The prognostic impact of histology and 1p/19q status in anaplastic oligodendroglial tumors.
BACKGROUND
It has been reported previously that the combined loss of chromosomal arms 1p and 19q is a significant predictor of outcome for patients with anaplastic oligodendroglial (AO) tumors and that such chromosomal loss correlates with classic histology in AO. The authors sought to determine whether histology was an equivalent or superior predictor of outcome compared with 1p/19q status in 131 patients with AO tumors.


METHODS
The status of 1p and 19q was determined using real-time, quantitative polymerase chain reaction analysis and/or fluorescence in situ hybridization. Clinical features (response to adjuvant therapy and tumor location) and molecular genetic abnormalities (9p and 10q deletions, overexpression of p53 and epidermal growth factor receptor) were determined on available specimens. Histologic assessments for classic oligodendroglial features were performed by five neuropathologists.


RESULTS
Classic histology was associated closely with 1p/19q loss, as reported previously. Patients who had tumors that were considered classic by at least four of the five neuropathologists showed significantly increased progression-free and overall survival compared with the patients who had less classic tumors. The authors also tested the correlation between 1p/19q status and outcome in subsets of patients stratified according to classic tumor features. The association of 1p/19q status with survival was related closely to the presence of classic histology. Loss of 1p/19q was predictive of improved outcome only among patients who had tumors with classic histologic features.


CONCLUSIONS
The current results suggested that, in addition to 1p/19q status, histologic features contribute information to the prediction of outcome in patients with AO. Loss of 1p and 19q appeared to be a prognostic marker only in the subset of patients who had AO tumors with classic histologic features.
McDonald
J Matthew
JM
Department of Pathology, The University of Texas M. D. Anderson Cancer Center, Houston, Texas 77030, USA.
See
Siew Ju
SJ
Tremont
Ivo W
IW
Colman
Howard
H
Gilbert
Mark R
MR
Groves
Morris
M
Burger
Peter C
PC
Louis
David N
DN
Giannini
Caterina
C
Fuller
Gregory
G
Passe
Sandra
S
Blair
Hilary
H
Jenkins
Robert B
RB
Yang
Helen
H
Ledoux
Alicia
A
Aaron
Joann
J
Tipnis
Ulka
U
Zhang
Wei
W
Hess
Kenneth
K
Aldape
Ken
K
D001483:Base Sequence; D001707:Biopsy, Needle; D001932:Brain Neoplasms / Q000235:genetics* / Q000401:mortality / Q000473:pathology* / Q000601:surgery; D002878:Chromosomes, Human, Pair 1; D002888:Chromosomes, Human, Pair 19; D015331:Cohort Studies; D004273:DNA, Neoplasm / Q000032:analysis; D005260:Female; D005819:Genetic Markers / Q000235:genetics; D006801:Humans; D017404:In Situ Hybridization, Fluorescence; D016015:Logistic Models; D019656:Loss of Heterozygosity; D008297:Male; D008969:Molecular Sequence Data; D009367:Neoplasm Staging; D009837:Oligodendroglioma / Q000235:genetics* / Q000401:mortality / Q000473:pathology* / Q000601:surgery; D016133:Polymerase Chain Reaction / Q000379:methods; D011379:Prognosis; D012189:Retrospective Studies; D018570:Risk Assessment; D016019:Survival Analysis
D004273:DNA, Neoplasm; D005819:Genetic Markers