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Swe Swe Myint

As seen in: Nature, PLOS, The American Journal of Human Genetics, Texas Medical Center
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Articles

Genome-wide association study and predictors of neonatal blood cell traits in Hispanic newborns

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By Yunqi Li, Zixuan Zhang, Jalen Langie, Swe Swe Myint, Michaela Ince, Rong Lu, Charleston W.K. Chiang, Steven Gazal, Nicholas Mancuso, Linda Kachuri, Adam de Smith, Benjamin Alonzo
| The American Journal of Human Genetics Verified
Keywords genome-wide association study GWAS blood cell traits immune cell traits newborns neonatal cord blood mode of delivery Hispanic Latino Get full text access Log in, subscribe or purchase for full access. References 1. Okada, Y. ∙ Kamatani, Y. Common genetic factors for hematological traits in humans J. Hum. Genet. 2012; 57:161-169 2. Horton, S. ∙ Fleming, K.A. ∙ Kuti, M. ... The Top 25 Laboratory Tests by Volume and Revenue in Five Different Countries Am. J. Clin. Pathol. 2019; 151:446-451 3. Orrù, V.
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"Epigenomic Signature of Major Congenital Heart Defects in Newborns Wit" by Julia S Mouat, Shaobo Li et al.

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By Julia S Mouat, Shaobo Li, Swe Swe Myint, Benjamin Laufer
| Texas Medical Center
BACKGROUND: Congenital heart defects (CHDs) affect approximately half of individuals with Down syndrome (DS), but the molecular reasons for incomplete penetrance are unknown. Previous studies have largely focused on identifying genetic risk factors associated with CHDs in individuals with DS, but comprehensive studies of the contribution of epigenetic marks are lacking.
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Early-life tobacco exposure is causally implicated in aberrant RAG-mediated recombination in childhood acute lymphoblastic leukemia - Leukemia

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By Swe Swe Myint, Libby Morimoto, Joseph L. Wiemels, Scott Kogan, Catherine Metayer
| Nature Verified
The development of childhood acute lymphoblastic leukemia (ALL) typically involves formation of preleukemic clones in early-life followed by the postnatal acquisition of “second-hit” mutations and copy-number alterations that drive progression to overt leukemia [1]. “Off-target” V(D)J recombination is a mechanism known to drive the formation of deletions in ALL [2, 3].
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