FISH 1p/19q deletion/imbalance for molecular subclassification of glioblastoma
FISH 1p/19q deletion/imbalance for molecular subclassification of glioblastoma
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DOI：
10.1007/s10014-006-0209-6
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发表时间：
2007-01-01
影响因子：
3.3
通讯作者：
Inao, Suguru
中科院分区：
文献类型：
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作者：
Nagasaka, Toru;Gunji, Masaharu;Inao, Suguru
胶质母细胞瘤是最恶性和最常见的胶质肿瘤。一小部分胶质母细胞瘤可能包含显示少突胶质细胞瘤样肿瘤细胞分化的区域。几位作者将此类肿瘤描述为具有少突胶质细胞成分的胶质母细胞瘤（GBMO）。GBMO可能代表了少突胶质细胞系的恶性程度。胶质母细胞瘤中少突胶质细胞成分和染色体臂1 p和19 q的联合缺失表明生存率增加。在我们的研究中，我们分析了一系列的12个胶质母细胞瘤和8个少突胶质细胞瘤的1 p和19 q状态，使用荧光原位杂交（FISH）石蜡包埋组织。在每种情况下，杂交状态分为缺失，不平衡，多体性，扩增，或正常模式。还评估了其他遗传改变，如CDKN 2A（p16）、RB和EGFR。在组织学检查中，12例胶质母细胞瘤中有2例（16.7%）被归类为GBMO。12例胶质母细胞瘤中3例（25%）存在染色体1 p/19 q缺失。相反，所有8例少突胶质细胞肿瘤均显示1 p/19 q缺失。所有GBMO均存在19 q缺失伴失衡，而10例普通胶质母细胞瘤中有1例（10%）表现为19 q缺失伴失衡。除1例普通胶质母细胞瘤（90%）外，所有胶质母细胞瘤均显示CDKN 2A（p16）缺失，但无GBMO显示此改变。我们的研究结果表明，GBMO可能是胶质母细胞瘤的一个独特的亚型，具有特征性的分子特征。石蜡包埋标本上的FISH是胶质母细胞瘤亚分类的有用方法。
Glioblastoma is the most malignant and frequent of the glial tumors. A minor fraction of glioblastoma may contain areas showing oligodendroglioma-like tumor cell differentiation. Several authors have described such tumors as glioblastoma with oligodendroglial component (GBMO). GBMO may represent the ultimate level of malignancy in the oligodendroglial lineage. The oligodendroglial component and combined loss of chromosomal arm 1p and 19q in glioblastoma indicate increased survival. In our study, we analyzed 1p and 19q status in a series of 12 glioblastoma and 8 oligodendroglial tumors using fluorescence in situ hybridization (FISH) on paraffin-embedded tissues. In each case, hybridization status was classified as deletion, imbalance, polysomy, amplification, or normal pattern. Other genetic alterations such as CDKN2A (p16), RB, and EGFR were also assessed. On histological review, 2 of 12 glioblastoma (16.7%) were classified as GBMO. Chromosome 1p/19q deletion was detected in 3 of 12 glioblastomas (25%). In contrast, all 8 oligodendroglial tumors showed 1p/19q deletion. All GBMO had 19q deletion with imbalance, whereas 1 of 10 ordinary glioblastoma (10%) demonstrated 19q deletion with imbalance. All but 1 ordinary glioblastoma (90%) showed CDKN2A (p16) deletion, but no GBMO displayed this alteration. Our results indicate that GBMO may be a distinct subtype of glioblastoma harboring a characteristic molecular profile. FISH on paraffin-embedded specimens is a useful method for subclassification of glioblastoma.