PMID- 20408960 OWN - NLM STAT- MEDLINE DCOM- 20110318 LR - 20171116 IS - 1440-1789 (Electronic) IS - 0919-6544 (Linking) VI - 30 IP - 6 DP - 2010 Dec TI - Utility of in situ demonstration of 1p loss and p53 overexpression in pathologic diagnosis of oligodendroglial tumors. PG - 586-96 LID - 10.1111/j.1440-1789.2010.01116.x [doi] AB - To improve the diagnostic accuracy of oligodendroglial tumors and to find more convenient parameters that could predict the cytogenetic status, oligodendroglial and astrocytic tumors were cytogenetically and immunohistochemically investigated. Materials included 22 oligodendroglial tumors (15 oligodendrogliomas and 7 oligoastrocytomas) and 20 astrocytic tumors. 1p loss was examined with the fluorescence in situ hybridization (FISH) method. Expression of GFAP, Olig2 and p53 was immunohistochemically investigated and co-localization of GFAP and Olig2 was evaluated on double-immunostained sections. Furthermore, TP53 mutation analyses were carried out on three oligodendroglial tumors showing p53 protein overexpression with a direct sequence analysis. Our FISH studies demonstrated 1p loss in 73% of oligodendroglial tumors (80% oligodendrogliomas and 57% oligoastrocytomas) and in only 10% of astrocytic tumors. There were no clear-cut morphologic differences between 1p-deleted and 1p-intact oligodendroglial tumors. GFAP and Olig2 were expressed in most oligodendroglial and astrocytic tumors, and their cellular localization was almost independent of each other. Overexpression of p53 was observed in five oligodendroglial tumors, all of which were 1p-intact. In comparison, 16 oligodendroglial tumors with 1p deletion showed no overexpression of p53. TP53 missense mutations were detected in three of the p53 overexpressed oligodendroglial tumors studied. Our results suggest that 1p loss is almost specific to oligodendroglial tumors. Although the prediction of 1p status based solely on the morphologic features seems to be difficult, the immunohistochemistry for p53 is a useful tool in that p53 overexpression is closely related to the 1p-intact status in oligodendroglial tumors. CI - (c) 2010 Japanese Society of Neuropathology. FAU - Hirose, Takanori AU - Hirose T AD - Department of Pathology, Saitama Medical School, Moroyama, Iruma-gun, Saitama, Japan. thirose@tph.gr.jp FAU - Ishizawa, Keisuke AU - Ishizawa K FAU - Shimada, Shio AU - Shimada S LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't PL - Australia TA - Neuropathology JT - Neuropathology : official journal of the Japanese Society of Neuropathology JID - 9606526 RN - 0 (Basic Helix-Loop-Helix Transcription Factors) RN - 0 (Glial Fibrillary Acidic Protein) RN - 0 (Nerve Tissue Proteins) RN - 0 (OLIG2 protein, human) RN - 0 (Oligodendrocyte Transcription Factor 2) RN - 0 (Tumor Suppressor Protein p53) SB - IM MH - Adult MH - Aged MH - Astrocytoma/*diagnosis/genetics/metabolism MH - Basic Helix-Loop-Helix Transcription Factors/biosynthesis MH - Brain Neoplasms/*diagnosis/genetics/metabolism MH - Chromosomes, Human, Pair 1/*genetics MH - Female MH - Gene Deletion MH - Glial Fibrillary Acidic Protein/biosynthesis MH - Humans MH - Immunohistochemistry MH - In Situ Hybridization, Fluorescence MH - Male MH - Middle Aged MH - Mutation MH - Nerve Tissue Proteins/biosynthesis MH - Oligodendrocyte Transcription Factor 2 MH - Oligodendroglioma/*diagnosis/genetics/metabolism MH - Tumor Suppressor Protein p53/*biosynthesis/genetics EDAT- 2010/04/23 06:00 MHDA- 2011/03/19 06:00 CRDT- 2010/04/23 06:00 PHST- 2010/04/23 06:00 [entrez] PHST- 2010/04/23 06:00 [pubmed] PHST- 2011/03/19 06:00 [medline] AID - NEU1116 [pii] AID - 10.1111/j.1440-1789.2010.01116.x [doi] PST - ppublish SO - Neuropathology. 2010 Dec;30(6):586-96. doi: 10.1111/j.1440-1789.2010.01116.x.