Personalized genomic medicine: lessons from the exome - PubMed (original) (raw)
Case Reports
. 2011 Sep-Oct;104(1-2):189-91.
doi: 10.1016/j.ymgme.2011.06.022. Epub 2011 Jul 5.
Daniel E Pineda-Alvarez, Donald W Hadley, NISC Comparative Sequencing Program, Jamie K Teer, Praveen F Cherukuri, Nancy F Hansen, Pedro Cruz, Alice C Young, Robert W Blakesley, Brendan Lanpher, Stephanie Mayfield Gibson, Murat Sincan, Settara C Chandrasekharappa, James C Mullikin
Affiliations
- PMID: 21767969
- PMCID: PMC3171610
- DOI: 10.1016/j.ymgme.2011.06.022
Case Reports
Personalized genomic medicine: lessons from the exome
Benjamin D Solomon et al. Mol Genet Metab. 2011 Sep-Oct.
Abstract
While genomic sequencing methods are powerful tools in the discovery of the genetic underpinnings of human disease, incidentally-revealed novel genomic risk factors may be equally important, both scientifically, and as relates to direct patient care. We performed whole-exome sequencing on a child with VACTERL association who suffered severe post-surgical neonatal pulmonary hypertension, and identified a potential novel genetic risk factor for this complication: a heterozygous mutation in CPSI. Newborn screening results from this patient's monozygotic twin provided evidence that this mutation, in combination with an environmental trigger (in this case, surgery), may have resulted in pulmonary artery hypertension due to inadequate nitric oxide production. Identification of this genetic risk factor allows for targeted medical preventative measures in this patient as well as relatives with the same mutation, and illustrates the power of incidental medical information unearthed by whole-exome sequencing.
Published by Elsevier Inc.
Figures
Fig.
Hypothesized explanation for pulmonary artery hypertension in the patient described here[–12, 14]. A loss-of-function mutation in the CPSI gene (1) leads to impaired production of citrulline (2) and arginine (3). The lack of availability of these precursors leads to decreased availability of nitric oxide (4), resulting in decreased pulmonary artery vasodilation, which becomes especially severe in concert with iatrogenic depletion of arginine and citrulline.
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