Kubuki Yoko, Yamaji Takumi, Hidaka Tomonori, Kameda Takuro, Shide Kotaro, Sekine Masaaki, Kamiunten Ayako, Akizuki Keiichi, Shimoda Haruko, Tahira Yuuki, Nakamura Kenichi, Abe Hiroo, Miike Tadashi, Iwakiri Hisayoshi, Tahara Yoshihiro, Sueta Mitsue, Yamamoto Shojiro, Hasuike Satoru, Nagata Kenji, Kitanaka Akira, Shimoda Kazuya
Department of Transfusion and Cell Therapy, University of Miyazaki Hospital.
J Clin Exp Hematop. 2017;56(3):145-149. doi: 10.3960/jslrt.56.145.
Ten-eleven translocation-2 (TET2) mutation is frequently observed in myeloid malignancies, and loss-of-function of TET2 is essential for the initiation of malignant hematopoiesis. TET2 mutation presents across disease entities and was reported in lymphoid malignancies. We investigated TET2 mutations in 27 diffuse large B-cell lymphoma (DLBCL) patients and found a frameshift mutation in 1 case (3.7%). TET2 mutation occurred in some populations of DLBCL patients and was likely involved in the pathogenesis of their malignancies.
十一-易位蛋白2（TET2）突变在髓系恶性肿瘤中经常被观察到，并且TET2功能丧失对于恶性造血的起始至关重要。TET2突变存在于多种疾病实体中，并且在淋巴系恶性肿瘤中也有报道。我们调查了27例弥漫性大B细胞淋巴瘤（DLBCL）患者的TET2突变情况，发现1例患者存在移码突变（3.7%）。TET2突变发生在部分DLBCL患者群体中，可能参与了其恶性肿瘤的发病机制。
