Literature DB >> 33094427

The genetic cause of intellectual deficiency and/or congenital malformations in two parental reciprocal translocation carriers and implications for assisted reproduction.

Dehua Cheng1,2, Shimin Yuan1,2, Liang Hu1,2,3,4,5, Duo Yi1,2, Keli Luo1,2, Fei Gong1,2,3,4,5, Changfu Lu1,2,3,4,5, Guangxiu Lu1,2,3,4,5, Ge Lin1,2,3,4,5, Yue-Qiu Tan6,7,8,9.   

Abstract

PURPOSE: To elucidate the genetic cause of intellectual deficiency and/or congenital malformations in two parental reciprocal translocation carriers and provide appropriate strategies of assisted reproductive therapy (ART).
MATERIALS AND METHODS: Two similar couples having a child with global developmental delay/intellectual disability symptoms attended the Reproductive and Genetic Hospital of CITIC-Xiangya (Changsha, China) in 2017 and 2019, respectively, in order to determine the cause(s) of the conditions affecting their child and to seek ART to have a healthy baby. Both of the healthy couples were not of consanguineous marriage, denied exposure to toxicants, and had no adverse life history. This study was approved by the Institutional Ethics Committee of the Reproductive & Genetic Hospital of CITIC-Xiangya, and written informed consent was obtained from the parents. Genetic diagnoses were performed by karyotype analysis, breakpoint mapping analysis of chromosomal translocation(s), single-nucleotide polymorphism (SNP) microarray analysis, and whole-exome sequencing (WES) for the two children and different appropriate reproductive strategies were performed in the two families.
RESULTS: Karyotype analysis revealed that both patients carried parental reciprocal translocations [46,XY,t(7;16)(p13;q24)pat and 46,XY,t(13;17)(q12.3;p11.2)pat, respectively]. Follow-up breakpoint mapping analysis showed no interruption of associated genes, and SNP microarray analysis identified no significant copy number variations (CNVs) in the two patients. Moreover, WES results revealed that patients 1 and 2 harbored candidate compound heterozygous mutations of MCOLN1 [c.195G>C (p.K65N) and c.1061G>A (p.W354*)] and MCPH1 [c.877A>G (p.S293G) and c.1869_1870delAT (p.C624*)], respectively, that were inherited from their parents and not previously reported. Furthermore, the parents of patient 1 obtained 10 embryos during ART cycle, and an embryo of normal karyotype and non-carrier of observed MCOLN1 mutations according to preimplantation genetic testing for structural rearrangement and monogenic defect was successfully transferred, resulting in the birth of a healthy boy. The parents of patient 2 chose to undergo ART with donor sperm to reduce the risk of recurrence.
CONCLUSIONS: Systematic genetic diagnosis of two carriers of inherited chromosomal translocations accompanied by clinical phenotypes revealed their cause of disease, which was critical for genetic counseling and further ART for these families.

Entities:  

Keywords:  Assisted reproductive therapy; Chromosome microdissection; Developmental delay; Intellectual disability; Reciprocal translocation; Whole-exome sequencing

Mesh:

Year:  2020        PMID: 33094427      PMCID: PMC7822985          DOI: 10.1007/s10815-020-01986-1

Source DB:  PubMed          Journal:  J Assist Reprod Genet        ISSN: 1058-0468            Impact factor:   3.412


  43 in total

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8.  A cytogenetic survey of 14,069 newborn infants. I. Incidence of chromosome abnormalities.

Authors:  J L Hamerton; N Canning; M Ray; S Smith
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9.  A foetus with 18p11.32-q21.2 duplication and Xp22.33-p11.1 deletion derived from a maternal reciprocal translocation t(X;18)(q13;q21.3).

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10.  Daily life changes and adaptations investigated in 154 families with a child suffering from a rare disability at a public centre for rare diseases in Northern Italy.

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Journal:  Ital J Pediatr       Date:  2016-08-31       Impact factor: 2.638

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