Breast cancer patients treated with adjuvant chemotherapy regimens containing alkylating agents and anthracyclines are at an increased risk for secondary myeloid malignancies, either acute myeloid leukemia (AML) or myelodysplastic syndrome (MDS). Complex genomic changes (karyotypes and/or gene amplification) accompany the development of the secondary neoplasms. Here we present a unique case of a breast cancer patient who developed secondary AML within 18 months of treatment with trastuzumab, pertuzumab, docetaxel, carboplatin (TCHP) and radiation. Leukemia cells had catastrophic alterations in chromosomes 8, 11, and 17. Genetic abnormalities in the leukemia cells included amplification of MYC and KMT2A as double minutes, and deletion and mutational inactivation of TP53 Concurrent amplification of different genes at different levels and on different double minutes, we have named “double minute heterogeneity.” Clinically, this case highlights the need to identify genes amplified in secondary myeloid malignancies by cytogenomic microarray (CMA) analysis since these may have therapeutic implications.

用含烷基化剂和蒽环类药物的辅助化疗方案治疗的乳腺癌患者罹患继发性髓样恶性肿瘤（急性髓性白血病（AML）或骨髓增生异常综合症（MDS））的风险增加。复杂的基因组变化（核型和/或基因扩增）伴随着继发性肿瘤的发展。在这里，我们介绍了一个乳腺癌患者的独特案例，该患者在接受曲妥珠单抗，帕妥珠单抗，多西他赛，卡铂（TCHP）和放射治疗后18个月内发生了继发性AML。白血病细胞在8号，11号和17号染色​​体上发生了灾难性的变化。白血病细胞的遗传异常包括MYC和KMT2A扩增两次，以及TP53的缺失和突变失活。在不同的水平和不同的双分钟同时扩增不同基因，我们将其命名为“双分钟异质性”。临床上，这种情况强调需要通过细胞基因组微阵列（CMA）分析鉴定继发性骨髓恶性肿瘤中扩增的基因，因为这些基因可能具有治疗意义。