Arbiser Jack L, Bonner Michael Y
Department of Dermatology, Emory School of Medicine, and Winship Cancer Institute, Atlanta, Georgia, USA; Dermatology Veterans Affairs Medical Center, Decatur, Georgia, USA.
Department of Dermatology, Emory School of Medicine, and Winship Cancer Institute, Atlanta, Georgia, USA.
J Invest Dermatol. 2016 Mar;136(3):564-566. doi: 10.1016/j.jid.2015.12.019.
Neel et al. have demonstrated that seborrheic keratosis, the most common of all skin tumors, is dependent on acutely transforming retrovirus AKT8 in rodent T-cell lymphoma signaling. The authors found that these lesions are hypersensitive to Akt inhibitors which bind to the ATP binding site of Akt. Cutaneous squamous cell carcinoma is resistant to Akt inhibitors. The implications of this study are not limited to seborrheic keratosis. The presence of wild type p53 (seborrheic keratosis) or mutant p53 (cutaneous squamous cell carcinoma) appears to dictate whether a lesion is sensitive to Akt inhibition or not.
尼尔等人已证明,脂溢性角化病是所有皮肤肿瘤中最常见的一种,在啮齿动物T细胞淋巴瘤信号传导中依赖于急性转化逆转录病毒AKT8。作者发现,这些病变对与Akt的ATP结合位点结合的Akt抑制剂高度敏感。皮肤鳞状细胞癌对Akt抑制剂具有抗性。这项研究的意义并不局限于脂溢性角化病。野生型p53(脂溢性角化病)或突变型p53(皮肤鳞状细胞癌)的存在似乎决定了病变是否对Akt抑制敏感。