Department of Dermatology and Venereology, Hôpital de Beaumont, Lausanne University Hospital Center, Lausanne, Switzerland.
J Invest Dermatol. 2013 Aug;133(8):1929-32. doi: 10.1038/jid.2013.90.
Recent studies of cancer patients revealed high diversity in oncogenic mechanisms, leading to increased treatment individualization for subgroups of patients with frequent cancers. A similar development may not be possible for patients with rare cancers, such as Merkel cell carcinoma (MCC). Finding shared disease mechanisms may open new options to understanding and treating such tumors. Tumor-infiltrating CD8+ T cells are frequently associated with favorable clinical outcome in a remarkably large spectrum of cancers. In this issue, Afanasiev et al. suggest a mechanism that may hinder the tumor homing of CD8+ T cells in MCC patients. It is possible that therapeutic mobilization of anti-cancer T cells may be useful in patients who share this specific immune biological feature.
最近对癌症患者的研究揭示了致癌机制的高度多样性,这导致了对常见癌症患者亚组的治疗个体化的增加。对于罕见癌症患者(如 Merkel 细胞癌[MCC]),可能无法进行类似的发展。寻找共同的疾病机制可能为理解和治疗此类肿瘤开辟新的选择。肿瘤浸润的 CD8+T 细胞通常与多种癌症的有利临床结局相关。在本期杂志中,Afanasiev 等人提出了一种可能阻碍 MCC 患者 CD8+T 细胞归巢肿瘤的机制。在具有这种特定免疫生物学特征的患者中,治疗性动员抗癌 T 细胞可能是有用的。