1646P - Analysis of a novel translocation, t(9;17)(q31;q24), in rosette-forming glioneuronal tumors

Date 28 September 2014
Event ESMO 2014
Session Poster Display session
Topics Central Nervous System Malignancies
Pathology/Molecular Biology
Basic Scientific Principles
Presenter MASAYA Nagaishi
Citation Annals of Oncology (2014) 25 (suppl_4): iv564-iv573. 10.1093/annonc/mdu359
Authors M. Nagaishi1, S. Nobusawa2, H. Yokoo2, A. Hyodo1, Y. Nakazato3
  • 1Neurosurgery, Koshigaya hospital Dokkyo University School of Medicine, 343-8555 - Saitama/JP
  • 2Human Pathology, Gunma University Graduate School of Medicine, 371-8511 - Gunma/JP
  • 3Pathology, Hidaka Hospital, 370-0001 - Gunma/JP



Papillary glioneuronal tumor (PGNT) and rosette-forming glioneuronal tumor (RGNT) were recently established unusual glioneuronal phenotypes and were categorized as a novel tumor entity in the 2007 World Health Organization classification. The molecular background of these glioneuronal tumors remains poorly understood due to a paucity of reports. Recently, the SLC44A1-PRKCA fusion has been identified in 3 cases of PGNT.


The aim of this study was to confirm it in our 3 cases of PGNT and analyze the presence of specific fusion in 2 cases of RGNT, using fluorescence in situ hybridization.


Two out of three PGNT cases showed one adjacent red-green signal pair representing the rearrangement on chromosome 9 and 17, but not a complete fused yellow signal. Normal signal pattern was observed in the other PGNT case. Neither of two RGNT cases revealed adjacent red-green signal pair or yellow signal.


The SLC44A1-PRKCA fusion is a characteristic alteration in PGNT but not in RGNT, and is suggested as a potential biomarker of PGNT. One adjacent red-green signal pair observed in the PGNTs may imply the presence of different breakpoints from those previously reported in the 9q31 and 17q24 genes.


All authors have declared no conflicts of interest.