PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 2464954

Intermediate filament expression in astrocytic neoplasms.

M Cosgrove·P L Fitzgibbons·A Sherrod·P T Chandrasoma·S E Martin
View original source ↗Export metadata ↓

Abstract

Immunohistochemical analysis of 30 paraffin-embedded astrocytic neoplasms was performed to correlate the expression of intermediate filament proteins with histologic subtype. Each tumor was studied with monoclonal antibodies to keratin, vimentin, desmin, 200-kd neurofilament protein, and glial fibrillary acidic protein (GFAP). Immunoreactivity with the anti-keratin monoclonal antibodies AE1 and AE3 was demonstrated in 24 cases (80%) including 4 of 6 (66%) well-differentiated astrocytomas (WDAs), 10 of 12 (83%) anaplastic astrocytomas (ANAs), and 10 of 12 (83%) glioblastomas multiforme (GBMs). These cases were further studied with the monoclonal antikeratin antibodies 34 beta E12 and 34 beta H11. Of the 24 AE1/AE3-positive cases, 14 (58%) reacted with 34 beta E12. None of the cases was reactive with 34 beta H11. Vimentin expression was demonstrated in 24 cases (80%), including 2 of 6 (33%) WDAs, 11 of 12 (92%) ANAs, and 11 of 12 (92%) GBMs. Coexpression of keratin and vimentin was observed in 20 cases (67%), including 2 of 6 WDAs, 9 of 12 (75%) ANAs, and 9 of 12 (75%) GBMs. Immunoreactivity with GFAP antibody was present in all 30 (100%) cases, but none of the tumors was reactive with antibodies to desmin or 200-kd neurofilament protein. These findings demonstrate that expression of both keratin and vimentin intermediate filaments is common in astrocytic neoplasms regardless of histologic grade.

Explore related subjects

AstrocytomaBiomarkers, TumorGlial Fibrillary Acidic ProteinGlioblastomaHumansImmunoenzyme TechniquesIntermediate Filament ProteinsKeratinsStaining and LabelingVimentinJournal Article

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

M Cosgrove, P L Fitzgibbons, A Sherrod, P T Chandrasoma, S E Martin. 1989. Intermediate filament expression in astrocytic neoplasms.. https://doi.org/10.1097/00000478-198902000-00007

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2007

Relative afferent pupillary defect with normal vision and vertical strabismus--implications for pupillary pathway anatomy.

BACKGROUND: A relative afferent pupillary defect (RAPD) is usually a sign of visual dysfunction. Here, an unusual case of an RAPD combined with vertical strabismus but normal vision is described. Implications for pupillary pathway anatomy are discussed. METHODS: A 12-year-old girl with chronic headache was shown to have a midbrain tumour. She presented to us with intermittent diplopia. Examination included visual acuity, visual fields, pupillary function, anterior and posterior segments, and strabismus evaluation with the tangent screen. RESULTS: There was a right-sided pathologic RAPD but no afferent visual impairment. Isocoria was present in light and darkness. There was a right-sided strabismus sursoadductorius. CONCLUSIONS: A pathologic RAPD with normal vision can be caused by tumour compression of the contralateral pretectal nucleus or its afferent or efferent fibres. As an implication for pupillary pathway anatomy, our case suggests that there is equal distribution between crossing and non-crossing intercalated neurons. An associated strabismus can show a non-paralytic pattern.

Astrocytoma↗
PubMed2007

Malignant transformation of high-grade astrocytoma associated with neurocysticercosis in a patient with Turcot syndrome.

A 45-year-old woman with anaplastic astrocytoma was clinically diagnosed with Turcot syndrome, and subsequently developed simultaneous neurocysticercosis and malignant transformation to glioblastoma. The parasitic cysts and glioblastoma were microsurgically removed. Histological examination of surgical specimens revealed neurocysticercosis between the normal brain tissue and glioblastoma. The clinical course and histological findings suggest that the parasitic infection and/or genetic changes contributed to the malignant transformation of the astrocytic tumour.

Astrocytoma↗
PubMed2007

Genetic analysis to complement histopathological diagnosis of brain tumors.

Gliomas, the most frequent tumors originating in the human nervous system, are divided into various subtypes. Currently, microscopic examination alone is insufficient for classification and grading so that genetic profiles are increasingly being emphasized in recognition of the emerging role of molecular diagnostic approaches to glioma classification. Glioblastomas (WHO grade IV) may develop de novo (primary glioblastomas) or through progression from lower-grade astrocytomas (secondary glioblastomas), while both glioblastomas show similar histological features. In contrast, they do constitute distinct disease entities that evolve through different genetic pathways, and are likely to differ in prognosis and response to therapy. Oligodendrogliomas (WHO grade II) account for 2.7% of brain tumors and 5-18% of all gliomas. Since this tumor is recognized as a particular subtype of glioma that shows remarkable responses to chemotherapy, a correct diagnosis is of prime importance. The difficulty is that histological differentiation of oligodendrogliomas from diffuse astrocytomas is highly subjective in cases without typical morphological features and there is a lack of reliable immunohistochemical markers. While histological distinction of low-grade gliomas from reactive astrocytes is also often difficult, reactive astrocytes usually lack genetic alterations. More biological and molecular approaches to glioma classification thus appear warranted to provide improved means to achieve correct diagnoses.

Astrocytoma↗