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At least 19 recordsLinked to original sources

PubMed1998

MIB-1 and p53 immunocytochemistry for differentiating pilocytic astrocytomas and astrocytomas from anaplastic astrocytomas and glioblastomas in children and young adults.

AIMS: To establish whether MIB-1 and p53 staining are useful for differentiating pilocytic astrocytomas and astrocytomas from anaplastic astrocytomas and glioblastomas. This study was restricted to children and young adults under 30 years of age because of the differences in p53 mutations between paediatric and adult astrocytomas. METHODS AND RESULTS: Forty-five astrocytic tumours, including 18 pilocytic astrocytomas, 14 astrocytomas, four anaplastic astrocytomas and nine glioblastomas, from 45 children and young adults, between 1 and 29 years (mean 11 years) of age, were examined pathologically, and sections from paraffin-embedded blocks were used for MIB-1 and p53 immunostaining. The MIB-1 labelling index and the frequency and intensity of p53 staining in both the pilocytic astrocytoma and the astrocytoma group were significantly lower than in the anaplastic astrocytoma plus glioblastoma group (P < 0.001). In 11.1% (two of 18) of pilocytic astrocytomas and 42.9% (six of 14) of astrocytomas, immunoreactivity of either MIB-1 or p53 staining was of almost the same intensity as that of anaplastic astrocytomas and glioblastomas. However, in these cases, results using both MIB-1 and p53 stain differed from those for anaplastic astrocytomas and glioblastomas. CONCLUSIONS: MIB-1 and p53 co-staining is very useful for differentiating pilocytic astrocytomas and astrocytomas from anaplastic astrocytomas and glioblastomas. However, MIB-1 or p53 staining alone cannot differentiate pilocytic astrocytomas and astrocytomas from anaplastic astrocytomas and glioblastomas.

Adolescent↗

PubMed1999

Supratentorial pilocytic astrocytomas, astrocytomas, anaplastic astrocytomas and glioblastomas are characterized by a differential expression of S100 proteins.

The levels of expression of the S100A1, S100A2, S100A3, S100A4, S100A5, S100A6 and S100B proteins were immunohistochemically assayed and quantitatively determined in a series of 95 astrocytic tumors including 26 World Health Organization (WHO) grade I (pilocytic astrocytomas), 23 WHO grade II (astrocytomas), 25 WHO grade III (anaplastic astrocytomas) and 21 WHO grade IV (glioblastomas) cases. The level of the immunohistochemical expression of the S100 proteins was quantitatively determined in the solid tumor tissue (tumor mass). In addition twenty blood vessel walls and their corresponding perivascular tumor astrocytes were also immunohistochemically assayed for 10 cases chosen at random from each of the four histopathological groups. The data showed modifications in the level of S100A3 protein expression; these modifications clearly identified the pilocytic astrocytomas from WHO grade II-IV astrocytic tumors as a distinct biological group. Modifications in the level of S100A6 protein expression enabled a clear distinction to be made between low (WHO grade I and II) and high (WHO grade III and IV) grade astrocytic tumors. Very significant modifications occurred in the level of S100A1 protein expression (and, to a lesser extent, in their of the S100A4 and S100B proteins) in relation to the increasing levels of malignancy. While the S100A5 protein was significantly expressed in all the astrocytic tumors (but without any significant modifications in the levels of malignancy), the S100A2 protein was never expressed in these tumors. These data thus indicate that several S100 proteins play major biological roles in human astrocytic tumors.

Adolescent↗

PubMed2001

Distinct differences in binding capacity to saccharide epitopes in supratentorial pilocytic astrocytomas, astrocytomas, anaplastic astrocytomas, and glioblastomas.

We monitored the expression of glycan-binding sites on a panel of 10 biotinylated neoglycoconjugates by means of quantitative computer-assisted microscopy to further study the molecular mechanisms in the extensive infiltration of the surrounding brain parenchyma by most astrocytic tumors. Three distinct histological compartments were analyzed for each of the 108 astrocytic tumors (15 pilocytic astrocytomas (WHO grade I), 25 astrocytomas (WHO grade II), 30 anaplastic astrocytomas (WHO grade III), and 38 glioblastomas (WHO grade IV) included in our series. These compartments were tumors (nonperivascular tumor astrocytes), perivascular tumor astrocytes, and blood vessel walls. Clear differences were observed between the pilocytic and the diffuse astrocytic tumors. Furthermore, malignant progression in the latter category was paralleled by a decrease in cells' ability to bind distinct sugar epitopes, especially the D-GalNAc(alpha1-3)-D-GalNAc-beta1-R determinant of the Forssman pentasaccharide in tumors, the alpha-L-fucose in perivascular tumor areas, and the beta-D-glucose in tumor vessel walls. Markedly, the level of binding site expression for alpha-D-mannose decreased in the tumors, the perivascular tumor areas, and the vessel walls. These glycohistochemical results imply the functional relevance of protein-carbohydrate interactions in this tumor system.

Adult↗

PubMed2000

Pilocytic astrocytomas do not show most of the genetic changes commonly seen in diffuse astrocytomas.

AIMS: While it is well known that pilocytic astrocytomas are clinically distinct from diffuse astrocytomas, few comprehensive studies have focused on their genetic differences. The aim of this study was to examine pilocytic astrocytomas for genetic alterations that are commonly seen in diffuse astrocytomas. METHODS AND RESULTS: By using molecular genetic and immunohistochemical techniques, we evaluated p16, p53, CDK4 and PTEN genes in 29 pilocytic astrocytomas. Mutation screening of p53 and PTEN was performed by single strand conformation polymorphism analysis followed by direct sequencing. Loss of heterozygosity (LOH) of p53, p16 and 10q23-25 loci was performed with microsatellite markers and genomic microsatellite instability (MSI) was also screened. Protein expression of p16, p53, CDK4 and PTEN was examined by immunohistochemistry. Five tumours were found to have single genetic alterations, which included a p53 mutation, a PTEN mutation, MSI at a single microsatellite marker of the p16 locus, and one single LOH at each p16 and 10q23 loci. Protein expressions of p16, CDK4 and PTEN were detected in 73%, 61% and 38% of tumours, respectively. Significantly and in sharp contrast to diffuse astrocytomas, no pilocytic astrocytoma in our series stained for p53 protein. CONCLUSION: Pilocytic astrocytomas have neither MSI phenotype nor recurrent alterations of the p53 and p116 genes. However, altered expression of PTEN may be important in the genesis of pilocytic astrocytomas. We conclude that pilocytic astrocytomas are genetically distinct from diffuse astrocytomas. Lack of p53 mutation/immunostaining may serve as a diagnostic adjunct for differentiating pilocytic astrocytomas from diffuse astrocytomas in small neurosurgical biopsies.

Adolescent↗

PubMed1999

Astrocytoma cell interaction with elastin substrates: implications for astrocytoma invasive potential.

Elastin has been identified within the meninges and the microvasculature of the normal human brain. However, the role that elastin plays in either facilitating astrocytoma cell attachment to these structures or modulating astrocytoma invasion has not been previously characterized. We have recently shown that astrocytoma cell lines and specimens produce tropoelastin, and express the 67 kDa elastin binding protein (EBP). In the present report, we have established that astrocytoma cells attach to elastin as a substrate in vitro. The U87 MG astrocytoma cell line demonstrated the greatest degree of adhesion. In addition, all astrocytoma cell lines examined were capable of penetrating and migrating through an intact elastin membrane, and of degrading tritiated-elastin, a process that could be prevented by the pre-incubation of astrocytoma cells with EDTA, but not with alpha1-antitrypsin. Astrocytoma cells were also capable of penetrating 1 mm sections of human brain tissue maintained as organotypic cultures. Interestingly, the invasive potential of cultured astrocytoma cells plated on organotypic cultures of human brain was significantly increased after exposure to elastin degradation products (kappa-elastin), which interact with astrocytoma cell surface EBP. Our data show that astrocytoma cells express a functional 67 kDa EBP, enabling them to potentially recognize and attach to elastin as a substrate. These data also suggest that this elastin receptor may be involved in processes which regulate regional astrocytoma invasion.

Astrocytoma↗

PubMed1990

Cell proliferation patterns in the diagnosis of astrocytomas, anaplastic astrocytomas and glioblastoma multiforme: a Ki-67 study.

Although astrocytomas, anaplastic astrocytomas and glioblastoma multiforme differ in their clinical courses, histological distinction between these three tumours and between astrocytomas and anaplastic astrocytomas in particular may be unclear on histology alone especially in small biopsies. In the present study, a more objective way of distinguishing between the three types of tumour is sought. Frozen sections from 26 astrocytomas, 26 anaplastic astrocytomas and 38 glioblastomas were stained by an indirect immunoperoxidase technique using the monoclonal antibody Ki-67 which binds to nuclear proteins in the G1, S, G2 and M phases of the cell cycle. The Ki-67 staining was assessed quantitatively through direct observation of the stained sections by the use of a drawing tube attached to a microscope. A minimum of 1000 cells was counted in each case and labelled cells were expressed as a percentage of the total number of cells. These results, when correlated in each case with the histology of the tumour in paraffin sections, showed Ki-67 labelling indices ranging from 0 to 1.9% (mean 0.5% SD +/- 0.54) in astrocytomas, 0.6 to 10.9% (mean 4.1% SD +/- 2.8) in anaplastic astrocytomas and 0.9 to 16.2% (mean 6.4% SD +/- 3.34) in glioblastoma multiforme. The differences in the three types of tumour were statistically significant. The results suggest that Ki-67 staining is a useful addition to the panel of techniques for distinguishing between astrocytomas, anaplastic astrocytomas and glioblastoma multiforme.

Antibodies, Monoclonal↗

PubMed1993

Astrocytomas of the cerebellum. A comparative clinicopathologic study of pilocytic and diffuse astrocytomas.

BACKGROUND: The majority of patients with astrocytomas of the cerebellum have an excellent prognosis; however, a small percentage of patients continue to do poorly. To clarify the clinical, pathologic, and treatment characteristics that determine prognosis and therapeutic recommendations, a large group of patients with astrocytic tumors of the cerebellum was reviewed and analyzed. METHODS: A clinicopathologic analysis was performed of all patients undergoing initial operation for astrocytomas in the cerebellum between 1960 and 1984. Of the 132 patients, 105 patients had pilocytic astrocytomas and 27 had diffuse astrocytomas. RESULTS: Multivariate analysis revealed that the division of pilocytic and diffuse histologic type was the most significant prognostic factor influencing survival. The 5-year, 10-year, and 20-year survival rates were 85%, 81%, and 79%, respectively, for patients with pilocytic astrocytomas and 7%, 7%, and 7%, respectively, for patients with diffuse astrocytomas (P < 0.001). Pilocytic astrocytomas occurred in a younger age group and were more commonly cystic and completely resected. CONCLUSIONS: Astrocytomas of the cerebellum can be divided into two principal groups, the pilocytic and the diffuse astrocytomas, each of which has distinct clinical, pathologic, and prognostic characteristics.

Adolescent↗

PubMed2001

Galectins are differentially expressed in supratentorial pilocytic astrocytomas, astrocytomas, anaplastic astrocytomas and glioblastomas, and significantly modulate tumor astrocyte migration.

Galectins, a family of mammalian lectins with specificity to beta-galactosides, are involved in growth-regulatory mechanisms and cell adhesion. A relationship is assumed to exist between the levels of expression of galectins and the level of malignancy in human gliomas. A comparative study of this aspect in the same series of clinical samples is required to prove this hypothesis. Using computer-assisted microscopy, we quantitatively characterized by immunohistochemistry the levels of expression of galectins-1, -3 and -8 in 116 human astrocytic tumors of grades I to IV. Extent of transcription of galectins-1, -3, and -8 genes was investigated in 8 human glioblastoma cell lines by means of RT-PCR techniques. Three of these cell lines were grafted into the brains of nude mice in order to characterize in vivo the galectins-1, -3 and -8 expression in relation to the patterns of the tumor invasion of the brain. The role of galectin-1, -3 and -8 in tumor astrocyte migration was quantitatively determined in vitro by means of computer-assisted phase-contrast videomicroscopy. The data indicate that the levels of galectin-1 and galectin-3 expression significantly change during the progression of malignancy in human astrocytic tumors, while that of galectin-8 remains unchanged. These three galectins are involved in tumor astrocyte invasion of the brain parenchyma since their levels of expression are higher in the invasive parts of xenografted glioblastomas than in their less invasive parts. Galectin-3, galectin-1, and to a lesser extent galectin-8, markedly stimulate glioblastoma cell migration in vitro. Since bands for the transcripts of human galectins-2, -4 and -9 were apparently less frequent and intense in the 8 human glioblastoma cell lines, this system provides an excellent model to assign defined roles to individual galectins and delineate overlapping and distinct functional aspects.

Adolescent↗

PubMed1996

Transfection of an invasive human astrocytoma cell line with a TIMP-1 cDNA: modulation of astrocytoma invasive potential.

Malignant astrocytomas are highly invasive tumors which infiltrate diffusely into regions of normal brain. The degradation of the extracellular matrix (ECM) by matrix metalloproteinases is thought to be one of the most important steps in the process of tumor invasion. However, the activity of most matrix metalloproteinases (MMPs) can be modulated by simultaneously secreted inhibitors (tissue inhibitors of metalloproteinases, TIMPs). We have previously shown that an imbalance between the levels of MMPs and TIMPs may be essential in the determination of the invasiveness of certain human malignant astrocytoma cell lines. To determine if the up-regulation of TIMP genes and gene products could modulate the invasiveness of human malignant astrocytoma cells, in the present study we have transfected a highly invasive astrocytoma cell line, SF-188, with an expression vector carrying a full-length TIMP-1 cDNA. The parental SF-188 astrocytoma cell line overexpresses the 72-kDa and 92-kDa type IV collagenases with little expression of TIMPs-1 and -2. Following transfection with TIMP-1, SF-188 astrocytoma clones expressed the 0.9 kb TIMP-1 message by northern analysis, and produced a 21 kDa metalloproteinase inhibitor by reverse zymography. The stable TIMP-1 SF-188 transformants demonstrated morphological changes and diminished growth rates in soft agar when compared to controls. The invasion of successfully TIMP-1 transfected astrocytoma cells across matrigel-coated filters was significantly decreased over controls. These results suggest that upregulation of TIMP-1 expression in SF-188 astrocytoma cells has decreased their in vitro invasive potential.

Astrocytoma↗

PubMed2000

Preferential inactivation of the p53 tumor suppressor pathway and lack of EGFR amplification distinguish de novo high grade pediatric astrocytomas from de novo adult astrocytomas.

Classification of high grade astrocytomas of children into genetic subtypes similar to the adult remains to be defined. Here we report an extensive characterization of 29 high grade pediatric astrocytomas, 7 WHO grade III and 22 WHO grade IV, for genetic alterations frequently observed in high grade adult astrocytomas occurring in either the p53/MDM2/p14ARF or Rb/CDK4/p16INK4a tumor suppressor pathways. In addition, we have assessed the contribution of EGFR overexpression and amplification and LOH for chromosome 10, two genetic alterations commonly associated with the development of de novo adult glioblastoma for their roles in the development of de novo astrocytomas of childhood. Our results suggest two major differences in the genetic pathway(s) leading to the formation of de novo high grade astrocytomas in children compared with those of the adult. Our findings show preferential inactivation of the p53 tumor suppressor pathway in >95% of pediatric astrocytomas versus inactivation of the Rb tumor suppressor pathway in <25% of the same tumors. In addition, de novo high grade pediatric astrocytomas lack amplification of the EGFR gene compared with EGFR amplification in one-third of adult glioblastomas. Since drug treatments and gene therapy strategies exploit specific genetic alterations in tumor cells, our findings have important implications for the future development of treatments for high grade pediatric astrocytomas.

Adolescent↗

PubMed2001

Increased microglia proliferation separates pilocytic astrocytomas from diffuse astrocytomas: a double labeling study.

It is not known how many non-tumorous cells in gliomas contribute to the proliferation rate. We investigated the proliferative activity of microglia in an immunohistochemical double-labeling study of pilocytic astrocytomas and astrocytomas WHO grade II-IV using the antibodies MIB-1 (Ki67) as proliferation-marker and Ki-M1P (CD68) as microglia marker. We found the highest indices of proliferating microglia in pilocytic astrocytomas with an average rate of 32% (+/- 6.8) of all proliferating cells. In contrast, the proliferation indices of microglia were lowest in fibrillary astrocytomas with 8.6% (+/- 2.5) of all proliferating cells. In anaplastic astrocytomas and glioblastomas the percentage of proliferating microglia showed a slight increase to 8.8% (+/- 3.6) and 13.4% (+/- 8.7), respectively. We conclude that microglial cells in astrocytic brain tumors proliferate and show different proliferative activities at different grades of malignancy with the highest rates of proliferating microglia especially in pilocytic astrocytomas. Thus, the proliferation rate does not solely reflect the proliferation of tumor cells, but also of non-tumorous cells. This should be considered in particular when proliferation rates are used as a criterion for prognosis and grading of pilocytic astrocytomas.

Antigens, CD↗

PubMed1982

Cell surface antigens of human astrocytoma defined by mouse monoclonal antibodies: identification of astrocytoma subsets.

The surface antigens of cultured human malignant astrocytomas were analyzed by using mouse monoclonal antibodies. BALB/c mice were immunized repeatedly with either SK-MG-1 [a glial fibrillary acidic protein (GFA)-negative astrocytoma line] or SK-AO2 (a GFA-positive astrocytoma line). After fusion with NS/1 mouse myeloma cells, 12 antibody-producing clones were selected for detailed study. Serological analysis permitted the identification of nine distinct antigenic systems. Four monoclonal antibodies (Ab AJ225, Ab AO10, Ab AJ8, and Ab AO122) identified cell surface antigens preferentially expressed on tumors of neuroectodermal origin, and these antibodies subdivided the astrocytoma panel into distinguishable subsets. The determinant detected by Ab AO10 and Ab AJ8 showed mutually exclusive expression on the astrocytoma lines. The AO10 and AJ8 phenotypes appeared to reflect the differentiation state of the cultured cells; 4/7 AO10-positive astrocytomas expressed GFA, an intracellular astrocyte differentiation antigen, whereas all AJ8-positive astrocytoma (9/9) were GFA-negative. Five antibodies (Ab AJ10, Ab AJ9, Ab AJ17, Ab AJ425, and Ab AJ2) recognized determinants widely distributed on normal and malignant cells. Four antibodies defined in this study precipitated proteins from reduced preparations of radioisotope-labeled SK-MG-1 and SK-AO2 cells: Ab AJ225 (Mr 145,000); Ab AO122 (Mr265,000); Ab AJ10 (Mrs 195,000 and 165,000); and Ab AJ2 (Mrs 170,000, 140,000, 140,000, and 28,000).

Animals↗

PubMed1994

[Recurrent astrocytoma versus primary astrocytoma: a comparative study of morphological changes of 32 cases].

The pathologic morphological changes of 32 cases of recurrent astrocytoma (RA) and primary astrocytoma were reported. During recurrence, 20 cases (62.5%) of astrocytomas transformed into cases at higher grades. Twelve cases remained at the same grades as primary tumors. Among 21 cases of RA at grades III and IV, 15 cases (71.4%) came from primary astrocytomas, grades I and II. The change from astrocytoma grade I to grade III or IV took time longer than that from grade II to grade III or IV. The recurrent time of astrocytomas with different grades showed no statistical differences. Postoperative radiotherapy/chemotherapy did not play a major role in grading changes and recurrent time.

Adult↗

PubMed2000

A clinicopathologic reappraisal of brain stem tumor classification. Identification of pilocystic astrocytoma and fibrillary astrocytoma as distinct entities.

BACKGROUND: Brain stem tumors in children have been classified pathologically as low grade or high grade gliomas and descriptively as diffuse gliomas, intrinsic gliomas, midbrain tumors, tectal gliomas, pencil gliomas, dorsal exophytic brain stem tumors, pontine gliomas, focal medullary tumors, cervicomedullary tumors, focal gliomas, or cystic gliomas. METHODS: To search for a simplified and prognostic clinicopathologic scheme for brain stem tumors, the authors reviewed a consecutive cohort of patients younger than age 21 years with tumors diagnosed from 1980 through 1997. Pathology specimens and neuroimaging were classified by masked review. Statistical and survival analysis along with Cox proportional hazards regression was performed. RESULTS: Seventy-six patients were identified, with initial diagnostic magnetic resonance imaging available for 51 and pathology specimens for 48 patients. Twenty cases were classified histologically as pilocytic astrocytoma (PA), 14 as fibrillary astrocytoma (FA), and 14 as other tumors or indeterminate pathology. For all tumors, characteristics significantly associated with a worse survival rate were: symptom duration less than 6 months before diagnosis (P = 0.004); abducens palsy at presentation (P < 0.0001); pontine location (P = 0.0002); and engulfment of the basilar artery (P = 0.006). Pilocytic astrocytoma was associated with location outside the ventral pons (P = 0.001) and dorsal exophytic growth (P = 0.013); Fibrillary astrocytoma was associated with symptoms less than 6 months (P = 0. 006), abducens palsy (P < 0.001), and engulfment of the basilar artery (P = 0.002). Pilocytic astrocytoma showed 5-year overall survival (OS) of 95% (standard error [SE], 5%) compared with FA 1-year OS of 23% (SE, 11%;P < 0.0001). CONCLUSIONS: Brain stem tumors can be succinctly and better biologically classified as diffusely infiltrative brain stem gliomas-generally FA located in the ventral pons that present with abducens palsy, often engulf the basilar artery, and carry a grim prognosis-and focal brain stem gliomas-frequently PA arising outside the ventral pons, often with dorsal exophytic growth, a long clinical prodrome, and outstanding prognosis for survival. Our findings emphasize the individuality of PA as a distinct clinicopathologic entity with an exceptional prognosis.

Adolescent↗

PubMed1992

Correlation of cytogenetic analysis and loss of heterozygosity studies in human diffuse astrocytomas and mixed oligo-astrocytomas.

The aims of this study were to correlate cytogenetic studies and molecular genetic loss of heterozygosity (LOH) analyses in human astrocytomas and mixed oligo-astrocytomas, and to locate putative tumor suppressor genes on chromosome 10. Paired blood and tumor samples from 53 patients were analyzed. The tumors included 45 diffuse astrocytomas (39 grade 4, 4 grade 3, and 2 grade 2), 1 astroblastoma, and 7 mixed oligo-astrocytomas (2 grade 4, 4 grade 3, and 1 grade 2). By cytogenetic analyses the most common numeric chromosome abnormalities were +7, -10, -13, -14, -17, +19, -22, and -Y. The most common structural abnormalities involved chromosome arms 1p, 1q, 5p, and 9p. By LOH and dosage analysis the most common molecular genetic abnormalities were of chromosome arms 5p, 6p, 7q, 9p, 10p, 10q, 13q, 14q, 17p, and 19p. When the results of all methods were combined, the most commonly abnormal chromosomes were, in descending frequency, 10, Y, 17, 7, 13, and 9. In 80 percent of cases the cytogenetic and molecular genetic studies were concordant. LOH studies were more sensitive in detecting loss of genetic material than cytogenetic analyses and accounted for 60% of the discordant results. When there were structural abnormalities, such as translocations or inversions, cytogenetic analysis was more sensitive in detecting an abnormality than molecular genetic studies. In addition to the 24 tumors which appeared to lose an entire copy of chromosome 10, there were 10 tumors with molecular genetic or cytogenetic evidence of loss of only a portion of chromosome 10. The genetic analyses of these tumors suggest that there are 2 regions on chromosome 10 that may contain potential tumor suppressor genes. One lies distal to locus D10S22 from 10q22 to 10qter, and the other lies proximal to locus TST1 on the 10q arm near the centromere or on the 10p arm.

Adult↗

PubMed1996

Classification of astrocytomas and malignant astrocytomas by principal components analysis and a neural net.

The classification of astrocytomas, astrocytomas with anaplastic foci and glioblastoma multiformes is not always straightforward because the tumors form a histological continuum. The use of principal component analysis (PCA) and neural nets in the classification of these tumors is explored. PCA was performed on 14 histological features recorded from 52 gliomas classified by the Radiation Therapy Oncology Group method (17 astrocytomas, 18 astrocytomas with anaplastic foci, 17 glioblastoma multiformes). Four of the 14 possible 'scores' derived from this analysis were selected to summarize the histological variability seen in all the tumors. These scores were mostly significantly different between tumor types and were thus used to successfully train a neural net to correctly classify these tumors. The first principal component (score) supported the use of increasing cellularity, mitoses, endothelial proliferation, and necrosis in differentiating between the tumor categories, but accounted for only 39% of the variability seen. Other histological features that were significant components of the other scores included the presence of multinucleated or giant cells, gemistocytes, atypical mitoses and changes in nuclear chromatin. Computer programs derived from the methodology described provide a way of standardizing glioma diagnosis and may be extended to assist with management decisions.

Astrocytoma↗

PubMed2002

Infiltrative astrocytomas with granular cell features (granular cell astrocytomas): a study of histopathologic features, grading, and outcome.

Granular cell astrocytomas (GCAs) are rare, incompletely characterized infiltrative gliomas that contain a prominent component of granular cells. Such tumors can readily be mistaken for reactive conditions. We studied 22 cases to explore their morphologic spectrum, establish features useful in distinguishing GCA from nonneoplastic diseases, and to determine which parameters correlate with biologic behavior. Tumors occurred in 17 men and five women, ranging in age from 29 to 75 years, who presented mainly with seizures, headache, aphasia, or hemiparesis. Radiologically, high-grade GCAs were contrast-enhancing, cerebral hemispheric masses with prominent peritumoral edema. All contained sheets or interspersed large, round cells packed with eosinophilic, PAS-positive granules. Lymphocytic infiltrates, either perivascular or admixed with neoplastic cells, were present in 14 tumors. Transition to typical infiltrating astrocytoma was noted in 16 cases; of these, granular cells comprised 30-95% of cells. Six tumors consisted almost entirely of atypical granular cells. By WHO criteria, four GCA were grade 2, seven were grade 3, and 11 were grade 4. Glial fibrillary acidic protein staining was seen in all but one tumor, and the majority were immunoreactive for S-100 protein, KP-1, ubiquitin, and epithelial membrane antigen. Although MIB-1 proliferation indices increased with tumor grade, granular cells accounted for only a minority of immunoreactive cells. Among 18 cases with follow-up, 15 recurred after surgery and resulted in death (mean survival, 7.6 months). Two patients died postoperatively, and one was alive at 51 months. Granular cell astrocytoma is an uncommon morphologic variant that appears to be rapidly progressive and usually fatal.

Adult↗

PubMedDate not supplied

Astrocytoma with angiomatoid vascular proliferation ("angiomatous astrocytoma").

We report a surgical case of unusual anaplastic astrocytoma which was accompanied by an exuberant proliferation of abnormal blood vessels with features resembling those of capillary telangiectasis or cavernous angioma. The patient was a 39-year-old man, who presented with a generalized convulsive seizure, and neuroradiological examination revealed a tumor in the left frontal lobe. The resected tumor showed the features of an anaplastic astrocytoma, grade 3. The proliferation of abnormal blood vessels with dilated lumina and thin walls was seen throughout the tumor, and in the central area these vessels were densely packed and almost replaced the neoplastic astrocytic tissue. Although these dense vascular aggregates in the central area closely simulated capillary telangiectasis or cavernous angioma, they were considered to be of a reactive nature. The term "angiomatous astrocytoma", which is analogous to angiomatous meningioma, seemed to be the most appropriate for the present tumor.

Adult↗