Immunohistochemical phenotype of malignant mesothelioma: Predictive value of CA125 and HBME-1 expression
Immunohistochemical phenotype of malignant mesothelioma: Predictive value of CA125 and HBME-1 expression
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DOI：
10.1046/j.1365-2559.1996.d01-562.x
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发表时间：
1997-01-01
期刊：
影响因子：
6.4
通讯作者：
Herbert, A
中科院分区：
文献类型：
--
作者：
Bateman, AC;AlTalib, RK;Herbert, A
恶性间皮瘤的组织学诊断以及与腺癌的鉴别往往很困难。恶性间皮瘤的病理学确诊需要适当的免疫组化表型。选择一个最佳的小组的免疫组化抗体的恶性间皮瘤的可靠鉴定是阻碍了间皮瘤细胞的特异性免疫组化标记的情况下。最近，我们发现卵巢癌细胞抗体CA 125标记恶性间皮瘤细胞，并且抗体HBME-1已被开发为敏感的间皮瘤细胞标记物。我们比较了CA 125和HBME-1的免疫组化染色模式，获得了使用一组8个进一步的抗体在17个恶性间皮瘤和14个原发性和继发性腺癌在肺和胸膜。CA 125标记恶性间皮瘤细胞15例（88%），腺癌细胞7例（50%）。HBME-1标记17例（100%）间皮瘤细胞，14例（71%）腺癌细胞中10例（71%）阳性; BerEP-4标记1例恶性间皮瘤，16例阴性，14例腺癌中9例（64%）阳性。抗CEA、AUA-1、CA19.9和LeuM 1单克隆抗体均未标记恶性间皮瘤，在14例腺癌中分别有10例（71%）、9例（64%）、8例（57%）和6例（43%）阳性。淀粉酶PAS染色检测中性粘蛋白在没有恶性间皮瘤，但在10（71%）的14个腺癌。我们的结论是，CA 125和HBME-1不标记间皮瘤细胞具有足够的特异性，可用于区分恶性间皮瘤腺癌，虽然阴性染色HBME-1作出诊断恶性间皮瘤不太可能。由于仍然缺乏特异性阳性间皮细胞标志物，因此使用包括以下至少两种的一组抗体进行这种区分仍然是最可靠的：抗CEA、AUA-1、BerEP 4、LeuM 1和CA 19.9，并结合中性粘蛋白产生的组织化学评估。
Histological diagnosis of malignant mesothelioma and differentiation from adenocarcinoma is often difficult. Definitive pathological confirmation of malignant mesothelioma requires demonstration of an appropriate immunohistochemical phenotype. Selection of an optimum panel of immunohistochemical antibodies for the reliable identification of malignant mesothelioma is hindered by the absence of a specific immunohistochemical label for mesothelioma cells. Recently, we have found that the ovarian carcinoma cell antibody CA125 labels malignant mesothelioma cells, and the antibody HBME-1 has been developed as a sensitive mesothelial cell marker. We have compared the immunohistochemical staining patterns achieved with CA125 and HBME-1 to those obtained using a panel of eight further antibodies in 17 malignant mesotheliomas and 14 primary and secondary adenocarcinomas within lung and pleura. CA125 labelled malignant mesothelioma cells in 15 of 17 cases (88%), and adenocarcinoma cells in seven of 14 cases (50%). HBME-1 labelled mesothelioma cells in all 17 cases (100%) but also labelled adenocarcinoma cells in 10 of 14 cases (71%), BerEP4 positively labelled one the malignant mesothelioma but was negative in the remaining 16 cases and positively labelled nine of 14 adenocarcinomas (64%). Monoclonal anti-CEA, AUA-1, CA19.9 and LeuM1 labelled no malignant mesotheliomas and were positive in 10 (71%), nine (64%), eight (57%) and six (43%) of 14 cases of adenocarcinoma, respectively. Diastase-PAS staining detected neutral mucin in none of the malignant mesotheliomas but in 10 (71%) of the 14 adenocarcinomas. We conclude that CA125 and HBME-1 do not label mesothelial cells with sufficient specificity to be useful for differentiating malignant mesothelioma from adenocarcinoma, although negative staining with HBME-1 makes a diagnosis of malignant mesothelioma unlikely. As there remains an absence of a specific positive mesothelial cell marker this distinction is still most reliably made using a panel of antibodies including at least two of the following: anti-CEA, AUA-1, BerEP4, LeuM1 and CA19.9, in combination with histochemical assessment of neutral mucin production.