FISH assay development for the detection of p16/CDKN2A deletion in malignant pleural mesothelioma.
FISH assay development for the detection of p16/CDKN2A deletion in malignant pleural mesothelioma.
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用于检测恶性胸膜间皮瘤中 p16/CDKN2A 缺失的 FISH 测定法的开发。
DOI：
10.1136/jcp.2010.076794
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发表时间：
2010-07
影响因子：
3.4
通讯作者：
Tsao, Ming-Sound
中科院分区：
文献类型：
--
作者：
Chung, Catherine T-S;Santos, Gilda Da Cunha;Hwang, David M.;Ludkovski, Olga;Pintilie, Melania;Squire, Jeremy A.;Tsao, Ming-Sound
开发一种荧光原位杂交 (FISH) 测定法，用于检测石蜡组织切片上的 p16/CDKN2A 缺失，作为区分反应性间皮增殖和恶性间皮增殖的辅助测试。对 11 例良性间皮增殖和 54 例恶性胸膜间皮瘤 (MPM) 病例进行 p16/CDKN2A 和 9 号染色体 (CEP-9) 的双色 FISH，以确定 p16/CDKN2A 缺失的临界值。第三个 MYC 探针用于验证显示纯合缺失的病例。使用八个模棱两可的活组织检查进行化验测试。 p16/CDKN2A 缺失的截止值是根据从良性对照获得的 FISH 信号模式（平均细胞核百分比加上三个标准差）计算的。半合子缺失被定义为 >44% 的细胞核显示出半合子（一个 p16/CDKN2A，两个 CEP-9 信号）或 >15% 的细胞核显示出单体性（一个 p16/CDKN2A，一个 CEP-9 信号）删除模式。良性病例均未表现出纯合缺失模式（无 p16/CDKN2A，至少有一个 CEP-9 信号）。在恶性病例中，显示纯合缺失的细胞核百分比范围为 1% 至 87%。因此，纯合缺失的截止值被定义为>10%。在 61% (33/54) 的 MPM 病例中检测到 P16/CDKN2A 缺失。在模棱两可的活检中，四份显示纯合子，一份显示半合子 p16/CDKN2A 缺失。年龄超过 60 岁、接触石棉和 p16/CDKN2A 缺失与较差的预后相关。区分良性和恶性间皮增殖在诊断上可能具有挑战性。 p16/CDKN2A 缺失的 FISH 是确认 MPM 诊断的有用测试。
To develop a fluorescence in-situ hybridisation (FISH) assay for detecting p16/CDKN2A deletion on paraffin tissue sections for use as an ancillary test to distinguish reactive from malignant mesothelial proliferations. Dual-colour FISH for p16/CDKN2A and chromosome 9 (CEP-9) was performed on 11 benign mesothelial proliferations and 54 malignant pleural mesothelioma (MPM) cases to establish cut-off values for p16/CDKN2A deletion. A third MYC probe was used to verify cases showing homozygous deletion. Eight equivocal biopsies were used for assay testing. Cut-off values for p16/CDKN2A deletion were calculated based on FISH signalling patterns obtained from the benign controls (mean percent nuclei plus three standard deviations). Hemizygous deletion was defined as >44% of nuclei showing the hemizygous (one p16/CDKN2A, two CEP-9 signals) or >15% of nuclei showing the monosomy (one p16/CDKN2A, one CEP-9 signal) deletion patterns. None of the benign cases showed a homozygous deletion pattern (no p16/CDKN2A, at least one CEP-9 signal). In the malignant cases, the percentage of nuclei showing homozygous deletion ranged from 1% to 87%. Therefore, the cut-off value for homozygous deletion was defined as >10%. P16/CDKN2A deletion was detected in 61% (33/54) of MPM cases. Among the equivocal biopsies, four showed homozygous and one showed hemizygous p16/CDKN2A deletion. Age over 60 years, asbestos exposure and p16/CDKN2A deletion were associated with a worse prognosis. Distinction between benign and malignant mesothelial proliferations can be diagnostically challenging. FISH for p16/CDKN2A deletion is a useful test for confirming the diagnosis of MPM.
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影响因子：
11.5
作者：
Borczuk, AC;Taub, RN;Powell, CA
通讯作者：
Powell, CA
影响因子：
3.5
作者：
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影响因子：
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作者：
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通讯作者：
VANMARCK, E
影响因子：
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作者：
Tibiletti, MG
通讯作者：
Tibiletti, MG
影响因子：
11.2
作者：
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通讯作者：
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