High IL2RA/CD25 expression is a prognostic stem cell biomarker for pediatric acute myeloid leukemia without a core-binding factor.

CD25 RNA sequencing acute myeloid leukemia children leukemic stem cells

Journal

Pediatric blood & cancer
ISSN: 1545-5017
Titre abrégé: Pediatr Blood Cancer
Pays: United States
ID NLM: 101186624

Informations de publication

Date de publication:
06 Dec 2023
Historique:
revised: 19 11 2023
received: 09 05 2023
accepted: 25 11 2023
medline: 6 12 2023
pubmed: 6 12 2023
entrez: 6 12 2023
Statut: aheadofprint

Résumé

CD25 is an aberrant marker expressed on the leukemic stem cell (LSC) surface and an immunotherapy target in acute myeloid leukemia (AML). However, the clinical prevalence and significance of CD25 expression in pediatric AML are unknown. High IL2RA/CD25 expression in pediatric AML showed a stem cell-like phenotype, and elevated CD25 expression was associated with lower overall survival (p < .001) and event-free survival (p < .001) in the Japanese Pediatric Leukemia/Lymphoma Study Group AML-05 study. This finding was reproduced in AML without a core-binding factor in the Children's Oncology Group study cohort. High CD25 expression has prognostic significance in pediatric AML.

Identifiants

pubmed: 38054691
doi: 10.1002/pbc.30803
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

e30803

Informations de copyright

© 2023 Wiley Periodicals LLC.

Références

van Gils N, Denkers F, Smit L. Escape from treatment; the different faces of leukemic stem cells and therapy resistance in acute myeloid leukemia. Front Oncol. 2021;11:659253.
Saito Y, Kitamura H, Hijikata A, et al. Identification of therapeutic targets for quiescent, chemotherapy-resistant human leukemia stem cells. Sci Transl Med. 2010;2:17ra9.
Itoh-Nakadai A, Saito Y, Murasawa-Tomizawa M, et al. CXCR4-expressing anti-CD25 CAR T-cells effectively eliminate human AML cells in vivo. Blood. 2020;136:S35-S36.
Gönen M, Sun Z, Figueroa ME, et al. CD25 expression status improves prognostic risk classification in AML independent of established biomarkers: ECOG phase 3 trial, E1900. Blood. 2012;120:2297-2306.
Nakase K, Kita K, Kyo T, Ueda T, Tanaka I, Katayama N. Prognostic relevance of cytokine receptor expression in acute myeloid leukemia: interleukin-2 receptor α-chain (CD25) expression predicts a poor prognosis. PLoS One. 2015;10:e0128998.
Bolouri H, Farrar JE, Triche T Jr, et al. The molecular landscape of pediatric acute myeloid leukemia reveals recurrent structural alterations and age-specific mutational interactions. Nat Med. 2018;24:103-112.
Koedijk JB, van der Werf I, Calkoen FG, et al. Paving the way for immunotherapy in pediatric acute myeloid leukemia: current knowledge and the way forward. Cancers (Basel). 2021;13:4364.
Tomizawa D, Tawa A, Watanabe T, et al. Excess treatment reduction including anthracyclines results in higher incidence of relapse in core binding factor acute myeloid leukemia in children. Leukemia. 2013;27:2413-2416.
Hasegawa D, Tawa A, Tomizawa D, et al. Attempts to optimize postinduction treatment in childhood acute myeloid leukemia without core-binding factors: a report from the Japanese Pediatric Leukemia/Lymphoma Study Group (JPLSG). Pediatr Blood Cancer. 2020;67:e28692.
Shiba N, Yoshida K, Hara Y, et al. Transcriptome analysis offers a comprehensive illustration of the genetic background of pediatric acute myeloid leukemia. Blood Adv. 2019;3:3157-3169.
Li J, Ran Q, Xu B, et al. Role of CD25 expression on prognosis of acute myeloid leukemia: a literature review and meta-analysis. PLoS One. 2020;15:e0236124.
Du W, He J, Zhou W, et al. High IL2RA mRNA expression is an independent adverse prognostic biomarker in core binding factor and intermediate-risk acute myeloid leukemia. J Transl Med. 2019;17:191.
Cerny J, Yu H, Ramanathan M, et al. Expression of CD25 independently predicts early treatment failure of acute myeloid leukemia (AML). Br J Haematol. 2013;160:262-266.
Döhner K, Thiede C, Jahn N, et al. Impact of NPM1/FLT3-ITD genotypes defined by the 2017 European LeukemiaNet in patients with acute myeloid leukemia. Blood. 2020;135:371-380.
Ostronoff F, Othus M, Gerbing RB, et al. NUP98/NSD1 and FLT3/ITD coexpression is more prevalent in younger AML patients and leads to induction failure: a COG and SWOG report. Blood. 2014;124:2400-2407.
Meshinchi S, Alonzo TA, Stirewalt DL, et al. Clinical implications of FLT3 mutations in pediatric AML. Blood. 2006;108:3654-3661.
Shiba N, Ohki K, Kobayashi T, et al. High PRDM16 expression identifies a prognostic subgroup of pediatric acute myeloid leukemia correlated to FLT3-ITD, KMT2A-PTD, and NUP98-NSD1: the results of the Japanese Pediatric Leukemia/Lymphoma Study Group AML-05 trial. Br J Haematol. 2016;172:581-591.
Cooper TM, Franklin J, Gerbing RB, et al. AAML03P1, a pilot study of the safety of gemtuzumab ozogamicin in combination with chemotherapy for newly diagnosed childhood acute myeloid leukemia: a report from the Children's Oncology Group. Cancer. 2012;118:761-769.
Gamis AS, Alonzo TA, Meshinchi S, et al. Gemtuzumab ozogamicin in children and adolescents with de novo acute myeloid leukemia improves event-free survival by reducing relapse risk: results from the randomized phase III Children's Oncology Group trial AAML0531. J Clin Oncol. 2014;32:3021-3032.
Terwijn M, Feller N, van Rhenen A, et al. Interleukin-2 receptor alpha-chain (CD25) expression on leukaemic blasts is predictive for outcome and level of residual disease in AML. Eur J Cancer. 2009;45:1692-1699.
van Galen P, Hovestadt V, Wadsworth Ii MH, et al. Single-cell RNA-Seq reveals AML hierarchies relevant to disease progression and immunity. Cell. 2019;176:1265-1281.e24.

Auteurs

Takahiro Aoki (T)

Department of Pediatrics, Graduate School of Medicine, Chiba University, Chiba, Japan.

Norio Shiba (N)

Department of Pediatrics, Yokohama City University Graduate School of Medicine, Yokohama, Japan.

Shinichi Tsujimoto (S)

Department of Pediatrics, Yokohama City University Graduate School of Medicine, Yokohama, Japan.

Genki Yamato (G)

Department of Pediatrics, Gunma University Graduate School of Medicine, Maebashi, Japan.

Yusuke Hara (Y)

Department of Pediatrics, Gunma University Graduate School of Medicine, Maebashi, Japan.

Shota Kato (S)

Department of Pediatrics, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.

Kenichi Yoshida (K)

Division of Cancer Evolution, National Cancer Center Research Institute, Tokyo, Japan.

Seishi Ogawa (S)

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.
Department of Medicine, Center for Hematology and Regenerative Medicine, Karolinska Institute, Stockholm, Sweden.

Yasuhide Hayashi (Y)

Institute of Physiology and Medicine, Jobu University, Takasaki, Japan.

Shotaro Iwamoto (S)

Department of Pediatrics, Mie University, Tsu, Japan.

Tomohiko Taki (T)

Department of Medical Technology, Kyorin University Faculty of Health Sciences, Mitaka, Japan.

Akira Shimada (A)

Department of Pediatrics, Jichi Medical University, Shimotsuke, Japan.

Yuka Iijima-Yamashita (Y)

Clinical Research Center, NHO Nagoya Medical Center, Nagoya, Japan.

Keizo Horibe (K)

Clinical Research Center, NHO Nagoya Medical Center, Nagoya, Japan.

Akio Tawa (A)

Higashiosaka Aramoto Heiwa Clinic, Higashiosaka, Japan.

Takashi Taga (T)

Department of Pediatrics, Shiga University of Medical Science, Shiga, Japan.

Souichi Adachi (S)

Department of Human Health Science, Kyoto University, Kyoto, Japan.

Daisuke Tomizawa (D)

Division of Leukemia and Lymphoma, Children's Cancer Center, National Center for Child Health and Development, Tokyo, Japan.

Classifications MeSH