Adult Low-Hypodiploid Acute Lymphoblastic Leukemia Evolves from TP53-Mutated Clonal Hematopoiesis

Ryunosuke Saiki; Seishi Ogawa

doi:10.1158/2643-3230.BCD-23-0006

Adult Low-Hypodiploid Acute Lymphoblastic Leukemia Evolves from TP53-Mutated Clonal Hematopoiesis

Blood Cancer Discov. 2023 Mar 1;4(2):102-105. doi: 10.1158/2643-3230.BCD-23-0006.

Authors

Ryunosuke Saiki^{1

2}, Seishi Ogawa^{1

2}

Affiliations

¹ Department of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
² Institute for the Advanced Study of Human Biology (WPI ASHBi), Kyoto University, Kyoto, Japan.

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).

Publication types

Editorial
Research Support, Non-U.S. Gov't
Comment

MeSH terms

Acute Disease
Adult
Aged
Aneuploidy
Child
Clonal Hematopoiesis* / genetics
Humans
Mutation
Precursor Cell Lymphoblastic Leukemia-Lymphoma* / genetics
Tumor Suppressor Protein p53 / genetics

Substances

TP53 protein, human
Tumor Suppressor Protein p53