Literature DB >> 22319038

Genetic overlap in Kallmann syndrome, combined pituitary hormone deficiency, and septo-optic dysplasia.

Taneli Raivio1, Magdalena Avbelj, Mark J McCabe, Christopher J Romero, Andrew A Dwyer, Johanna Tommiska, Gerasimos P Sykiotis, Louise C Gregory, Daniel Diaczok, Vaitsa Tziaferi, Mariet W Elting, Raja Padidela, Lacey Plummer, Cecilia Martin, Bihua Feng, Chengkang Zhang, Qun-Yong Zhou, Huaibin Chen, Moosa Mohammadi, Richard Quinton, Yisrael Sidis, Sally Radovick, Mehul T Dattani, Nelly Pitteloud.   

Abstract

CONTEXT: Kallmann syndrome (KS), combined pituitary hormone deficiency (CPHD), and septo-optic dysplasia (SOD) all result from development defects of the anterior midline in the human forebrain.
OBJECTIVE: The objective of the study was to investigate whether KS, CPHD, and SOD have shared genetic origins. DESIGN AND PARTICIPANTS: A total of 103 patients with either CPHD (n = 35) or SOD (n = 68) were investigated for mutations in genes implicated in the etiology of KS (FGFR1, FGF8, PROKR2, PROK2, and KAL1). Consequences of identified FGFR1, FGF8, and PROKR2 mutations were investigated in vitro.
RESULTS: Three patients with SOD had heterozygous mutations in FGFR1; these were either shown to alter receptor signaling (p.S450F, p.P483S) or predicted to affect splicing (c.336C>T, p.T112T). One patient had a synonymous change in FGF8 (c.216G>A, p.T72T) that was shown to affect splicing and ligand signaling activity. Four patients with CPHD/SOD were found to harbor heterozygous rare loss-of-function variants in PROKR2 (p.R85G, p.R85H, p.R268C).
CONCLUSIONS: Mutations in FGFR1/FGF8/PROKR2 contributed to 7.8% of our patients with CPHD/SOD. These data suggest a significant genetic overlap between conditions affecting the development of anterior midline in the human forebrain.

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Year:  2012        PMID: 22319038      PMCID: PMC3319178          DOI: 10.1210/jc.2011-2938

Source DB:  PubMed          Journal:  J Clin Endocrinol Metab        ISSN: 0021-972X            Impact factor:   5.958


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