Absence of histological signs of tumor progression in recurrences of completely resected meningiomas.
In meningioma recurrences a tumor progression has been proposed on a molecular genetic basis. From the histological point of view the problem has not been sufficiently investigated. Recurrences mainly depend on tumor location, histology, resection type and on the tumor growth in the adjacent nervous tissue. Seventy-six completely resected recurrent meningiomas have been studied. Most tumors were convexity or parasagittal meningiomas. The number of recurrences studied per tumor varied from 1 to 5. Besides histological methods, immunohistochemistry for Ki-67 MIB-1, TUNEL for apoptosis, counts of mitoses and molecular genetics for CDKN2A were performed. No variation of the mitotic index (MI) or MIB-1 labeling index (LI) was observed in recurrences. Histological features, the number of mitoses and the MIB-1 LI showed a great regional variability. Loss of heterozygosity (LOH) of CDKN2A was found to be slightly more frequent in the first recurrence than in the initial tumor, but it was lower in the following recurrences. The nervous tissue adjacent to the tumor could contain meningothelial cells and be responsible for recurrences. The number of mitoses appeared to be the most important criterion for establishing the tumor grade. The histological aspect does not change in recurrences and there is no progression. The greater number of recurrences in atypical and anaplastic tumors depends on their initial higher proliferation capacity. The occurrence of tumor meningothelial cells in the adjacent nervous tissue or in the thickened arachnoidal membrane can be responsible for recurrence.
Department of Neuroscience, University of Turin, Foundation Gruppo Policlinico di Monza, Via Cherasco 15, 10126 Turin, Italy. davide.schiffer@unito.it
Davide
D
Schiffer
Chiara
C
Ghimenti
Valentina
V
Fiano
D000328:Adult; D000368:Aged; D019941:Cyclin-Dependent Kinase Inhibitor p16 / Q000235:genetics; D003937:Diagnosis, Differential; D018450:Disease Progression; D005260:Female; D006801:Humans; D019394:Ki-67 Antigen / Q000378:metabolism*; D019656:Loss of Heterozygosity; D008297:Male; D008577:Meningeal Neoplasms / Q000378:metabolism / Q000473:pathology* / Q000601:surgery*; D008579:Meningioma / Q000378:metabolism / Q000473:pathology* / Q000601:surgery*; D008875:Middle Aged; D008940:Mitotic Index; D009361:Neoplasm Invasiveness / Q000235:genetics / Q000473:pathology*; D009364:Neoplasm Recurrence, Local / Q000235:genetics / Q000378:metabolism / Q000473:pathology*; D009367:Neoplasm Staging; D018365:Neoplasm, Residual
D019941:Cyclin-Dependent Kinase Inhibitor p16; D019394:Ki-67 Antigen