title: Cortical architectural abnormalities and MIB1 immunoreactivity in gangliogliomas: a study of 60 patients with intracranial tumors.
abstract: Gangliogliomas are generally low grade neoplasms composed of mixtures of neoplastic glial and neuronal elements whose origin and exact nature are still controversial. We studied a series of 60 intracranial gangliogliomas looking for coexistent cortical architectural abnormalities (cortical dysplasia, microdysgenesis) and to determine if tumor behavior correlates with MIB1 (marker of cellular proliferation) labeling. The patients included 34 males and 26 females who ranged in age from 6 months to 55 years (mean 20 years). Thirty-eight tumors (63%) were located in the temporal lobe and 6 (10%) in the frontal lobe. Fifty-four patients (90%) presented with seizures (most with intractable epilepsy) and the duration of seizures ranged from 1 to 38 years (mean 14 years). In all cases, the predominant glioma component resembled a low grade fibrillary astrocytoma. In 14 tumors (23%), an oligodendroglial component was present. In one case, the glial component resembled an anaplastic astrocytoma. The tumors were characterized variously by perivascular chronic inflammation (N = 45, 75%), vascular proliferation (N = 36, 60%), granular bodies (N = 54, 90%), binucleated neurons (N = 36, 60%), calcification (N = 28, 47%), and cystic degeneration (N = 26, 43%). Meningeal involvement by tumor was observed in five (8%) cases. In 38 patients, sufficient tissue was resected to evaluate for the presence of concomitant cortical architectural abnormalities. Cortical architectural abnormalities were identified near to but clearly separate from the tumor in 19 (50%) patients. Only four patients including the anaplastic tumor died with tumor progression. MIB1 indices (positive tumor cells/1,000 tumor cells counted) in 54 cases ranged from 0 to 10.2 (mean 1.1 +/- 1.0).(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Department of Anatomic Pathology, Cleveland Clinic Foundation, Ohio 44195, USA.
authors.forename: R A
authors.initials: RA
authors.lastname: Prayson
authors.forename: K
authors.initials: K
authors.lastname: Khajavi
authors.forename: Y G
authors.initials: YG
authors.lastname: Comair
mesh_terms: D000328:Adult; D000368:Aged; D000911:Antibodies, Monoclonal / Q000276:immunology; D000951:Antigens, Neoplasm / Q000032:analysis*; D001254:Astrocytoma / Q000737:chemistry / Q000648:ultrastructure; D001932:Brain Neoplasms / Q000098:blood supply / Q000737:chemistry / Q000150:complications / Q000401:mortality / Q000648:ultrastructure*; D002114:Calcinosis; D002467:Cell Nucleus / Q000648:ultrastructure; D002648:Child; D002675:Child, Preschool; D004827:Epilepsy / Q000209:etiology; D005260:Female; D005625:Frontal Lobe / Q000098:blood supply / Q000737:chemistry / Q000648:ultrastructure*; D018303:Ganglioglioma / Q000098:blood supply / Q000737:chemistry / Q000150:complications / Q000401:mortality / Q000648:ultrastructure*; D006801:Humans; D002479:Inclusion Bodies / Q000648:ultrastructure; D007223:Infant; D007249:Inflammation; D019394:Ki-67 Antigen; D008297:Male; D008578:Meninges / Q000473:pathology; D008875:Middle Aged; D009363:Neoplasm Proteins / Q000032:analysis*; D009389:Neovascularization, Pathologic; D009474:Neurons / Q000276:immunology / Q000648:ultrastructure; D009687:Nuclear Proteins / Q000032:analysis*; D009837:Oligodendroglioma / Q000737:chemistry / Q000648:ultrastructure; D012189:Retrospective Studies; D013702:Temporal Lobe / Q000098:blood supply / Q000737:chemistry / Q000648:ultrastructure*
chemical_list: D000911:Antibodies, Monoclonal; D000951:Antigens, Neoplasm; D019394:Ki-67 Antigen; D009363:Neoplasm Proteins; D009687:Nuclear Proteins