomide. Repeated and systematic blood sampling in a large cohort of patients is needed for the detection of CTCs in glioma patients with systemic tumour spread. Future studies investigating how intrinsic factors in glioma cell biology cause rare metastases in these tumours are needed.

AB - BACKGROUND: The incidence of extraneural metastases of glioma is low. Metastases occur at different sites and, infrequently, as diffuse bone marrow infiltration. Direct contact of a glioma with extrameningeal tissues might be a reason for extraneural metastases. However, the role of haematogenous spread remains unclear.METHODS: We report on a young patient who suffered from a left frontal anaplastic WHO grade III astrocytoma, which was treated with gross total resection and irradiation (60 Gy). No local relapse occurred during the following course, but a diffuse infiltration of the bone marrow was diagnosed 12 months after the initial diagnosis. The patient died 6 months later, as a result of hypercalcaemia and pancytopenia. The histopathological properties of the tumour and its bone metastases were analysed, as well as the mutations of the isocitrate dehydrogenase 1 gene (IDH1). To study the route of tumour dissemination, the peripheral blood of the patient was analysed for circulating tumour cells (CTCs).RESULTS: This study describes a rare case of an extraneurally metastasised WHO grade III anaplastic astrocytoma. The occurrence of bone marrow infiltration coinciding with the finding of a stable intracranial tumour is a notably unusual situation. The properties of the primary tumour were maintained within the metastases in our patient. No CTCs were found in the peripheral blood at one random time point after the diagnosis of bone metastases.CONCLUSIONS: Despite young patient age, a stable intracranial course with a single location and mutations in the IDH1 gene, the patient's overall survival was short at 18 months after diagnosis. This finding illustrates the therapeutic dilemma in patients with bone marrow involvement complicating the use of alkylating agents, such as temozolomide. Repeated and systematic blood sampling in a large cohort of patients is needed for the detection of CTCs in glioma patients with systemic tumour spread. Future studies investigating how intrinsic factors in glioma cell biology cause rare metastases in these tumours are needed.

KW - Adult

KW - Astrocytoma

KW - Biological Markers

KW - Biopsy

KW - Bone Marrow Neoplasms

KW - Bone Neoplasms

KW - Brain Neoplasms

KW - C-Reactive Protein

KW - DNA Modification Methylases

KW - DNA Repair Enzymes

KW - Fatal Outcome

KW - Glial Fibrillary Acidic Protein

KW - Humans

KW - Hypercalcemia

KW - Immunohistochemistry

KW - Isocitrate Dehydrogenase

KW - Magnetic Resonance Imaging

KW - Male

KW - Neoplastic Cells, Circulating

KW - Neurosurgical Procedures

KW - Polymerase Chain Reaction

KW - Tomography, X-Ray Computed

KW - Tumor Suppressor Proteins

U2 - 10.1016/j.clineuro.2012.05.025

DO - 10.1016/j.clineuro.2012.05.025

M3 - SCORING: Journal article

C2 - 22704562

VL - 115

SP - 323

EP - 328

JO - CLIN NEUROL NEUROSUR

JF - CLIN NEUROL NEUROSUR

SN - 0303-8467

IS - 3

M1 - 3

ER -