Characterisation of TP53 mutational features and outcomes of acute myeloid leukaemia after allogeneic haematopoietic cell transplantation.

Authors

Martina Reuss, Thomas Meyer, Florian Ingelfinger, Rouven Hoefflin, Miriam Mozaffari Jovein, Hosna Baniadam, Dietmar Pfeifer, Justus Duyster, Jesus Duque-Afonso, Kristina Maas-Bauer, Ralph Wäsch, Armin Zebisch, Annkristin Heine, Tobias Holderried, Jürgen Finke, Claudia Wehr, Robert Zeiser, Tobias Wertheimer

Published in

Bone marrow transplantation. Sep 04, 2026. Epub Sep 04, 2026.

Abstract

TP53 mutations define a clinically distinct subset of acute myeloid leukaemia (AML) associated with complex cytogenetics and therapy resistance. We performed a retrospective single-centre analysis of 61 consecutive TP53-altered AML patients undergoing first allogeneic haematopoietic cell transplantation (allo-HCT) at the Medical Center Freiburg (2007-2025), compared with 636 TP53-wild-type controls. TP53-altered patients had markedly inferior overall survival (median 379 vs. 1694 days; 5-year OS 18% vs. 50%; p < 0.001). Excess relapse was the primary driver (5-year cumulative incidence 55% vs. 33%; p < 0.001), whereas non-relapse mortality did not differ (28.5% vs. 23%; p = 0.426). On multivariable Cox analysis, TP53 alteration was the strongest independent predictor of inferior OS (HR 2.54, 95% CI 1.77-3.64; p < 0.001), and this association persisted after adjustment for cytogenetic risk and for the refined Disease Risk Index. In an exploratory hierarchical clustering analysis extended by seven patients from a second centre, two subgroups emerged: a del(17p)-enriched cluster (n = 12; median OS 5.7 months) and a TP53 point mutation-enriched cluster (n = 56; median OS 15.1 months). TP53-altered AML is confirmed as the strongest independent adverse prognostic factor after allo-HCT, and molecular heterogeneity within this subtype may inform trial stratification and targeted post-transplant interventions.

PMID:
42697934
Bibliographic data and abstract were imported from PubMed on 05 Sep 2026.

Read full publication at:
Please sign in to see all details.

Stats

1-terrible, 9-excellent. How would you rate this publication? Sign in in to submit your rating.

Post a comment

You need to be signed in to post comments. You can sign in here.

Comments

There are no comments yet.