Expression of p63 TA and △N isoforms) in human primary well differentiated buccal carcinomas
Expression of p63 TA and △N isoforms) in human primary well differentiated buccal carcinomas
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DOI：
10.1016/j.ijom.2003.10.023
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发表时间：
2004-07-01
影响因子：
2.4
通讯作者：
Lin, LM
中科院分区：
文献类型：
--
作者：
Chen, YK;Hsue, SS;Lin, LM
P53基因的缺失被认为是头颈部鳞状细胞癌发生中最一致的遗传异常。p53基因家族的两个新成员，p73和p63，最近已被确定。我们研究了两个N端p63亚型（TA和AN亚型）在人原发性高分化颊鳞癌中的表达。TAp 63和triangleNp 63亚型在所有5例正常颊粘膜标本的基底/基底上层中均检测到。在23例原发性高分化颊癌组织中，Np 63均呈三角形，而TAp 63则有18例（78.3%）缺失。TAp 63和triangleNp 63亚型的免疫染色模式相似，p63阳性主要见于肿瘤巢的外周细胞，而阴性染色见于角蛋白珍珠形成的区域。T3-T4期患者和复发患者TAp 63表达阴性的人数高于T1-T2期患者和未复发患者，但差异无统计学意义。这些结果表明，特定的p63亚型与人类口腔鳞状细胞癌的发生。三角形Np 63亚型可能参与上皮细胞的分化和增殖在人类口腔癌的发生，而有证据表明，在人类口腔肿瘤的发生TAp 63低表达的可能作用。
Abnormalities in the P53 gene have been regarded as the most consistent genetic abnormalities detected in head and neck squamous cell carcinogenesis. Two new members of the p53 gene family, p73 and p63, have recently been identified. We investigated the expression of the two N-terminal p63 isoforms (TA and AN isoforms) in human primary well-differentiated buccal squamous cell carcinoma. Both TAp63 and triangleNp63 isoforms were detected in the basal/suprabasal layers of all of the five specimens of normal buccal mucosa. The triangleNp63 isoform was found in all of the 23 specimens of human primary well-differentiated buccal carcinoma whereas TAp63 isoform was absent in 18 (78.3%) of the 23 specimens. The immunostaining patterns of both TAp63 and triangleNp63 isoforms were similar in that the p63 positivity was noted mainly in the peripheral cells of tumor nests whereas negative staining was observed in the areas with keratin pearl formation. A higher number of T3-T4 patients and patients with recurrence showed negative staining of TAp63 than T1-T2 patients and patients without recurrence but the difference was not statistically significant. These results suggested that specific p63 isoforms were associated with human oral squamous cell carcinogenesis. The triangleNp63 isoforms might be involved in epithelial differentiation and proliferation in human oral carcinogenesis whereas there was evidence for a possible role of TAp63 under-expression in human oral tumongenesis.