成人低倍体急性淋巴细胞白血病由 TP53 突变的克隆性造血演变而来。
Adult Low-Hypodiploid Acute Lymphoblastic Leukemia Evolves from TP53-Mutated Clonal Hematopoiesis.
机构信息
Department of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Institute for the Advanced Study of Human Biology (WPI ASHBi), Kyoto University, Kyoto, Japan.
出版信息
Blood Cancer Discov. 2023 Mar 1;4(2):102-105. doi: 10.1158/2643-3230.BCD-23-0006.
Abstract
Low-hypodiploid acute lymphoblastic leukemia (LH-ALL) in both children and adults is characterized by biallelic TP53 alterations in virtually all cases. However, in contrast to a common germline origin of the TP53 mutations in pediatric cases, those in adult cases are mostly somatic and are derived from age-related clonal hematopoiesis (ARCH), highlighting the role of TP53-mutant ARCH in the development not only of myeloid leukemogenesis but also of LH-ALL in aged populations. See related article by Kim et al., p. 134 (4).
摘要
儿童和成人中的低倍体急性淋巴细胞白血病（LH-ALL）几乎所有病例均存在双等位基因 TP53 改变。然而，与儿科病例中 TP53 突变的常见种系起源不同，成人病例中的 TP53 突变大多是体细胞的，源自与年龄相关的克隆性造血（ARCH），这突出了 TP53 突变型 ARCH 在不仅髓系白血病发生发展中而且在老年人群 LH-ALL 发生发展中的作用。见 Kim 等人的相关文章，第 134 页（4）。
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