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Swee Lay Thein

Researcher at National Institutes of Health

Publications -  335
Citations -  21617

Swee Lay Thein is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Fetal hemoglobin & Population. The author has an hindex of 62, co-authored 316 publications receiving 19670 citations. Previous affiliations of Swee Lay Thein include King's College & University of Oxford.

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HBS1L-MYB intergenic variants modulate fetal hemoglobin via long-range MYB enhancers.

TL;DR: It is found that several HBS1L-MYB intergenic variants reduce transcription factor binding, affecting long-range interactions with MYB and MYB expression levels, and designate MYB as a target for therapeutic induction of HbF to ameliorate sickle cell and β-thalassemia disease severity.
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Dissecting the loci controlling fetal haemoglobin production on chromosomes 11p and 6q by the regressive approach.

TL;DR: It is demonstrated that in addition to the two factors (β thalassaemia and Xmn l-Gγ site) on chromosome 11 p, there is a third major genetic determinant for fetal Hb production localized on chromosome 6q.
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cMYB is involved in the regulation of fetal hemoglobin production in adults

TL;DR: Observations suggest that differences in the intrinsic levels of cMYB may account for some of the variation in adult HbF levels, and the possible mechanism of c MYB influencing gamma- to beta-globin switching is discussed.
Journal Article

cMYB is involved in the regulation of fetal hemoglobin production in adults. Commentary

TL;DR: In this article, a quantitative trait locus (QTL) controlling HbF levels has been mapped to chromosome 6q23 in an Asian-Indian kindred with β thalassemia and heterocellular hereditary persistence of fetal hemoglobin (HPFH).
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Systematic documentation and analysis of human genetic variation in hemoglobinopathies using the microattribution approach

TL;DR: This project provides the first example of implementing microattribution to incentivise submission of all known genetic variation in a defined system and is likely to serve as a model for other systems and for the analysis of other common and/or complex human genetic diseases.