Akiyama Hiroki, Yamamoto Masahide, Sakashita Chizuko, Umezawa Yoshihiro, Kurosu Tetsuya, Murakami Naomi, Miura Osamu
Department of Hematology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Japan.
Intern Med. 2015;54(6):651-5. doi: 10.2169/internalmedicine.54.3535. Epub 2015 Jan 15.
A 40-year-old woman developed therapy-related acute myeloid leukemia (t-AML) with inv(16)(p13.1q22) and a rare type D form of core-binding factor β-subunit gene-myosin heavy chain 11 gene (CBFB-MYH11) fusion transcript approximately 2.5 years after receiving chemoradiotherapy for uterine cervical cancer. t-AML with inv(16)(p13.1q22) and rare non-type A CBFB-MYH11 typically develops after exposure to a topoisomerase II inhibitor, with a short period of latency of one to five years. As the patient had no history of exposure to topoisomerase II inhibitors, among her previously used chemotherapeutics, the topoisomerase I inhibitor, irinotecan, was speculated to be the most plausible cause of t-AML in this case. The present case suggests that irinotecan may cause t-AML resembling that associated with topoisomerase II inhibitors.
一名40岁女性在接受子宫颈癌放化疗约2.5年后，发生了伴有inv(16)(p13.1q22)的治疗相关急性髓系白血病（t-AML），并出现了罕见的D型核心结合因子β亚基基因-肌球蛋白重链11基因（CBFB-MYH11）融合转录本。伴有inv(16)(p13.1q22)和罕见非A型CBFB-MYH11的t-AML通常在接触拓扑异构酶II抑制剂后发生，潜伏期较短，为1至5年。由于该患者无接触拓扑异构酶II抑制剂的病史，在其先前使用的化疗药物中，拓扑异构酶I抑制剂伊立替康被推测是本例中t-AML最可能的病因。本病例提示，伊立替康可能导致类似于与拓扑异构酶II抑制剂相关的t-AML。
