Journal of Neuro-Oncology

, Volume 125, Issue 2, pp 249–251 | Cite as

Prognostic significance of relative 1p/19q codeletion in oligodendroglial tumors

  • Marc C. Chamberlain
  • Donald Born
Laboratory Investigation


1p/19q codeletion is a favorable prognostic marker for oligodendroglial tumors (OT). Compare outcome in OT with simple deletions of 1p or 19q to those with relative deletions defined as the presence of both increased copy number (polysomy) and 1p/19q codeletion. 525 cases were examined by fluorescence in situ hybridization (FISH) using dual color probes to determine the deletion status of chromosome arms 1p and 19q. Categories included simple deletions defined as a proportion of either 1p32 or 19q13 FISH signals compared to 1q42 or 19p13 signals less than 0.80 and relative deletions (1p or 19q) defined as the combination of a <0.80 proportion with >30 % of nuclei showing increased chromosome number (based on enumeration of 1q25 or 19p13). 464 (80 %) were WHO Grade II or III OT of which 209 (48 %) had both 1p and 19q deleted (codeletion). 72 (16 %) had relative deletions for either one or both 1p and 19q of which 28 (6 %) had relative deletions of 1p and 19q (relative codeletion). Overall survival in WHO Grade II OT was 13 + years when 1p/19q codeleted (n = 156); 5 + years in uni- or nondeleted (n = 86); 6 + years in relative deletion for either 1p or 19q (n = 41); and 6 + years in relative 1p/19q codeletion (n = 15). Similarly in WHO Grade III OT (n = 168) overall survival was 11 + years in 1p/19q codeleted (n = 54) OT; 2.5 years in uni- or nondeleted (n = 70); 3 years in relative deletion for one or both 1p or 19q (n = 31); and 4 + years in relative 1p/19q codeletion (n = 13). Survival for OT regardless of grade with relative codeletion of 1p/19q was approximately one half that of 1p/19q codeleted tumors. The presence of relative 1p/19q codeletion is of prognostic significance.


Oligodendroglioma Polysomy Relative1p/19q codeletion 


Compliance with ethical standards

Conflict of interest

Authors report no conflict of interest related to this article.


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Copyright information

© Springer Science+Business Media New York 2015

Authors and Affiliations

  1. 1.Department of NeurologyUniversity of WashingtonSeattleUSA
  2. 2.Department of Pathology-NeuropathologyStanford UniversityPalo AltoUSA
  3. 3.University of Washington/Fred Hutchison Cancer Research CenterSeattle Cancer Care AllianceSeattleUSA

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