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|Title:||Glioblastomatous recurrence of oligodendroglioma remote from the original site: A case report|
|Authors:||Uludağ Üniversitesi/Tıp Fakültesi/Beyin Cerrahisi Anabilim Dalı.|
Uludağ Üniversitesi/Tıp Fakültesi/Tıbbi Genetik Anabilim Dalı.
Uludağ Üniversitesi/Tıp Fakültesi/Patoloji Anabilim Dalı.
|Keywords:||Neurosciences & neurology|
|Citation:||Kocaeli, H. vd. (2006). ''Glioblastomatous recurrence of oligodendroglioma remote from the original site: A case report''. Surgical Neurology, 65(6), 627-631.|
|Abstract:||Background: As in all diffuse gliomas, recurrence is an inherent feature of oligodendrogliomas, either as the same or higher grade neoplasm at the primary site. The rate of remote recurrence after surgery for the primary tumor cannot be estimated from the scarce literature, but delayed treatment of the primary tumor and genetic alterations may be associated with this phenomenon. Case Description: A 40-year-old man presented with generalized seizures. A magnetic resonance imaging scan disclosed a right frontal mass lesion showing features of a low-grade glioma for which he refused any treatment. Seven months after diagnosis upon uncontrollable seizures, he underwent a stereotactic biopsy, which was followed by a right frontal craniotomy, both of which confirmed the lesion as a grade 2 oligodendroglioma. Six months after surgery, the patient presented with a left frontal lobe GBM without evidence of recurrence at the primary site. The genetic analysis of the primary and recurrent tumors showed trisomy 7, monosomy 10, but not 1p or 19q deletions, which have been proposed as markers for favorable prognosis. Conclusion: Recurrence of a frontal lobe oligodendroglioma remote from the primary site as a GBM is a rare occurrence. Single-cell invasion across the corpus callosum with subsequent or simultaneous malignant degeneration into a secondary GBM is the likely mechanism. As the genetic analysis suggests, conversion of oligodendroglioma to GBM may be associated with gain of chromosome 7, loss of chromosome 10, and other genetic markers that may represent late events in the oncogenesis of oligodendroglial tumors.|
|Appears in Collections:||Scopus|
Web of Science
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