Galectin-3 predicts acute GvHD and overall mortality post reduced intensity allo-HCT: a BMT-CTN biorepository study

Philip L. McCarthy, Kristopher M. Attwood, Xiaojun Liu, George L. Chen, Hans Minderman, Amin Alousi, Asad Bashey, Robert Lowsky, David B. Miklos, John Hansen, Peter Westervelt, Gregory Yanik, Edmund K. Waller, Alan Howard, Bruce R. Blazar, Paul K. Wallace, Ran Reshef, Mary M. Horowitz, Richard T. Maziarz, John E. LevineHemn Mohammadpour

Research output: Contribution to journalArticlepeer-review

Abstract

Identifying plasma biomarkers early after allo-HCT may become crucial to prevent and treat severe aGvHD. We utilized samples from 203 allo-HCT patients selected from the Blood & Marrow Transplant Clinical Trials Network (BMT CTN) to identify new biomarker models to predict aGvHD and overall mortality. Two new biomarkers (Gal-3 and LAG-3), and previously identified biomarkers (ST2/IL33R, IL6, Reg3A, PD-1, TIM-3, TNFR1) were screened. Increased Gal-3 levels measured at Day +7 post-transplant predicted the development of aGvHD (grade 2–4) in the total population [AUC: 0.602; P = 0.045] while higher Day +14 levels predicted overall mortality due to toxicity among patients receiving reduced intensity conditioning [P = 0.028] but not myeloablative conditioning. Elevated LAG-3 levels (Day +21) were associated with less severe aGvHD [159.1 ng/mL vs 222.0 ng/mL; P = 0.046]. We developed a model utilizing Gal-3, LAG-3, and PD-1 levels at Days +14 and +21 with an improved performance to predict aGvHD and overall non-relapse mortality. We confirmed four informative biomarkers (Reg3A, ST2, TIM-3, and TNFR1) predict severe aGvHD at day +14 and day +21 (grade 3–4). In conclusion, the combination of Gal-3 alone or in combination with LAG-3, and PD-1 is a new informative model to predict aGvHD development and overall non-relapse mortality after allo-HCT. Graphical abstract: (Figure presented.).

Original languageEnglish (US)
Pages (from-to)334-343
Number of pages10
JournalBone marrow transplantation
Volume59
Issue number3
DOIs
StatePublished - Mar 2024

Bibliographical note

Publisher Copyright:
© The Author(s), under exclusive licence to Springer Nature Limited 2023.

PubMed: MeSH publication types

  • Journal Article

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