Impact of 9p deletion and p16, Cyclin D1, and Myc hyperexpression on the outcome of anaplastic oligodendrogliomas

PloS One
Karine MichaudStéphan Saikali

Abstract

To study the presence of 9p deletion and p16, cyclin D1 and Myc expression and their respective diagnostic and prognostic interest in oligodendrogliomas. We analyzed a retrospective series of 40 consecutive anaplastic oligodendrogliomas (OIII) from a single institution and compared them to a control series of 10 low grade oligodendrogliomas (OII). Automated FISH analysis of chromosome 9p status and immunohistochemistry for p16, cyclin D1 and Myc was performed for all cases and correlated with clinical and histological data, event free survival (EFS) and overall survival (OS). Chromosome 9p deletion was observed in 55% of OIII (22/40) but not in OII. Deletion was highly correlated to EFS (median = 29 versus 53 months, p<0.0001) and OS (median = 48 versus 83 months, p<0.0001) in both the total cohort and the OIII population. In 9p non-deleted oligodendrogliomas, p16 hyperexpression correlated with a shorter OS (p = 0.02 in OII and p = 0.0001 in OIII) whereas lack of p16 expression was correlated to a shorter EFS and OS in 9p deleted OIII (p = 0.001 and p = 0.0002 respectively). Expression of Cyclin D1 was significantly higher in OIII (median expression 45% versus 14% for OII, p = 0.0006) and was correlated with MIB-1 expression (...Continue Reading

References

Feb 1, 1993·Radiology·K T ShimizuM T Selch
Jan 1, 1997·Journal of Neuro-oncology·F G BarkerM A Israel
Sep 18, 1997·Journal of Neuropathology and Experimental Neurology·A PerryD A Carson
Mar 14, 1998·Acta Neuropathologica·P CavallaD Schiffer
Jun 8, 1999·Journal of Neuro-oncology·H MiettinenH Haapasalo
Nov 4, 2000·International Journal of Cancer. Journal International Du Cancer·S BortolottoD Schiffer
Mar 14, 2001·Journal of Neuropathology and Experimental Neurology·C GianniniH Altermatt
Apr 22, 2004·Journal of Neuropathology and Experimental Neurology·Kenneth B FallonArie Perry
Jun 29, 2004·Journal of Neuro-oncology·Stella M RanuncoloLydia Puricelli
Mar 8, 2005·Journal of Clinical Neuroscience : Official Journal of the Neurosurgical Society of Australasia·Xiang ZhangXi-Ling Wang
Sep 20, 2005·Cancer Cell·Chi V DangTarja Juopperi
Oct 12, 2007·The New England Journal of Medicine·John GearhartMegana K Prasad
Mar 29, 2008·Acta Neuropathologica·Mário Henrique FariaSilvia Helena Rabenhorst
Feb 22, 2012·Upsala Journal of Medical Sciences·Fredrik J Swartling
Oct 17, 2012·Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology·Gregory CairncrossMinesh Mehta
Apr 8, 2015·Nature Genetics·Hiromichi SuzukiSeishi Ogawa
May 7, 2015·Acta Neuropathologica·Pieter WesselingArie Perry
Jun 11, 2015·The New England Journal of Medicine·UNKNOWN Cancer Genome Atlas Research NetworkJianan Zhang
Aug 4, 2015·Brain Tumor Pathology·Nozomi MatsumuraYoichi Nakazato
Sep 20, 2015·Neurology·Agustí AlentornUNKNOWN POLA Network
Oct 4, 2016·Journal of Molecular Medicine : Official Organ of the Gesellschaft Deutscher Naturforscher Und Ärzte·Shuo Qie, J Alan Diehl

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Citations

Feb 2, 2020·Diagnostic Pathology·Thi My Hanh LuongMasahiro Nakashima

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Methods Mentioned

BETA
surgical resections
biopsies
biopsy

Software Mentioned

Metafer
R

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