A homozygous splice site ROBO1 mutation in a patient with a novel syndrome with combined pituitary hormone deficiency.
Child, Preschool
Corpus Callosum
/ diagnostic imaging
Hearing Loss, Sensorineural
/ complications
Humans
Hypopituitarism
/ complications
Intellectual Disability
/ complications
Magnetic Resonance Imaging
Male
Mutation
Nerve Tissue Proteins
/ genetics
RNA Splice Sites
/ genetics
Receptors, Immunologic
/ genetics
Exome Sequencing
Roundabout Proteins
Journal
Journal of human genetics
ISSN: 1435-232X
Titre abrégé: J Hum Genet
Pays: England
ID NLM: 9808008
Informations de publication
Date de publication:
Apr 2019
Apr 2019
Historique:
received:
14
11
2018
accepted:
09
01
2019
revised:
06
01
2019
pubmed:
30
1
2019
medline:
15
3
2019
entrez:
30
1
2019
Statut:
ppublish
Résumé
The genetic causes of combined pituitary hormone deficiency remain elusive in most patients. Recently, incompletely penetrant heterozygous mutations in ROBO1 have been described in patients with pituitary stalk interruption syndrome. Herein, we identified a novel homozygous slice site mutation in ROBO1 (c.1342+1G>A) using a trio whole-exome sequencing strategy in a 5-year-old Japanese boy who had combined pituitary hormone deficiency, psychomotor developmental delay, severe intellectual disability, sensorineural hearing loss, strabismus, and characteristic facial features, including a broad forehead, micrognathia, and arched eyebrows. Magnetic resonance imaging delineated anterior pituitary hypoplasia, ectopic posterior pituitary, invisible pituitary stalk, thinning of the corpus callosum, and hypoplasia of the pons and midbrain. The phenotypically normal parents (first cousins) were heterozygous for the mutation. The results provide further evidence of ROBO1 being involved in the development of the pituitary gland. A recessive mutation of ROBO1 is a potential novel cause of a syndromic disorder associated with combined pituitary hormone deficiency.
Identifiants
pubmed: 30692597
doi: 10.1038/s10038-019-0566-8
pii: 10.1038/s10038-019-0566-8
doi:
Substances chimiques
Nerve Tissue Proteins
0
RNA Splice Sites
0
Receptors, Immunologic
0
Types de publication
Case Reports
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
341-346Subventions
Organisme : Japan Agency for Medical Research and Development (AMED)
ID : 18gk0110012h0101
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