OBJECT: The malignant progression of benign tumors is well documented in gliomas and other systemic lesions. It is also well known that some meningiomas become progressively aggressive despite their original benign status. The theory of clonal evolution is widely believed to explain malignant progression in meningioma; however, the data used to explain stepwise progression have typically been derived from the cytogenetic analysis of different types of tumors of different grades and in different patients. In this study, the authors examined the data obtained in a group of patients with meningiomas that showed clear histopathological progression toward a higher grade of malignancy and then analyzed the underlying cytogenetic findings. METHODS: Among 175 patients with recurrent meningiomas, 11 tumors showed a histopathological progression toward a higher grade that was associated with an aggressive clinical course. Six tumors progressed to malignancy and five to the atypical category over a period averaging 112 months. Tests for MIB-1 and p53 and cytogenetic studies with the fluorescence in situ hybridization (FISH) method were performed in successive specimens obtained in four patients. The MIB-1 value increased in subsequent samples of tumors. Cytogenetic analysis with FISH showed deletions of 22, 1p, and 14q. In all but one case, these aberrations were also present in the previous specimen despite its lower hispathological grade. CONCLUSIONS: The authors documented the progression of meningiomas from benign to a higher histological grade. These tumors were associated with a complex karyotype that was present ab initio in a histologically lower-grade tumor, contradicting the stepwise clonal evolution model. Although it was limited to the tested probes, the FISH method appears to be more accurate than the standard cytogenetic one in detecting these alterations. Tumors that present with complex genetic alterations, even those with a benign histological grade, are potentially aggressive and require closer follow up.
OBJECT: The malignant progression of benign tumors is well documented in gliomas and other systemic lesions. It is also well known that some meningiomas become progressively aggressive despite their original benign status. The theory of clonal evolution is widely believed to explain malignant progression in meningioma; however, the data used to explain stepwise progression have typically been derived from the cytogenetic analysis of different types of tumors of different grades and in different patients. In this study, the authors examined the data obtained in a group of patients with meningiomas that showed clear histopathological progression toward a higher grade of malignancy and then analyzed the underlying cytogenetic findings. METHODS: Among 175 patients with recurrent meningiomas, 11 tumors showed a histopathological progression toward a higher grade that was associated with an aggressive clinical course. Six tumors progressed to malignancy and five to the atypical category over a period averaging 112 months. Tests for MIB-1 and p53 and cytogenetic studies with the fluorescence in situ hybridization (FISH) method were performed in successive specimens obtained in four patients. The MIB-1 value increased in subsequent samples of tumors. Cytogenetic analysis with FISH showed deletions of 22, 1p, and 14q. In all but one case, these aberrations were also present in the previous specimen despite its lower hispathological grade. CONCLUSIONS: The authors documented the progression of meningiomas from benign to a higher histological grade. These tumors were associated with a complex karyotype that was present ab initio in a histologically lower-grade tumor, contradicting the stepwise clonal evolution model. Although it was limited to the tested probes, the FISH method appears to be more accurate than the standard cytogenetic one in detecting these alterations. Tumors that present with complex genetic alterations, even those with a benign histological grade, are potentially aggressive and require closer follow up.
Authors: David A Reardon; Andrew D Norden; Annick Desjardins; James J Vredenburgh; James E Herndon; April Coan; John H Sampson; Sridharan Gururangan; Katherine B Peters; Roger E McLendon; Julie A Norfleet; Eric S Lipp; Jan Drappatz; Patrick Y Wen; Henry S Friedman Journal: J Neurooncol Date: 2011-09-22 Impact factor: 4.130
Authors: Elia Guadagno; Marialaura Del Basso De Caro; Sara Pignatiello; Concetta Sciammarella; Domenico Solari; Paolo Cappabianca; Francesco Maiuri; Flavia Dones Journal: J Neurooncol Date: 2016-07-09 Impact factor: 4.130
Authors: Varun R Kshettry; Quinn T Ostrom; Carol Kruchko; Ossama Al-Mefty; Gene H Barnett; Jill S Barnholtz-Sloan Journal: Neuro Oncol Date: 2015-05-24 Impact factor: 12.300
Authors: Suganth Suppiah; Farshad Nassiri; Wenya Linda Bi; Ian F Dunn; Clemens Oliver Hanemann; Craig M Horbinski; Rintaro Hashizume; Charles David James; Christian Mawrin; Houtan Noushmehr; Arie Perry; Felix Sahm; Andrew Sloan; Andreas Von Deimling; Patrick Y Wen; Kenneth Aldape; Gelareh Zadeh Journal: Neuro Oncol Date: 2019-01-14 Impact factor: 12.300
Authors: Yohan Lee; Jason Liu; Shilpa Patel; Timothy Cloughesy; Albert Lai; Haumith Farooqi; David Seligson; Jun Dong; Linda Liau; Donald Becker; Paul Mischel; Soheil Shams; Stanley Nelson Journal: Brain Pathol Date: 2009-11-20 Impact factor: 6.508