Magee J W, McCalmont T H, LeBoit P E
Department of Pathology, University of California, San Francisco.
Arch Dermatol. 1994 Feb;130(2):187-90.
p53 is a tumor suppressor nucleoprotein. Mutations of the p53 gene have been found in a variety of malignant neoplasms. Wild-type p53 has a short half-life, possibly only 20 to 30 minutes, and is not present in the nucleus at levels that are detectable with routine immunohistochemical techniques. Mutant p53 has a longer half-life, and is readily detectable with immunoperoxidase staining.
We studied 17 specimens from patients with either porokeratosis of Mibelli or actinic porokeratosis, using immunoperoxidase staining with an antibody directed against the p53. There was staining of lesional keratinocyte nuclei in 16 of 17 specimens, limited in most cases to the zone between cornoid lamellae. Staining for proliferating cell nuclear antigen was increased above background levels in only six of 13 specimens.
The finding of p53 immunoperoxidase staining in porokeratosis suggests genetic mutation, as occurs in other cutaneous keratinocytic neoplasms, and the lack of corresponding proliferating cell nuclear antigen expression in many specimens indicates that p53 overexpression is not simply a reflection of increased cellular proliferation.
p53是一种肿瘤抑制核蛋白。p53基因的突变已在多种恶性肿瘤中被发现。野生型p53半衰期短，可能仅20至30分钟，并且用常规免疫组化技术无法检测到其在细胞核中的存在水平。突变型p53半衰期较长，可通过免疫过氧化物酶染色轻易检测到。
我们使用针对p53的抗体进行免疫过氧化物酶染色，研究了17例米贝利汗孔角化症或光化性汗孔角化症患者的标本。17例标本中有16例病变角质形成细胞核出现染色，在大多数情况下局限于鸡眼样板之间的区域。13例标本中只有6例增殖细胞核抗原染色高于背景水平。
汗孔角化症中p53免疫过氧化物酶染色的发现提示存在基因突变，这与其他皮肤角质形成细胞肿瘤中发生突变的情况相同，并且许多标本中缺乏相应的增殖细胞核抗原表达表明p53过表达并非仅仅是细胞增殖增加的反映。
