Literature DB >> 23057549

KLF10 gene expression is associated with high fetal hemoglobin levels and with response to hydroxyurea treatment in β-hemoglobinopathy patients.

Joseph Borg1, Marios Phylactides, Marina Bartsakoulia, Christina Tafrali, Carsten Lederer, Alexander E Felice, Adamantia Papachatzopoulou, Alexandra Kourakli, Eleana F Stavrou, Soteroula Christou, Jun Hou, Sophia Karkabouna, Christina Lappa-Manakou, Zeliha Ozgur, Wilfred van Ijcken, Marieke von Lindern, Frank G Grosveld, Marianthi Georgitsi, Marina Kleanthous, Sjaak Philipsen, George P Patrinos.   

Abstract

AIM: In humans, fetal hemoglobin (HbF) production is controlled by many intricate mechanisms that, to date, remain only partly understood. PATIENTS &
METHODS: Pharmacogenomic analysis of the effects of hydroxyurea (HU) on HbF production was undertaken in a collection of Hellenic β-thalassemia and sickle cell disease (SCD) compound heterozygotes and a collection of healthy and KLF1-haploinsufficient Maltese adults, to identify genomic signatures that follow high HbF patterns.
RESULTS: KLF10 emerged as a top candidate. Moreover, genotype analysis of β-thalassemia major and intermedia patients and an independent cohort of β-thalassemia/SCD compound heterozygous patients that do or do not respond to HU treatment showed that the homozygous mutant state of a tagSNP in the KLF10 3'UTR is not present in β-thalassemia intermedia patients and is underrepresented in β-thalassemia/SCD compound heterozygous patients that respond well to HU treatment.
CONCLUSION: These data suggest that KLF10 may constitute a pharmacogenomic marker to discriminate between response and nonresponse to HU treatment.

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Year:  2012        PMID: 23057549     DOI: 10.2217/pgs.12.125

Source DB:  PubMed          Journal:  Pharmacogenomics        ISSN: 1462-2416            Impact factor:   2.533


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