Matsuno Akira, Murakami Mineko, Hoya Katsumi, Yamada Shoko M, Miyamoto Shinya, Yamada So, Son Jae-Hyun, Nishido Hajime, Ide Fuyuaki, Nagashima Hiroshi, Sugaya Mutsumi, Hirohata Toshio, Mizutani Akiko, Okinaga Hiroko, Ishii Yudo, Tahara Shigeyuki, Teramoto Akira, Osamura R Yoshiyuki
Department of Neurosurgery, Teikyo University Chiba Medical Center, 3426-3 Anesaki, Ichihara, Chiba, 299-0111, Japan,
Med Mol Morphol. 2014 Mar;47(1):1-7. doi: 10.1007/s00795-013-0050-z. Epub 2013 Aug 17.
There have been several reports of temozolomide (TMZ) treatment of pituitary carcinomas and atypical adenomas. O(6)-methyl-guanine-DNA methyltransferase is not the sole molecule determining the sensitivity to TMZ in pituitary carcinomas and atypical adenomas. The Japan Society of Hypothalamic and Pituitary Tumors study suggests that MSH6, one of mismatch repair pathway enzyme, fulfills a contributory role to the efficacy of TMZ treatment for pituitary carcinomas and atypical adenomas. The preserved MSH6 function might be essential for the responsiveness to TMZ treatment in pituitary carcinomas and atypical adenomas.
已有多篇关于替莫唑胺(TMZ)治疗垂体癌和非典型腺瘤的报道。O(6)-甲基鸟嘌呤-DNA甲基转移酶并非决定垂体癌和非典型腺瘤对TMZ敏感性的唯一分子。日本下丘脑和垂体肿瘤学会的研究表明,错配修复途径酶之一的MSH6对TMZ治疗垂体癌和非典型腺瘤的疗效起辅助作用。保留的MSH6功能可能对垂体癌和非典型腺瘤对TMZ治疗的反应至关重要。