Katherine S Panageas1, Anne S Reiner1, Fabio M Iwamoto1, Timothy F Cloughesy1, Kenneth D Aldape1, Andreana L Rivera1, April F Eichler1, David N Louis1, Nina A Paleologos1, Barbara J Fisher1, Lynn S Ashby1, J Gregory Cairncross1, Gloria B Roldán Urgoiti1, Patrick Y Wen1, Keith L Ligon1, David Schiff1, H Ian Robins1, Brandon G Rocque1, Marc C Chamberlain1, Warren P Mason1, Susan A Weaver1, Richard M Green1, Francois G Kamar1, Lauren E Abrey1, Lisa M DeAngelis1, Suresh C Jhanwar1, Marc K Rosenblum1, Andrew B Lassman1. 1. Departments of Neurology (A.B.L., F.M.I., L.E.A., L.M.D.), Pathology (S.C.J., M.K.R.), Epidemiology & Biostatistics (A.S.R., K.S.P.), and the Brain Tumor Center, Memorial Sloan-Kettering Cancer Center, New York, New York; University of California, Los Angeles, Los Angeles, California (T.F.C.); Department of Pathology, The University of Texas MD Anderson Cancer Center, Houston, Texas (K.D.A., A.L.R.); Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts (A.F.E., D.N.L.); NorthShore University Health System, Evanston Hospital Kellogg Cancer Center, University of Chicago, Pritzker School of Medicine, Evanston, Illinois (N.A.P.); London Regional Cancer Program, London, Ontario, Canada (B.J.F.); Barrow Neurological Institute, Phoenix, Arizona (L.S.A.); University of Calgary, Calgary, Alberta, Canada (J.G.C., G.B.R.U.); Brigham and Women's Hospital and Dana-Farber Cancer Institute, Boston, Massachusetts (P.Y.W.); Center for Molecular Oncologic Pathology, Dana-Farber Cancer Institute, Children's Hospital Boston, Brigham and Women's Hospital, Boston, Massachusetts (K.L.L.); University of Virginia Health System, Charlottesville, Virginia (D.S.); University of Wisconsin, Madison, Wisconsin (H.I.R., B.G.R.); University of Washington, Fred Hutchinson Cancer Research Center and Seattle Cancer Care Alliance, Seattle, Washington (M.C.C.); Princess Margaret Hospital, Toronto, Ontario, Canada (W.P.M.); Albany Medical Center, Albany, New York (S.A.W.); Kaiser Permanente-Los Angeles Medical Center, Los Angeles, California (R.M.G.); Clemenceau Medical Center, Beirut, Lebanon and Université Saint-Esprit de Kaslik, Byblos, Lebanon (F.G.K.).
Abstract
BACKGROUND: Anaplastic oligodendroglial tumors are rare, and median survival varies widely. Analysis of 1p19q deletion is performed commonly and is an important prognostic factor. However, age and other clinical variables also carry prognostic value, and it is unclear how to incorporate them into clinical decision making or to combine them for prognostication. METHODS: We compiled a retrospective database of 1013 patients with newly diagnosed anaplastic oligodendrogliomas or oligoastrocytomas and performed a recursive partitioning analysis to generate independent prognostic classes among 587 patients with informative 1p19q status. Variables included for survival classification were age (continuous), history of prior low-grade glioma, 1p19q deletion status, histology (presence or absence of an astrocytic component), tumor lobe, tumor hemisphere, gender, extent of resection, postresection treatment, and performance status at diagnosis. RESULTS: Recursive partitioning analysis identified 5 prognostic groups based on hazard similarity: class I (age <60 y, 1p19q codeleted), class II (age <43 y, not codeleted), class III (age 43-59 y, not codeleted, frontal lobe tumor or age ≥60 y, codeleted), class IV (age 43-59 y, not codeleted, not frontal lobe tumor or age 60-69 y, not codeleted), and class V (age ≥70 y, not codeleted). Survival differences were highly significant (P < .0001), with medians ranging from 9.3 years (95% CI: 8.4-16.0) for class I to 0.6 years (95% CI: 0.5-0.9) for class V. CONCLUSIONS: These 5 distinct classification groups were defined using prognostic factors typically obtained during routine management of patients with anaplastic oligodendroglial tumors. Validation in a prospective clinical trial may better differentiate patients with respect to treatment outcome.
BACKGROUND:Anaplastic oligodendroglial tumors are rare, and median survival varies widely. Analysis of 1p19q deletion is performed commonly and is an important prognostic factor. However, age and other clinical variables also carry prognostic value, and it is unclear how to incorporate them into clinical decision making or to combine them for prognostication. METHODS: We compiled a retrospective database of 1013 patients with newly diagnosed anaplastic oligodendrogliomas or oligoastrocytomas and performed a recursive partitioning analysis to generate independent prognostic classes among 587 patients with informative 1p19q status. Variables included for survival classification were age (continuous), history of prior low-grade glioma, 1p19q deletion status, histology (presence or absence of an astrocytic component), tumor lobe, tumor hemisphere, gender, extent of resection, postresection treatment, and performance status at diagnosis. RESULTS: Recursive partitioning analysis identified 5 prognostic groups based on hazard similarity: class I (age <60 y, 1p19q codeleted), class II (age <43 y, not codeleted), class III (age 43-59 y, not codeleted, frontal lobe tumor or age ≥60 y, codeleted), class IV (age 43-59 y, not codeleted, not frontal lobe tumor or age 60-69 y, not codeleted), and class V (age ≥70 y, not codeleted). Survival differences were highly significant (P < .0001), with medians ranging from 9.3 years (95% CI: 8.4-16.0) for class I to 0.6 years (95% CI: 0.5-0.9) for class V. CONCLUSIONS: These 5 distinct classification groups were defined using prognostic factors typically obtained during routine management of patients with anaplastic oligodendroglial tumors. Validation in a prospective clinical trial may better differentiate patients with respect to treatment outcome.
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