Smolyannikova V A, Aleksandrova A K
I.M. Sechenov First Moscow State Medical University, Ministry of Health of Russia, Moscow, Russia.
Arkh Patol. 2020;82(2):30-34. doi: 10.17116/patol20208202130.
Seborrheic keratosis (SK) is a benign skin tumor of unknown etiology and pathogenesis. Many details remain unclear despite that there have been a number of studies of cell-cycle abnormalities.
to investigate the expression of the cell-cycle regulatory proteins p53 and p16 and the cell proliferation marker Ki-67 in SK.
The investigation used intraoperative SK material obtained from 130 patients. Tumors were removed from UV-exposed parts of the body in 63 (48%) patients and from the places that were more often closed in 67 (51.5%). An immunohistochemical (IHC) study was performed using monoclonal antibodies to p53, p16, and Ki-67.
A positive reaction with monoclonal antibodies to p53 was recorded in 66 (50.7%) SK samples. In 92.1% of cases, the expression of p53 was found in SK located at the sites that were most exposed to UV radiation (p=0.00001). A positive reaction with monoclonal antibodies to p16 was observed in all SK cases as cytoplasmic staining of more than 50% of the tumor cells: a strong staining in 63 SK samples (overexpression) and a weak staining in 67 SK ones. The level of p16 expression correlated with age (R=0.21; p=0.019) and SK location at the sites exposed to increased insolation (R=0.35; p=0.000038). Overexpressions of p53 and p16 were significantly more commonly recorded in irritated SK. The tumor proliferative activity by the level of Ki-67 expression was low (3.0 to 11.3%). The largest number (8.5±4.8%) of proliferating cells was recorded in irritated SK (p=0.0000001).
The found disorders in the expression of cell-cycle regulatory proteins in SK are suggestive of tumor suppressor activation and keratinocyte senescence. There may be malignant tumor transformation in irritated SK in terms of the significant increase in the expression of p53, p16 in the presence of high cell proliferative activity.
脂溢性角化病（SK）是一种病因和发病机制不明的良性皮肤肿瘤。尽管已经对细胞周期异常进行了多项研究，但许多细节仍不清楚。
研究细胞周期调节蛋白p53和p16以及细胞增殖标志物Ki-67在SK中的表达。
本研究使用了从130例患者获取的术中SK材料。63例（48%）患者的肿瘤取自身体暴露于紫外线的部位，67例（51.5%）患者的肿瘤取自经常封闭的部位。使用针对p53、p16和Ki-67的单克隆抗体进行免疫组织化学（IHC）研究。
66例（50.7%）SK样本中记录到与p53单克隆抗体的阳性反应。在92.1%的病例中，p53的表达见于位于最暴露于紫外线辐射部位的SK（p=0.00001）。在所有SK病例中均观察到与p16单克隆抗体的阳性反应，表现为超过50%的肿瘤细胞胞质染色：63例SK样本中染色强（过表达），67例SK样本中染色弱。p16表达水平与年龄相关（R=0.21；p=0.019），且与SK位于日照增加部位相关（R=0.35；p=0.000038）。p53和p16的过表达在有炎症的SK中显著更常见。根据Ki-67表达水平，肿瘤增殖活性较低（3.0%至11.3%）。在有炎症的SK中记录到的增殖细胞数量最多（8.5±4.8%）（p=0.0000001）。
SK中细胞周期调节蛋白表达的异常发现提示肿瘤抑制激活和角质形成细胞衰老。在有炎症的SK中，鉴于p53、p16表达显著增加且细胞增殖活性高，可能存在恶性肿瘤转化。
