PubMed · 9583899
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B Eyden. 1998. Magnification of electron micrographs.. https://doi.org/10.1093/ajcp%2F109.2.237
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INTRODUCTION: In the surgical management of juvenile nasopharyngeal angiofibromas the possibility of recurrences and residual tumours is always there. This study was undertaken to predict the prognostic factors determining recurrence of juvenile nasopharyngeal angiofibroma and to find out the usual sites of these tumours. MATERIAL AND METHODS: The medical records of 95 patients with histologically proven juvenile nasopharyngeal angiofibroma were reviewed retrospectively. The commonest surgical approach used was a combined transpalatal and transmaxillary approach with a lazy S incision. A conservative lateral infratemporal approach was used in three cases. RESULTS: Complete removal of the juvenile nasopharyngeal angiofibroma was achieved in 78 (82 per cent) of the cases in a single operation. A residual tumour was found in 17 (18 per cent) cases and recurrences occurred in 13 (13.7 per cent) cases. CONCLUSIONS: Extensions into the pterygoid fossa and basisphenoid, erosion of the clivus, intracranial extensions medial to the cavernous sinus, invasion of the sphenoid diploe through a widened pterygoid canal, feeders from the internal carotid artery, a young age and a residual tumour were risk factors found associated with recurrence of juvenile nasopharyngeal angiofibroma.
BACKGROUND: Frequent beta-catenin mutations have been detected in juvenile angiofibromas, but the tumor pathogenesis remains unknown. METHODS: Metaphase-comparative genomic hybridization (CGH) was used to identify chromosomal aberrations in 29 tumor specimens. Two tumors were investigated using genome DNA microarrays. RESULTS: Three hundred eleven chromosomal gains and losses were detected by metaphase-CGH. Frequent chromosomal gains were detected at 4q, 6, 12, and X, while frequent chromosomal losses affected regions of chromosomes 8, 16, 17, 22, and Y. Genome DNA microarray analysis in 2 tumors of the series confirmed chromosomal aberrations, detected by metaphase-CGH, and indicated genes such as AURKA (20q13.2) not being recognized by metaphase-CGH. CONCLUSION: Metaphase-CGH results confirmed numerous chromosomal aberrations in juvenile angiofibromas. The most frequent aberrations affected sex chromosomes. Further consensus regions of chromosomal aberrations were detected at 4q, 6, 8, 12, 16, 17, and 22. AURKA and MDM2 were identified as interesting novel amplified genes in juvenile angiofibromas.
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