Hui Chen1, Cheddhi Thomas2, Felipe Andres Munoz3, Sanda Alexandrescu4, Craig M Horbinski5, Adriana Olar6, Declan McGuone6, Sandra Camelo-Piragua7, Lu Wang1, Elena Pentsova8, Joanna Phillips9, Kenneth Aldape6, Wen Chen8, A John Iafrate10, Andrew S Chi11, David Zagzag12, John G Golfinos12, Dimitris G Placantonakis12,13, Marc Rosenblum1, Pamela Ohman-Strickland3, Meera Hameed1, Matija Snuderl2. 1. Department of Pathology, Memorial Sloan-Kettering Cancer Center, New York, New York. 2. Department of Pathology, NYU Langone Health, New York, New York. 3. Department of Biostatistics and Epidemiology, Rutgers University, School of Public Health, Piscataway Township, New Jersey. 4. Department of Pathology, University of California San Francisco, San Francisco, California. 5. Department of Pathology, Northwestern University Feinberg School of Medicine, Chicago, Illinois. 6. Department of Pathology, The University of Texas MD Anderson Cancer Center, Houston, Texas. 7. Department of Pathology, University of Michigan School of Medicine, Ann Arbor, Michigan. 8. Department of Neurology, Memorial Sloan-Kettering Cancer Center, New York, New York. 9. Department of Neurological Surgery, University of California San Francisco, San Francisco, California. 10. Pathology Service, Massachusetts General Hospital, Boston, Massachusetts. 11. Neuro-Oncology Program, Perlmutter Cancer Center, NYU Langone Health, New York, New York. 12. Department of Neurosurgery, Perlmutter Cancer Center, NYU Langone Health, New York, New York. 13. Kimmel Center for Stem Cell Biology, Neuroscience Institute, NYU Langone Health, New York, New York.
Abstract
BACKGROUND: Chromosomal instability is associated with earlier progression in isocitrate dehydrogenase (IDH)-mutated astrocytomas. Here we evaluated the prognostic significance of polysomy in gliomas tested for 1p/19q status. METHODS: We analyzed 412 histologic oligodendroglial tumors with use of 1p/19q testing at 8 institutions from 1996 to 2013; fluorescence in situ hybridization (FISH) for 1p/19q was performed. Polysomy was defined as more than two 1q and 19p signals in cells. Tumors were divided into groups on the basis of their 1p/19q status and polysomy and were compared for progression-free survival (PFS) and overall survival (OS). RESULTS: In our cohort, 333 tumors (81%) had 1p/19q loss; of these, 195 (59%) had concurrent polysomy and 138 (41%) lacked polysomy, 79 (19%) had 1p/19q maintenance; of these, 30 (38%) had concurrent polysomy and 49 (62%) lacked polysomy. In agreement with prior studies, the group with 1p/19q loss had significantly better PFS and OS than did the group with 1p/19q maintenance (P < 0.0001 each). Patients with 1p/19q loss and polysomy showed significantly shorter PFS survival than patients with 1p/19q codeletion only (P < 0.0001), but longer PFS and OS than patients with 1p/19q maintenance (P < 0.01 and P < 0.0001). There was no difference in survival between tumors with >30% polysomic cells and those with <30% polysomic cells. Polysomy had no prognostic significance on PFS or OS in patients with 1p/19q maintenance. CONCLUSIONS: The presence of polysomy in oligodendroglial tumors with codeletion of 1p/19q predicts early recurrence and short survival in patients with 1p/19q codeleted tumors.
BACKGROUND: Chromosomal instability is associated with earlier progression in isocitrate dehydrogenase (IDH)-mutated astrocytomas. Here we evaluated the prognostic significance of polysomy in gliomas tested for 1p/19q status. METHODS: We analyzed 412 histologic oligodendroglial tumors with use of 1p/19q testing at 8 institutions from 1996 to 2013; fluorescence in situ hybridization (FISH) for 1p/19q was performed. Polysomy was defined as more than two 1q and 19p signals in cells. Tumors were divided into groups on the basis of their 1p/19q status and polysomy and were compared for progression-free survival (PFS) and overall survival (OS). RESULTS: In our cohort, 333 tumors (81%) had 1p/19q loss; of these, 195 (59%) had concurrent polysomy and 138 (41%) lacked polysomy, 79 (19%) had 1p/19q maintenance; of these, 30 (38%) had concurrent polysomy and 49 (62%) lacked polysomy. In agreement with prior studies, the group with 1p/19q loss had significantly better PFS and OS than did the group with 1p/19q maintenance (P < 0.0001 each). Patients with 1p/19q loss and polysomy showed significantly shorter PFS survival than patients with 1p/19q codeletion only (P < 0.0001), but longer PFS and OS than patients with 1p/19q maintenance (P < 0.01 and P < 0.0001). There was no difference in survival between tumors with >30% polysomic cells and those with <30% polysomic cells. Polysomy had no prognostic significance on PFS or OS in patients with 1p/19q maintenance. CONCLUSIONS: The presence of polysomy in oligodendroglial tumors with codeletion of 1p/19q predicts early recurrence and short survival in patients with 1p/19q codeleted tumors.
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