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Article ; Online: Chromosomal rearrangement in the 22q11.2 region: a critical locus for sociability and attentional skills.

Babinet, Marie-Noëlle / Thomas, Nadine / Pons, Linda / Schluth-Bolard, Caroline / Sanlaville, Damien / Demily, Caroline

2023 Volume 33, Issue 5, Page(s) 202–205

Abstract: Rearrangements of 22q11.2 region, most often deletions and duplications, are responsible for multiple congenital disorders. These rearrangements are involved in syndromes that share some phenotypic similarities. To date, 22q11.2 triplication remains very ...

Abstract	Rearrangements of 22q11.2 region, most often deletions and duplications, are responsible for multiple congenital disorders. These rearrangements are involved in syndromes that share some phenotypic similarities. To date, 22q11.2 triplication remains very rare, with few cases described in the literature. Here, we report for the first time the clinical, neurocognitive, social cognition and psychiatric properties of a 6-year-old child with 22q11.2 triplication, in comparison with a patient with 22q11.2 duplication and 16 cases of patients with 22q11.2 deletion. Chromosomal region 22q11.2 seems to be a critical locus for sociability and attentional skills and rearrangements could be interpreted as a predisposing factor for the development of psychotic symptoms (22q11.2 deletion), a protective factor (22q11.2 duplication) or a tendency factor for hypersociability (22q11.2 triplication).
MeSH term(s)	Child ; Humans ; DiGeorge Syndrome/genetics ; Abnormalities, Multiple ; Syndrome
Language	English
Publishing date	2023-07-03
Publishing country	England
Document type	Journal Article
ZDB-ID	1067837-2
ISSN	1473-5873 ; 0955-8829
ISSN (online)	1473-5873
ISSN	0955-8829
DOI	10.1097/YPG.0000000000000351
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Article ; Online: Creatinine levels in French children with Down syndrome up to ten years old.

Pautonnier, Joanna / Goutte, Sylvie / Dubourg, Laurence Derain / Bacchetta, Justine / Ranchin, Bruno / Rabilloud, Muriel / Sanlaville, Damien

European journal of pediatrics

2024 Volume 183, Issue 4, Page(s) 1953–1957

Abstract: Assess creatinine levels in French children with Down syndrome (DS) on the basis of the relationship between creatinine levels and age. The study included 279 children with DS aged 0 to 10 years who had been regularly monitored between 2004 and 2021 in a ...

Abstract	Assess creatinine levels in French children with Down syndrome (DS) on the basis of the relationship between creatinine levels and age. The study included 279 children with DS aged 0 to 10 years who had been regularly monitored between 2004 and 2021 in a single genetics department and who had had at least one creatinine measurement. The creatinine level curves were established by estimating the median and the quantiles of order 2.5 and 97.5% according to age. A Generalized Additive Model for Location, Scale, and Shape was used. The results showed higher creatinine levels in children with DS than in children from the general population. Conclusion: The present results allow to propose an original chart of creatinine levels according to age in French children with DS, which should help optimize their medical management and improve the early detection of renal diseases. What is Known: • Creatinine is a product of muscle breakdown and depends on muscle mass and children with Down syndrome have muscle and growth characteristics that differ from those of the general paediatric population. • Serum creatinine values in Japanese children with DS are higher than those of children from the general Japanese population. What is New: • Creatinine values in French children with DS are higher than those of children from the general French population. • The proposed original chart for creatinine values according to age, specifically designed for individuals up to 10 years old, should serve for further investigation, prevention, and follow-up of children with DS.
MeSH term(s)	Child ; Humans ; Down Syndrome/diagnosis ; Down Syndrome/epidemiology ; Creatinine
Chemical Substances	Creatinine (AYI8EX34EU)
Language	English
Publishing date	2024-02-06
Publishing country	Germany
Document type	Journal Article
ZDB-ID	194196-3
ISSN	1432-1076 ; 0340-6199 ; 0943-9676
ISSN (online)	1432-1076
ISSN	0340-6199 ; 0943-9676
DOI	10.1007/s00431-024-05460-3
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Article ; Online: Kidney and urological involvement in Down syndrome: frequent, underestimated, but associated with impaired quality of life and risk of kidney failure.

Ranchin, Bruno / Bidault, Valeska / Zekre, Franck / DeMul, Aurelie / Sanlaville, Damien / Bacchetta, Justine

Pediatric nephrology (Berlin, Germany)

2023 Volume 39, Issue 2, Page(s) 347–355

Abstract: Patients with Down syndrome (DS) are at risk of multiorgan dysfunction; kidney and urological impairment are common. This is due to a likely increased risk of congenital kidney and urological malformations (odds ratio of 4.5 compared to the general ... ...

Abstract	Patients with Down syndrome (DS) are at risk of multiorgan dysfunction; kidney and urological impairment are common. This is due to a likely increased risk of congenital kidney and urological malformations (odds ratio of 4.5 compared to the general population in one study), more frequent associated comorbidities at risk of kidney dysfunction (such as prematurity in 9-24% of children, intrauterine growth retardation or low birth weight in 20%, and congenital heart disease in 44%), and more frequent lower urinary tract dysfunction (reported in 27-77% of children with DS). If present, malformations and comorbidities at risk of kidney dysfunction warrant regular kidney monitoring in addition to their treatment. Serum creatinine in children with DS has been shown to be higher than in the general population and asymptomatic hyperuricemia is reported in 12-33% of children or young adults with DS. Moreover cryptorchidism and testicular cancer are also more common and should be detected by clinical examination. Thus, persons with DS at risk of presenting kidney and urological impairment should be identified by prenatal ultrasonography, comorbidities at risk of kidney sequelae considered, and during regular medical follow-up, clinically examined and questioned to diagnose testicular anomalies and lower urinary tract dysfunction. This is of importance as such kidney and urological impairments are associated with impaired quality of life and mental health, and risk of kidney failure.
MeSH term(s)	Male ; Child ; Pregnancy ; Female ; Humans ; Down Syndrome/complications ; Down Syndrome/epidemiology ; Down Syndrome/diagnosis ; Testicular Neoplasms/complications ; Quality of Life ; Kidney/abnormalities ; Renal Insufficiency/complications
Language	English
Publishing date	2023-06-29
Publishing country	Germany
Document type	Journal Article ; Review
ZDB-ID	631932-4
ISSN	1432-198X ; 0931-041X
ISSN (online)	1432-198X
ISSN	0931-041X
DOI	10.1007/s00467-023-05986-y
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Article ; Online: Plan France Médecine génomique 2025 : la France entre dans l’ère de la médecine génomique.

Sanlaville, Damien / Vidaud, Michel / Thauvin-Robinet, Christel / Nowak, Frédérique / Lethimonnier, Franck

La Revue du praticien

2022 Volume 71, Issue 10, Page(s) 1061–1064

Title translation	French Genomic Medicine Plan 2025 (PFMG2025): France enters the era of genomic medicine.
MeSH term(s)	France ; Genomic Medicine ; Genomics ; Humans
Language	French
Publishing date	2022-02-11
Publishing country	France
Document type	Journal Article
ZDB-ID	205365-2
ISSN	2101-017X ; 0035-2640
ISSN (online)	2101-017X
ISSN	0035-2640
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Article: Case report: 7p22.3 deletion and 8q24.3 duplication in a patient with epilepsy and psychomotor delay-Does both possibly act to modulate a candidate gene region for the patient's phenotype?

Touhami, Rahma / Foddha, Hajer / Alix, Eudeline / Jalloul, Afef / Mougou-Zerelli, Soumaya / Saad, Ali / Sanlaville, Damien / Haj Khelil, Amel

Frontiers in genetics

2023 Volume 13, Page(s) 1061539

Abstract: Background: ...

Abstract	Background:
Language	English
Publishing date	2023-01-09
Publishing country	Switzerland
Document type	Case Reports
ZDB-ID	2606823-0
ISSN	1664-8021
ISSN	1664-8021
DOI	10.3389/fgene.2022.1061539
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Article ; Online: Variations pathogènes de NDE1 et microlissencéphalie - De la pathologie au développement cérébral normal.

Cabet, Sara / Guibaud, Laurent / Sanlaville, Damien

Medecine sciences : M/S

2020 Volume 36, Issue 10, Page(s) 866–871

Abstract: Pathogenic variants of the gene NDE1 (Nuclear Distribution Element 1) in humans lead to microlissencephaly which associates a reduced head circumference and a simplified gyration. Microlissencephaly is the most severe deficit of neurogenesis described to ...

Title translation	Microlissencephaly due to pathogenic variants of NDE1: from pathology to normal brain development.
Abstract	Pathogenic variants of the gene NDE1 (Nuclear Distribution Element 1) in humans lead to microlissencephaly which associates a reduced head circumference and a simplified gyration. Microlissencephaly is the most severe deficit of neurogenesis described to date but its precise physiopathological mechanism is not yet well known. The NDE1 gene encodes a phosphoprotein that is essential to neurogenesis and that is expressed in various cell compartments of neuroblasts. More than 60 interaction partners with NDE1 have been reported, notably various proteins involved in formation of the mitotic spindle, in ciliation, in genome protection of dividing neuroblasts or even in apoptosis (like LIS1, dynein or cohesin), which are all avenues that we explore in this review.
MeSH term(s)	Brain/embryology ; Brain/growth & development ; Humans ; Microcephaly/genetics ; Microcephaly/pathology ; Microtubule-Associated Proteins/genetics ; Mitosis/genetics ; Neural Stem Cells/physiology ; Neurogenesis/genetics
Chemical Substances	Microtubule-Associated Proteins ; Nde1 protein, human
Language	French
Publishing date	2020-10-07
Publishing country	France
Document type	Journal Article ; Review
ZDB-ID	632733-3
ISSN	1958-5381 ; 0767-0974
ISSN (online)	1958-5381
ISSN	0767-0974
DOI	10.1051/medsci/2020157
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Zs.B 2872: Show issues

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Article ; Online: Comprehensive analysis of F8 large deletions: Characterization of full breakpoint junctions and description of a possible DNA breakage hotspot in intron 6.

Jourdy, Yohann / Chatron, Nicolas / Fretigny, Mathilde / Dericquebourg, Amy / Sanlaville, Damien / Vinciguerra, Christine

Journal of thrombosis and haemostasis : JTH

2022 Volume 20, Issue 10, Page(s) 2293–2305

Abstract: Background: Large F8 deletions represent 3-5% of the variations found in severe hemophilia A patients, but only a few deletion breakpoints have been characterized precisely.: Objectives: Resolving at the nucleotide level 24 F8 large deletions to ... ...

Abstract	Background: Large F8 deletions represent 3-5% of the variations found in severe hemophilia A patients, but only a few deletion breakpoints have been characterized precisely. Objectives: Resolving at the nucleotide level 24 F8 large deletions to provide new data on the mechanisms involved in these rearrangements. Methods: Breakpoint junctions of 24 F8 large deletions were characterized using a combination of long-range polymerase chain reaction, whole F8 NGS sequencing, and Sanger sequencing. Repeat elements, non-B DNA, and secondary structures were analyzed around the breakpoints. Results: Deletions ranged from 1.667 kb to 0.5 Mb in size. Nine involved F8 neighboring genes. Simple blunt ends and 2-4 bp microhomologies were identified at the breakpoint junctions of 10 (42%) and 8 (33%) deletions, respectively. Five (21%) deletions resulted from homeologous recombination between two Alu elements. The remaining case corresponded to a more complex rearrangement with an insertion of a 19 bp-inverted sequence at the junction. Four different breakpoints were located in a 562-bp region in F8 intron 6. This finding suggested that this region, composed of two Alu elements, is a DNA breakage hotspot. Non-B DNA and secondary structures were identified in the junction regions and may contribute to DNA breakage. Conclusion: Molecular characterization of deletion breakpoints revealed that non-homologous non-replicative DNA repair mechanisms and replication-based mechanisms seemed to be the main causative mechanisms of F8 large deletions. Moreover, we identified a possible F8 DNA breakage hotspot involved in non-recurrent rearrangements.
MeSH term(s)	Base Sequence ; DNA/genetics ; Humans ; Introns ; Nucleotides ; Sequence Deletion
Chemical Substances	Nucleotides ; DNA (9007-49-2)
Language	English
Publishing date	2022-08-16
Publishing country	England
Document type	Journal Article
ZDB-ID	2112661-6
ISSN	1538-7836 ; 1538-7933
ISSN (online)	1538-7836
ISSN	1538-7933
DOI	10.1111/jth.15835
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Zs.A 5805: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Whole F8 gene sequencing identified pathogenic structural variants in the remaining unsolved patients with severe hemophilia A.

Jourdy, Yohann / Chatron, Nicolas / Frétigny, Mathilde / Zawadzki, Christophe / Lienhart, Anne / Stieltjes, Natalie / Rohrlich, Pierre-Simon / Thauvin-Robinet, Christel / Volot, Fabienne / Hamida, Yasmine Ferhat / Hariti, Ghania / Leuci, Alexandre / Dargaud, Yesim / Sanlaville, Damien / Vinciguerra, Christine

Journal of thrombosis and haemostasis : JTH

2024

Abstract: Background: No F8 genetic abnormality is detected in approximately 1% to 2% of patients with severe hemophilia A (HA) using conventional genetic approaches. In these patients, deep intronic variation or F8 disrupting genomic rearrangement could be ... ...

Abstract	Background: No F8 genetic abnormality is detected in approximately 1% to 2% of patients with severe hemophilia A (HA) using conventional genetic approaches. In these patients, deep intronic variation or F8 disrupting genomic rearrangement could be causal. Objectives: The study aimed to identify the causal variation in families with a history of severe HA for whom genetic investigations failed. Methods: We performed whole F8 gene sequencing in 8 propositi. Genomic rearrangements were confirmed by Sanger sequencing of breakpoint junctions and/or quantitative polymerase chain reaction. Results: A structural variant disrupting F8 was found in each propositus, so that all the 815 families with a history of severe HA registered in our laboratory received a conclusive genetic diagnosis. These structural variants consisted of 3 balanced inversions, 3 large insertions of gained regions, and 1 retrotransposition of a mobile element. The 3 inversions were 105 Mb, 1.97 Mb, and 0.362 Mb in size. Among the insertions of gained regions, one corresponded to the insertion of a 34 kb gained region from chromosome 6q27 in F8 intron 6, another was the insertion of a 447 kb duplicated region from chromosome 9p22.1 in F8 intron 14, and the last one was the insertion of an Xq28 349 kb gained in F8 intron 5. Conclusion: All the genetically unsolved cases of severe HA in this cohort were due to structural variants disrupting F8. This study highlights the effectiveness of whole F8 sequencing to improve the molecular diagnosis of HA when the conventional approach fails.
Language	English
Publishing date	2024-03-13
Publishing country	England
Document type	Journal Article
ZDB-ID	2112661-6
ISSN	1538-7836 ; 1538-7933
ISSN (online)	1538-7836
ISSN	1538-7933
DOI	10.1016/j.jtha.2024.03.002
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Zs.A 5805: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Clinical and molecular cytogenetic studies of five new patients with 20q11q12 deletion and review of the literature: Proposition of two critical regions.

Bensaid, Souad / Bendahmane, Malika / Loddo, Sara / Poke, Gemma / Januel, Louis / Nicolle, Romain / Malan, Valérie / Chatron, Nicolas / Ottombrino, Silvia / Dentici, Maria Lisa / Novelli, Antonio / Digilio, Maria Cristina / Sanlaville, Damien

American journal of medical genetics. Part A

2024 , Page(s) e63580

Abstract: Deletions of the long arm of chromosome 20 (20q) are rare, with only 16 reported patients displaying a proximal interstitial 20q deletion. A 1.62 Mb minimal critical region at 20q11.2, encompassing three genes GDF5, EPB41L1, and SAMHD1, is proposed to be ...

Abstract	Deletions of the long arm of chromosome 20 (20q) are rare, with only 16 reported patients displaying a proximal interstitial 20q deletion. A 1.62 Mb minimal critical region at 20q11.2, encompassing three genes GDF5, EPB41L1, and SAMHD1, is proposed to be responsible for this syndrome. The leading clinical features include growth retardation, intractable feeding difficulties with gastroesophageal reflux, hypotonia and psychomotor developmental delay. Common facial dysmorphisms including triangular face, hypertelorism, and hypoplastic alae nasi were additionally reported. Here, we present the clinical and molecular findings of five new patients with proximal interstitial 20q deletions. We analyzed the phenotype and molecular data of all previously reported patients with 20q11.2q12 microdeletions, along with our five new cases. Copy number variation analysis of patients in our cohort has enabled us to identify the second critical region in the 20q11.2q12 region and redefine the first region that is initially identified. The first critical region spans 359 kb at 20q11.2, containing six MIM genes, including two disease-causing genes, GDF5 and CEP250. The second critical region spans 706 kb at 20q12, encompassing four MIM genes, including two disease-causing genes, MAFB and TOP1. We propose GDF5 to be the primary candidate gene generating the phenotype of patients with 20q11.2 deletions. Moreover, we hypothesize TOP1 as a potential candidate gene for the second critical region at 20q12. Of note, we cannot exclude the possibility of a synergistic role of other genes involved in the deletion, including a contiguous gene deletion syndrome or position effect affecting both critical regions. Further studies focusing on patients with proximal 20q deletions are required to support our hypothesis.
Language	English
Publishing date	2024-03-21
Publishing country	United States
Document type	Journal Article
ZDB-ID	2108614-X
ISSN	1552-4833 ; 0148-7299 ; 1552-4825
ISSN (online)	1552-4833
ISSN	0148-7299 ; 1552-4825
DOI	10.1002/ajmg.a.63580
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Article ; Online: Idiopathic generalized epilepsy in a family with SCN4A-related myotonia.

Talarico, Mariagrazia / Fortunato, Francesco / Labalme, Audrey / Januel, Louis / Chatron, Nicolas / Sanlaville, Damien / Sammarra, Ilaria / Gagliardi, Monica / Procopio, Radha / Valentino, Paola / Annesi, Grazia / Lesca, Gaetan / Gambardella, Antonio

Epilepsia open

2024

Abstract: Objectives: Myotonia is a clinical sign typical of a group of skeletal muscle channelopathies, the non-dystrophic myotonias. These disorders are electrophysiologically characterized by altered membrane excitability, due to specific genetic variants in ... ...

Abstract	Objectives: Myotonia is a clinical sign typical of a group of skeletal muscle channelopathies, the non-dystrophic myotonias. These disorders are electrophysiologically characterized by altered membrane excitability, due to specific genetic variants in known causative genes (CLCN1 and SCN4A). Juvenile Myoclonic Epilepsy (JME) is an epileptic syndrome identified as idiopathic generalized epilepsy, its genetics is complex and still unclarified. The co-occurrence of these two phenotypes is rare and the causes likely have a genetic background. In this study, we have genetically investigated an Italian family in which co-segregates myotonia, JME, or abnormal EEG without seizures was observed. Methods: All six individuals of the family, 4 affected and 2 unaffected, were clinically evaluated; EMG and EEG examinations were performed. For genetic testing, Exome Sequencing was performed for the six family members and Sanger sequencing was used to confirm the candidate variant. Results: Four family members, the mother and three siblings, were affected by myotonia. Moreover, EEG recordings revealed interictal generalized sharp-wave discharges in all affected individuals, and two siblings were affected by JME. All four affected members share the same identified variant, c.644 T > C, p.Ile215Thr, in SCN4A gene. Variants that could account for the epileptic phenotype alone, separately from the myotonic one, were not identified. Significance: These results provide supporting evidence that both myotonic and epileptic phenotypes could share a common genetic background, due to variants in SCN4A gene. SCN4A pathogenic variants, already known to be causative of myotonia, likely increase the susceptibility to epilepsy in our family. Plain language summary: This study analyzed all members of an Italian family, in which the mother and three siblings had myotonia and epilepsy. Genetic analysis allowed to identify a variant in the SCN4A gene, which appears to be the cause of both clinical signs in this family.
Language	English
Publishing date	2024-03-27
Publishing country	United States
Document type	Journal Article
ISSN	2470-9239
ISSN (online)	2470-9239
DOI	10.1002/epi4.12920
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