Department of Translational Hematology and Oncology Research, Taussig Cancer Institute, Cleveland Clinic, Cleveland, OH.
Munich Leukemia Laboratory, Munich, Germany.
Blood. 2021 Nov 11;138(19):1885-1895. doi: 10.1182/blood.2020010603.
Although genomic alterations drive the pathogenesis of acute myeloid leukemia (AML), traditional classifications are largely based on morphology, and prototypic genetic founder lesions define only a small proportion of AML patients. The historical subdivision of primary/de novo AML and secondary AML has shown to variably correlate with genetic patterns. The combinatorial complexity and heterogeneity of AML genomic architecture may have thus far precluded genomic-based subclassification to identify distinct molecularly defined subtypes more reflective of shared pathogenesis. We integrated cytogenetic and gene sequencing data from a multicenter cohort of 6788 AML patients that were analyzed using standard and machine learning methods to generate a novel AML molecular subclassification with biologic correlates corresponding to underlying pathogenesis. Standard supervised analyses resulted in modest cross-validation accuracy when attempting to use molecular patterns to predict traditional pathomorphologic AML classifications. We performed unsupervised analysis by applying the Bayesian latent class method that identified 4 unique genomic clusters of distinct prognoses. Invariant genomic features driving each cluster were extracted and resulted in 97% cross-validation accuracy when used for genomic subclassification. Subclasses of AML defined by molecular signatures overlapped current pathomorphologic and clinically defined AML subtypes. We internally and externally validated our results and share an open-access molecular classification scheme for AML patients. Although the heterogeneity inherent in the genomic changes across nearly 7000 AML patients was too vast for traditional prediction methods, machine learning methods allowed for the definition of novel genomic AML subclasses, indicating that traditional pathomorphologic definitions may be less reflective of overlapping pathogenesis.
虽然基因组改变驱动急性髓系白血病(AML)的发病机制,但传统分类主要基于形态学,而典型的遗传创始病变仅定义了一小部分 AML 患者。原发性/新发 AML 和继发性 AML 的历史细分与遗传模式相关,但相关性不同。AML 基因组结构的组合复杂性和异质性可能迄今为止阻止了基于基因组的分类,以确定更能反映共同发病机制的明确分子定义亚型。我们整合了来自 6788 名 AML 患者的多中心队列的细胞遗传学和基因测序数据,这些数据使用标准和机器学习方法进行分析,以生成一种新的 AML 分子分类,其生物学相关性与潜在发病机制相对应。标准监督分析在尝试使用分子模式预测传统病理形态 AML 分类时,仅产生适度的交叉验证准确性。我们通过应用贝叶斯潜在类别方法进行无监督分析,该方法确定了 4 个具有不同预后的独特基因组簇。提取驱动每个簇的不变基因组特征,并在用于基因组分类时可达到 97%的交叉验证准确性。通过分子特征定义的 AML 亚类与当前的病理形态学和临床定义的 AML 亚型重叠。我们对内部和外部结果进行了验证,并为 AML 患者共享一个开放访问的分子分类方案。尽管近 7000 名 AML 患者的基因组变化存在固有的异质性,但对于传统预测方法来说太大了,机器学习方法允许定义新的基因组 AML 亚类,表明传统的病理形态学定义可能不太反映重叠的发病机制。