Biomedical subjects
Publications and source records attributed to J Alwasiak.
We report here neuropathology of vascular brain neoplastic tumors. These include haemangioblastoma, haemangiopericytoma, angiosarcoma. The most recent molecular data on the histogenesis of gliosarcoma are also discussed.
We report here immunohistochemical and ultrastructural studies of the pattern of brain degeneration being a consequence of the presence of brain tumors. Robust microglial reaction with upregulation of MHC II type antigens within and around the brain tumor were seen along with the purely degenerative phenomena like neuroaxonal dystrophy (NAD) and myelin dilatation ("ballooning"). The reaction was monotonous and independent of the histological type of the brain tumor.
Paraffin-embedded surgical specimens from 56 human astrocytomas (8 pilocytic [I degree] astrocytomas, 9 low grade [II degrees] fibrillary astrocytomas, 9 high grade [III degrees] astrocytomas and 30 glioblastomas) were immunostained with the anti-PCNA, anti-p53, anti-Ki-67 and anti EGFR antibodies. Approximately 41% of all cases were p53 protein-positive while 23% were EGFR positive. Five cases (8.9%) were positive for both p53 protein and EGFR. Low grade gliomas showed low PCNA LI while high PCNA LI was observed in high grade gliomas. The same trend was observed with anti-Ki-67 antibodies but the proportion of Ki-67 immunolabelled cells was always much lower. In conclusion, we found two populations of astrocytic tumors with EGFR and with p53 protein overexpression but no dependence between p53 immunoreactivity and PCNA or Ki-67 LI.
Neuroectodermal tumors demonstrate a relatively high incidence of proto-oncogenes amplification. This study attempted to determine the frequency of overexpression of three genes: N-myc, c-myc and c-erbB-1, in human PNET. Immunohistochemical studies revealed 5 to 74% neoplastic cells with positive immunoreactivity to anti-c-myc antibody in all investigated samples. In 3 cases the reactivity was particularly strong and present in more than 50% of tumor cells. Northern blot analysis revealed normal (2.3-kb in size) but significantly higher level of c-myc transcripts in these cases. By using anti-EGFR antibody 3 tumors disclosed 10 to 65% neoplastic cells with positive immunoreactivity. There was no rearrangement detected of their c-erbB-1 or N-myc genes by means of applied methods. Our results suggest that overexpression of c-myc gene is present in 10% of PNET but it is not the consequence of gene amplification. Amplification of N-myc and c-erbB-1 are rare events during PNET development.
We report here immunohistochemical study of two cases of dysplastic gangliocytoma of cerebellum (Lhermitte-Duclos disease) a rare entity which is recently classified as a tumor but which hamartomatous nature is also considered. Dysplastic cells of our cases expressed neuronal markers (synaptophysin and NFP), thus their origin from neurons or neuronal precursor is clearly demonstrated. The exact progenitor cell is, however, unknown. The glial involvement was not easily judged based on our histochemical study. While a few GFAP-immunopositive astrocytes were seen in all specimens, including the recurrence of the first case, they appeared of normal size and non hypertrophic in the second case. Furthermore, they did not much increased in number in the recurrent tumor. Thus, it seems that they are not the primary target for the pathogenetic process, whatever it is, of Lhermitte-Duclos disease.
We report a case of a 24-year-old woman with left temporal pleomorphic xanthoastrocytoma (PXA) with atypical neuronal cells. Many neoplastic cells, otherwise typical of PXA, expressed glial fibrillary acidic protein, while neuronal cells with marked atypia were immunopositive for synaptophysin and neurofilament protein. This report supports a notion that PXA, like other astrocytic tumors, may has its gangliogliomatous counterpart as superficial cerebral astrocytoma of infancy has it in desmoplastic infantile ganglioglioma.
We report a prospective series of consecutive cases of primitive neuroectodermal tumor (PNET) studied by electron microscopy. Virtually all specimens showed a differentiation along neuroblastic lines as evidenced by the presence of neurites, dense-cored vesicles, microtubules and adhesive plaque junctions. We observed also numerous intracytoplasmic cilia and autophagic vacuoles. Synaptic specializations were only rarely seen. We conclude that PNET is a tumor category which is not undifferentiated ("primitive") and clearly exhibits features of neuroblastic differentiation.
We report a case of fetal endocarditis coexisting with a congenital heart defect: a common atrium (left atrial isomerism) with complete congenital heart block. The case was studied by echocardiography from 32 to 39 weeks of gestation. A postmortem examination was carried out a few hours after Cesarean section. The autopsy, histopathological and immunohistochemical findings revealed endocarditis. We think that abnormal turbulent systolic and diastolic flow of the semilunar valve, seen in fetal Doppler echocardiography, may be a sign of fetal endocarditis even though clear evidence of vegetations were not seen.
Tubulovesicular structures (TVS) have been consistently observed in brain tissue of the transmissible spongiform virus encephalopathies such as natural and experimental scrapie, bovine spongiform encephalopathy and experimentally induced Creutzfeldt-Jakob disease (CJD). TVS were recently demonstrated in 3 cases of naturally occurring CJD. We report here the presence of TVS in another human brain with CJD, as detected in all 3 specimens by thin section electron microscopy. Their occurrence in all types of spongiform encephalopathies, irrespective of the affected host and the strain of infectious agent, emphasizes their biological significance.
The tumor necrosis factor alpha (TNF-alpha) is a cytokine released within central nervous system from activated astrocytes and macrophages and involved in several pathologic processes including AIDS-myelopathy, multiple sclerosis and myelin dilatation in panencephalic type of Creutzfeldt-Jakob disease. We studied the expression of the TNF-alpha in brain tumors. Only tumors of astrocytic lineage like astrocytomas and glioblastomas, or tumors of mixed lineage as oligo-astrocytomas and multipotential primitive neuroectodermal tumors (PNET) expressed TNF-alpha-like immunoreactivity. We conclude that this lymphokine is expressed in neoplastic astrocytes. We postulate that TNF-alpha may participate in neoplastic transformation of astrocytes via cascade of interactions with receptor for TNF-alpha.
We report the immunolocalization of extensive amyloid beta-protein in senile plaques, cerebrovascular amyloid deposits, neurofibrillary tangles and preamyloid in a 32-year-old man with progressive dementia not due to trisomy 21 or trauma. These amyloid deposits were non-reactive to antibodies directed against scrapie amyloid. Our data indicate that the presence of amyloid beta-protein is not limited to normal aging, Alzheimer's disease and related disorders but is also found in younger individuals with progressive dementia.
G6PD activity in erythrocytes was examined in 129 people with malignant neoplasms (83 males, 46 females). In all these subjects G6PD activity in erythrocytes was markedly higher than in the controls. Tumour surgery resulted in decreased activity of that enzyme in the erythrocytes. The controls were 53 healthy persons (38 males, 15 females) not exposed occupationally to carcinogens.
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A 32-year-old man with rapidly progressive dementia, pyramidal signs, myoclonic jerks and dystonic movements died following brain biopsy. neuropathological examination revealed minimal neuronal loss accompanied by mild spongiform change and astrocytic reaction. Numerous plaques and neurofibrillary tangles composed of paired helical filaments dominated the ultrastructural picture. This patient had features of both Creutzfeldt-Jakob disease and Alzheimer's disease, providing additional support for the existence of an overlap between these disorders.
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