PMID- 18781279 OWN - NLM STAT- MEDLINE DCOM- 20090428 LR - 20211020 IS - 0167-594X (Print) IS - 0167-594X (Linking) VI - 91 IP - 1 DP - 2009 Jan TI - Chromosome 1p and 19q deletions in malignant glioneuronal tumors with oligodendroglioma-like component. PG - 33-8 LID - 10.1007/s11060-008-9690-6 [doi] AB - Malignant glioneuronal tumors (MGNT) are suggested to be a new entity of glioma defined morphologically as any malignant glioma showing immunohistoichemical evidence of neuronal differentiation. We encountered seven cases of MGNT with oligodendroglioma-like component and investigated alternations of chromosome 1p and 19q in these tumors. Seven patients ranged from 33 to 62 years of age, four females and three males. Immunohistochemical study of these tumors was performed using neuronal markers (synaptophysin, neurofilament, beta-tubulin, chromogranin A and NeuN), astrocytic marker (GFAP) and Ki-67. We undertook a molecular cytogenetic study of tumor specimens obtained from seven patients using fluorescence in situ hybridization (FISH) with DNA probes mapping to chromosome 1p36, 1q25, 19p13 and 19q13. Histologically, these tumors resembled anaplastic oligodendroglioma. Immunohistochemically, tumor cells were immunoreactive for synaptophysin (7/7), neurofilament (6/7), beta-tubulin (5/7), chromogranin A (4/7), NeuN (2/7) and GFAP (7/7). The Ki-67 labeling index ranged from 4.5% to 20.7%. FISH analysis demonstrated either 1p or 19q deletion in all seven cases (100%) and both 1p and 19q deletions in five cases (71%). The 1p deletion was detected in six of seven cases (86%) and 19q deletion was also detected in six (86%). 1p and 19q deletions were present in MGNT, especially those with oligodendroglial components. We suggest that the oligodendroglial-like feature was associated with not only 1p or 19q loss but also differentiation along neuronal cell lines as a factor of favorable prognosis in glial tumors. It is inappropriate to make a diagnosis of oligodendroglioma based only on morphological resemblance to oligodendroglia. FAU - Takeuchi, Hiroaki AU - Takeuchi H AD - Department of Neurosurgery, Faculty of Medical Sciences, University of Fukui, 23-3 Matsuoka-Shimoaizuki, Eiheiji, Fukui, 910-1193, Japan. takeu@u-fukui.ac.jp FAU - Kubota, Toshihiko AU - Kubota T FAU - Kitai, Ryuhei AU - Kitai R FAU - Matsuda, Ken AU - Matsuda K FAU - Hashimoto, Norichika AU - Hashimoto N FAU - Sato, Kazufumi AU - Sato K LA - eng PT - Journal Article DEP - 20080910 PL - United States TA - J Neurooncol JT - Journal of neuro-oncology JID - 8309335 RN - 0 (Ki-67 Antigen) RN - 0 (Nerve Tissue Proteins) SB - IM MH - Adult MH - Aged MH - Brain Neoplasms/genetics/*metabolism MH - *Chromosome Deletion MH - *Chromosomes, Human, Pair 1 MH - *Chromosomes, Human, Pair 19 MH - Female MH - Humans MH - Ki-67 Antigen/metabolism MH - Male MH - Middle Aged MH - Nerve Tissue Proteins/metabolism MH - Oligodendroglia/metabolism/pathology MH - Oligodendroglioma/genetics/*metabolism EDAT- 2008/09/11 09:00 MHDA- 2009/04/29 09:00 CRDT- 2008/09/11 09:00 PHST- 2008/06/10 00:00 [received] PHST- 2008/08/11 00:00 [accepted] PHST- 2008/09/11 09:00 [pubmed] PHST- 2009/04/29 09:00 [medline] PHST- 2008/09/11 09:00 [entrez] AID - 10.1007/s11060-008-9690-6 [doi] PST - ppublish SO - J Neurooncol. 2009 Jan;91(1):33-8. doi: 10.1007/s11060-008-9690-6. Epub 2008 Sep 10.