TY - JOUR
T1 - Clinical and histological characteristics of recurrent oligodendroglial tumors
T2 - Comparison between primary and recurrent tumors in 18 cases
AU - Kanamori, Masayuki
AU - Kumabe, Toshihiro
AU - Shibahara, Ichiyo
AU - Saito, Ryuta
AU - Yamashita, Yoji
AU - Sonoda, Yukihiko
AU - Suzuki, Hiroyoshi
AU - Watanabe, Mika
AU - Tominaga, Teiji
PY - 2013/7
Y1 - 2013/7
N2 - Changes in histological and genetic characteristics were investigated in 18 paired primary and recurrent oligodendroglial tumors, using sequencing analysis for isocitrate dehydrogenase (IDH) 1 and 2 gene mutation, Ki-67 and p53 immunohistochemistry, and fluorescent in situ hybridization for loss of heterozygosity of chromosomes 1p and 19q (1p/19q co-deletion). Malignant transformation occurred in 5 of 8 cases with World Health Organization (WHO) grade II tumors, but in 0 of 10 cases with WHO grade III tumors progressing to glioblastoma. Thirteen of the 18 cases carried IDH1 gene mutation. Tumors with IDH1 mutation tended to survive for longer, even after recurrence, but newly developed microvascular proliferation, tumor necrosis, and elevated Ki-67 labeling index were common. Eleven of the 13 IDH1-mutation tumors had either 1p/19q co-deletion or nuclear expression of p53, but all 5 IDH1/2 wild-type tumors had neither. All cases had the same profile for 1p/19q status at recurrence, but nuclear expression of p53 changed from negative to positive in 2 of 6 cases with IDH1 mutation and 1p/19q co-deletion. WHO grade II oligodendroglial tumors show a high rate of malignant transformation, possibly involving p53 in tumors with IDH1 mutation and 1p/19q co-deletion. Tumors with IDH1 mutation had a more aggressive histological phenotype despite their better prognosis.
AB - Changes in histological and genetic characteristics were investigated in 18 paired primary and recurrent oligodendroglial tumors, using sequencing analysis for isocitrate dehydrogenase (IDH) 1 and 2 gene mutation, Ki-67 and p53 immunohistochemistry, and fluorescent in situ hybridization for loss of heterozygosity of chromosomes 1p and 19q (1p/19q co-deletion). Malignant transformation occurred in 5 of 8 cases with World Health Organization (WHO) grade II tumors, but in 0 of 10 cases with WHO grade III tumors progressing to glioblastoma. Thirteen of the 18 cases carried IDH1 gene mutation. Tumors with IDH1 mutation tended to survive for longer, even after recurrence, but newly developed microvascular proliferation, tumor necrosis, and elevated Ki-67 labeling index were common. Eleven of the 13 IDH1-mutation tumors had either 1p/19q co-deletion or nuclear expression of p53, but all 5 IDH1/2 wild-type tumors had neither. All cases had the same profile for 1p/19q status at recurrence, but nuclear expression of p53 changed from negative to positive in 2 of 6 cases with IDH1 mutation and 1p/19q co-deletion. WHO grade II oligodendroglial tumors show a high rate of malignant transformation, possibly involving p53 in tumors with IDH1 mutation and 1p/19q co-deletion. Tumors with IDH1 mutation had a more aggressive histological phenotype despite their better prognosis.
KW - 1p/19q co-deletion
KW - IDH1/2 gene
KW - Ki-67 labeling index
KW - p53
KW - Recurrent oligodendroglial tumor
UR - http://www.scopus.com/inward/record.url?scp=84880784237&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84880784237&partnerID=8YFLogxK
U2 - 10.1007/s10014-012-0119-8
DO - 10.1007/s10014-012-0119-8
M3 - Article
C2 - 23053495
AN - SCOPUS:84880784237
SN - 1433-7398
VL - 30
SP - 151
EP - 159
JO - Brain Tumor Pathology
JF - Brain Tumor Pathology
IS - 3
ER -