Title:	Single-Nucleotide Polymorphisms in MICA and MICB Genes Could Play a Role in the Outcome in AML Patients after HSCT
Authors:	Machuldová, Alena Houdová, Lucie Kratochvílová, Kateřina Leba, Martin Jindra, Pavel Ostašov, Pavel Macečková, Diana Klieber, Robin Gmucová, Hana Šrámek, Jiří Holubová, Monika
Citation:	MACHULDOVÁ, A. HOUDOVÁ, L. KRATOCHVÍLOVÁ, K. LEBA, M. JINDRA, P. OSTAŠOV, P. MACEČKOVÁ, D. KLIEBER, R. GMUCOVÁ, H. ŠRÁMEK, J. HOLUBOVÁ, M. Single-Nucleotide Polymorphisms in MICA and MICB Genes Could Play a Role in the Outcome in AML Patients after HSCT. Journal of Clinical Medicine, 2021, roč. 10, č. 20, s. 1-16. ISSN: 2077-0383
Issue Date:	2021
Publisher:	MDPI
Document type:	článek article
URI:	2-s2.0-85116620392 http://hdl.handle.net/11025/47012
ISSN:	2077-0383
Keywords in different language:	allogeneic hematopoietic cell transplantationgraft-versus-host diseasegraft-versus-tumor effectNKG2DMICAMICBNK cells
Abstract in different language:	NKG2D and its ligands, MICA and MICB, are known as the key regulators of NK cells. NK cells are the first reconstituted cells after the allogeneic hematopoietic stem cell transplantation (HSCT); therefore, it is crucial to understand their role in HSCT outcome. In the presented study, we investigated the single amino acid changes across the exons 2–4 of MICA and MICB genes, and point mutations within the NKG2D gene, which defines the type of NKG2D haploblock (HNK/LNK) in the donors (n = 124), as well as in patients with acute myeloid leukemia (n = 78). In our cohort, we found that graft from a donor with at least one MICA allele containing glycine at position 14 (MICA-14Gly) is significantly associated with deterioration of a patient’s overall survival (OS) (p < 0.05). We also observed a negative effect of MICB-58 (Lys → Glu) polymorphism on relapse-free survival (RFS), although it was not statistically significant in multivariate analysis (p = 0.069). To our knowledge, this is the first work describing the role of MICA-14 and MICB-58 polymorphisms on HSCT outcome.
Rights:	© authors
Appears in Collections:	Články / Articles (NTIS) OBD

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