No abstract

The immunoreactivity of a panel of poly- and monoclonal antibodies raised against different glial and neuronal antigens was investigated in paraffin-embedded specimens of 116 human tumors of the central and peripheral nervous system. We used antibodies against the HNK-1 epitope, which is shared between natural killer cells and the nervous system, glial fibrillary acidic protein (GFAP), vimentin, neurofilaments, S-100 protein, neuron-specific enolase (NSE) and myelin basic protein (MBP). HNK-1 immunoreactivity was detectable in nearly all neuroectodermal tumors. Especially in those derived from the neuroepithelium, which include the various types of gliomas, we observed a strong staining with this antibody. The only exceptions were the choroid plexus papillomas and individual ependymomas. In tumors derived from the neural crest HNK-1 reactivity was more variable and less intense. In other tumors of the nervous system HNK-1 was not detectable, except for two out of four malignant lymphomas. In addition to its reactivity with human lymphocytes HNK-1, therefore, seems to be a useful 'marker' for neurogenic tumors in general. GFAP expression was prominent in all astrocytomas and the astrocytic cells within mixed gliomas and gangliogliomas. Immunoreactivity was more variable in glioblastomas and ependymomas, while only isolated GFAP-positive cells were present in oligodendrogliomas, medulloblastomas, one plexus papilloma, and some neurinomas. Vimentin immunoreactivity was found in tumor cells of nearly all tumors of the central nervous system with the exception of oligodendrogliomas, most plexus papillomas, neuronal tumors and most medulloblastomas.

Olfactory neuroblastoma (esthesioneuroblastoma) is a very rare tumour of the olfactory mucosa. Morphological features and cytogenetic studies strongly suggest a neuro-ectodermal origin. Up to now, cytogenetic studies are inconsistent. Some of them have proposed that the tumour belongs to the pPNET family. In the present study we describe genomic imbalances in olfactory neuroblastoma in a 46-year-old woman by using the molecular cytogenetic technique--comparative genomic hybridization (CGH)--in order to define the spectrum of genetic abnormalities in the tumour. The anatomical location and morphological findings were the basis for the diagnosis of esthesionearoblastoma. Immunohistochemical reactions for NSE, synaptophysin, chromogranin A, HNK-1/Leu-7 and S-100 revealed a characteristic immunophenotype. The CGH analysis showed multiple changes including DNA overrepresentations of chromosomes 4, 8, 11 and 14, partial DNA gains of the long arms of chromosomes 1 and 17, deletions of the entire chromosomes 16, 18, 19 and X, and partial losses of chromosomes 5q and 17p. This study represents an early utilisation of the CGH technique in olfactory neuroblastoma and demonstrates that the tumour carries complex chromosomal aberrations.

The glial fibrillary acidic protein (GFAP) have been quantitatively determined in over 200 samples of liquid content of brain tumours and in cerebrospinal fluid (CSF) of cases with various tumours of the cerebral nervous system. For establishing the GFAP value, the rocket radioimmunoelectrophoresis was used. The studies were performed in three series of patients. The GFAP value of fluids from 26 cysts of both neoplastic and non-neoplastic type had a wide range of 0.6 microgram/ml to 40 micrograms/ml. Significant elevation of GFAP was usually recorded in fluid from cysts of anaplastic tumour with astroglial differentiation. In this series of 24 cases with various brain tumours, the GFAP value of the CSF ranged from 0.2 microgram/ml to 50 micrograms/ml. In gliomas, as in astrocytoma and glioblastoma, these values were on a higher level, of over 4 micrograms/ml. In other tumours and in cerebral lesions of other aetiology, the GFAP values were lower, below 3 micrograms/ml and 0.3 microgram/ml respectively. In another series of 32 patients with brain tumour treated surgically, a significant increase of GFAP (to 30 micrograms/ml) was noted in the CSF during the first week after operation, and that was always associated with an increase of the total protein of the CSF. During the second and third week after operation, when the total protein of the CSF was reduced to a normal level, the values of GFAP were still elevated, first of all in those cases of astrocytoma and glioblastoma which were not radically excised. These findings suggest that investigation of GFAP in the CSF of patients with brain tumour may be helpful in diagnosis and prognosis.

Tumours were produced in the adult cat brain by injection of the rapidly growing anaplastic rat glioma clone F98 in order to study their neuropathology, pathophysiology, regional biochemistry and magnetic reasonance imaging. We report here the neuropathological behaviour of cell suspensions in the basal ganglia and the left cerebral hemisphere one, two, three, four and six weeks after stereotactic implantation with respect to tumour growth, immunological tumour regression and alterations of the blood-brain barrier with associated vasogenic brain oedema. Injected cell suspensions produce consistently growing tumours during the first, second and third weeks. Tumour sizes varied according to the survival time and were only slightly dependent on the inoculated cell number, i.e., 3 and 6 x 10(6) tumour cells, respectively. Immunohistochemistry with respect to proteins of the cytoskeleton and other cell markers showed positive tumour cell immunoreactions for vimentin and S 100, but not for GFAP, Leu-7, Leu-M1 and MBP. While leucocyte infiltration is apparent after only one week, major tumour regression phenomena develop after three weeks in conjunction with severe lymphocytic reactions of the host, resulting in complete tumour rejection with scar gliosis after four and six weeks, respectively. This transplantation glioma model is accompanied by vasogenic brain oedema both within the tumour area and in the homolateral hemisphere. Immunohistochemistry of serum proteins, i.e. total serum protein, albumin and IgG reveals impairment of the blood-brain barrier after one week, reaching its maximum after two and three weeks. The oedematous changes decrease dramatically after four and six weeks, when most of the serum proteins are reabsorbed by cellular activities in the tumour scar. The vasogenic brain oedema in this xenogeneic glioma transplantation model may be enhanced by the immunological reactions in the brain.