A family case of a rare Xq28 duplication
Genetic factors contribute to the etiology of intellectual disability in 25–50 % of cases. Chromosomal abnormalities, such as microdeletions and microduplications, are the most significant genetic causes. We examined a family where two boys, aged 8 and 7, were diagnosed with mild intellectual dis...
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| Published in: | Vavilovskiĭ zhurnal genetiki i selekt͡s︡ii Vol. 29; no. 5; pp. 636 - 643 |
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| Main Authors: | , , , , , , , , , , , , , |
| Format: | Journal Article |
| Language: | English |
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Russia (Federation)
Siberian Branch of the Russian Academy of Sciences, Federal Research Center Institute of Cytology and Genetics, The Vavilov Society of Geneticists and Breeders
01.09.2025
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| ISSN: | 2500-3259, 2500-0462, 2500-3259 |
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| Abstract | Genetic factors contribute to the etiology of intellectual disability in 25–50 % of cases. Chromosomal abnormalities, such as microdeletions and microduplications, are the most significant genetic causes. We examined a family where two boys, aged 8 and 7, were diagnosed with mild intellectual disability. Using array-based comparative genomic hybridization, we detected a duplication of Xq28 in both brothers on the X chromosome inherited from a healthy mother with skewed (88 %) X-chromosome inactivation. The size of the rearrangement is 439.6 kilobases (kb). Eight genes are located in this region, including F8, MTCP1, BRCC3, VBP1, RAB39B, CLIC2, FUNDC2, and CMC4. This chromosomal region overlaps with the region of Xq28 duplication syndrome (OMIM 300815), characterized by intellectual disability, behavioral and psychiatric disorders, recurrent infections, atopic diseases, and specific facial features in affected male individuals. Whole-exome sequencing did not reveal pathogenic or likely pathogenic variants associated with neurodevelopmental disorders. These disorders have been previously linked to X-linked recessive single-nucleotide variants in RAB39B (OMIM 300271, 311510) and CLIC2 (OMIM 300886). An assessment of the clinical significance of the identified duplication, using the AutoCNV internet resource and original data, allowed us to classify this variant as pathogenic. This implies that the identified duplication may be the cause of intellectual disability in patients. |
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| AbstractList | Genetic factors contribute to the etiology of intellectual disability in 25-50 % of cases. Chromosomal abnormalities, such as microdeletions and microduplications, are the most significant genetic causes. We examined a family where two boys, aged 8 and 7, were diagnosed with mild intellectual disability. Using array-based comparative genomic hybridization, we detected a duplication of Xq28 in both brothers on the X chromosome inherited from a healthy mother with skewed (88 %) X-chromosome inactivation. The size of the rearrangement is 439.6 kilobases (kb). Eight genes are located in this region, including F8, MTCP1, BRCC3, VBP1, RAB39B, CLIC2, FUNDC2, and CMC4. This chromosomal region overlaps with the region of Xq28 duplication syndrome (OMIM 300815), characterized by intellectual disability, behavioral and psychiatric disorders, recurrent infections, atopic diseases, and specific facial features in affected male individuals. Whole-exome sequencing did not reveal pathogenic or likely pathogenic variants associated with neurodevelopmental disorders. These disorders have been previously linked to X-linked recessive single-nucleotide variants in RAB39B (OMIM 300271, 311510) and CLIC2 (OMIM 300886). An assessment of the clinical significance of the identified duplication, using the AutoCNV internet resource and original data, allowed us to classify this variant as pathogenic. This implies that the identified duplication may be the cause of intellectual disability in patients.К настоящему времени известно, что на долю генетических факторов, вносящих вклад в этиоло- гию нарушения интеллектуального развития, приходится от 25 до 50 % случаев. Среди генетических причин наиболее существенную роль играют хромосомные аномалии, в том числе микроделеции и микродупли- кации. Нами обследована семья, в которой у двух мальчиков в возрасте 8 и 7 лет диагностирована легкая интеллектуальная недостаточность. С помощью матричной сравнительной геномной гибридизации у обоих братьев была обнаружена дупликация Xq28. Мать мальчиков является носительницей такой же дупликации с 88 % смещением инактивации Х-хромосомы. Размер перестройки составил 439.6 т. п. н. В данном регионе локализовано восемь генов (F8, MTCP1, BRCC3, VBP1, RAB39B, CLIC2, FUNDC2, CMC4). Рассматриваемый хромо- сомный регион перекрывается с областью синдрома дупликации Xq28 (OMIM 300815), характеризующегося интеллектуальной недостаточностью, поведенческими и психиатрическими нарушениями, рецидивирую- щими инфекциями, атопическими заболеваниями и характерными чертами лица у мужчин. Ранее описаны нарушения интеллектуального развития, обусловленные рецессивными однонуклеотидными вариантами в генах RAB39B (OMIM 300271, OMIM 311510) и CLIC2 (OMIM 300886). Полноэкзомное секвенирование не выяви- ло дополнительных патогенных и потенциально патогенных вариантов, ассоциированных с нарушениями интеллектуального развития. Оценка клинической значимости обнаруженной дупликации с помощью ин- тернет-ресурса AutoCNV и собственных данных позволила классифицировать этот вариант как патогенный, что предполагает, что он может быть причиной интеллектуальной недостаточности у пациентов. Genetic factors contribute to the etiology of intellectual disability in 25–50 % of cases. Chromosomal abnormalities, such as microdeletions and microduplications, are the most significant genetic causes. We examined a family where two boys, aged 8 and 7, were diagnosed with mild intellectual disability. Using array-based comparative genomic hybridization, we detected a duplication of Xq28 in both brothers on the X chromosome inherited from a healthy mother with skewed (88 %) X-chromosome inactivation. The size of the rearrangement is 439.6 kilobases (kb). Eight genes are located in this region, including F8, MTCP1, BRCC3, VBP1, RAB39B, CLIC2, FUNDC2, and CMC4. This chromosomal region overlaps with the region of Xq28 duplication syndrome (OMIM 300815), characterized by intellectual disability, behavioral and psychiatric disorders, recurrent infections, atopic diseases, and specific facial features in affected male individuals. Whole-exome sequencing did not reveal pathogenic or likely pathogenic variants associated with neurodevelopmental disorders. These disorders have been previously linked to X-linked recessive single-nucleotide variants in RAB39B (OMIM 300271, 311510) and CLIC2 (OMIM 300886). An assessment of the clinical significance of the identified duplication, using the AutoCNV internet resource and original data, allowed us to classify this variant as pathogenic. This implies that the identified duplication may be the cause of intellectual disability in patients. Genetic factors contribute to the etiology of intellectual disability in 25–50 % of cases. Chromosomal abnormalities, such as microdeletions and microduplications, are the most significant genetic causes. We examined a family where two boys, aged 8 and 7, were diagnosed with mild intellectual disability. Using array-based comparative genomic hybridization, we detected a duplication of Xq28 in both brothers on the X chromosome inherited from a healthy mother with skewed (88 %) X-chromosome inactivation. The size of the rearrangement is 439.6 kilobases (kb). Eight genes are located in this region, including F8, MTCP1, BRCC3, VBP1, RAB39B, CLIC2, FUNDC2, and CMC4. This chromosomal region overlaps with the region of Xq28 duplication syndrome (OMIM 300815), characterized by intellectual disability, behavioral and psychiatric disorders, recurrent infections, atopic diseases, and specific facial features in affected male individuals. Whole-exome sequencing did not reveal pathogenic or likely pathogenic variants associated with neurodevelopmental disorders. These disorders have been previously linked to X-linked recessive single-nucleotide variants in RAB39B (OMIM 300271, 311510) and CLIC2 (OMIM 300886). An assessment of the clinical significance of the identified duplication, using the AutoCNV internet resource and original data, allowed us to classify this variant as pathogenic. This implies that the identified duplication may be the cause of intellectual disability in patients. |
| Author | Miroshnikova, V. V. Makarov, I. V. Vasilyeva, O. Yu Lebedev, I. N. Mazo, G. E. Usenko, T. S. Fonova, E. A. Lobanov, A. D. Glotov, O. S. Kopytova, A. E. Kasyanov, E. D. Emelina, D. A. Pchelina, S. N. Tolmacheva, E. N. |
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| Snippet | Genetic factors contribute to the etiology of intellectual disability in 25–50 % of cases. Chromosomal abnormalities, such as microdeletions and... Genetic factors contribute to the etiology of intellectual disability in 25-50 % of cases. Chromosomal abnormalities, such as microdeletions and... Genetic factors contribute to the etiology of intellectual disability in 25–50 % of cases. Chromosomal abnormalities, such as microdeletions and... |
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| SubjectTerms | array-based comparative genomic hybridization clic2 copy number variations (cnvs) intellectual disability rab39b xq28 duplication syndrome |
| Title | A family case of a rare Xq28 duplication |
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