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Article ; Online: PHGDH-related microcephalic dwarfism in two fetuses: Expanding the phenotypical spectrum of L-serine biosynthesis defect.

Cuinat, Silvestre / Quélin, Chloé / Pasquier, Laurent / Loget, Philippe / Aussel, Dominique / Odent, Sylvie / Laquerrière, Annie / Proisy, Maia / Mazoyer, Sylvie / Delous, Marion / Edery, Patrick / Chatron, Nicolas / Lesca, Gaetan / Putoux, Audrey

European journal of medical genetics

2023 Volume 66, Issue 11, Page(s) 104852

Abstract: Defects in L-serine biosynthesis are a group of autosomal recessive diseases resulting in a wide phenotypic spectrum ranging from viable to lethal presentations and caused by variants in the three genes encoding the L-serine biosynthesis enzymes, PHGDH, ... ...

Abstract	Defects in L-serine biosynthesis are a group of autosomal recessive diseases resulting in a wide phenotypic spectrum ranging from viable to lethal presentations and caused by variants in the three genes encoding the L-serine biosynthesis enzymes, PHGDH, PSAT1, and PSPH. Neu-Laxova syndrome (NLS) is the fetal form of this group, characterized by multiple congenital anomalies including severe intrauterine growth retardation, cutaneous lesions extending from ichthyosis to severe restrictive dermopathy with ectropion and eclabion, edema, microcephaly, central nervous system abnormalities, and flexion contractures. Here we report on two unrelated fetuses with an attenuated phenotype of NLS, that initially evoked Taybi-Linder syndrome. They carry biallelic pathogenic variants in the PHGDH gene. These observations expand the phenotypic continuum of L-serine biosynthesis defects, and illustrate the phenotypic overlap between NLS and microcephalic primordial dwarfism.
MeSH term(s)	Female ; Humans ; Microcephaly/genetics ; Microcephaly/pathology ; Fetus/pathology ; Dwarfism/genetics ; Fetal Growth Retardation/genetics ; Fetal Growth Retardation/pathology ; Serine
Chemical Substances	Serine (452VLY9402)
Language	English
Publishing date	2023-09-25
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	2184135-4
ISSN	1878-0849 ; 1769-7212
ISSN (online)	1878-0849
ISSN	1769-7212
DOI	10.1016/j.ejmg.2023.104852
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Article ; Online: Functional Assessment of a New PBX1 Variant in a 46,XY Fetus with Severe Syndromic Difference of Sexual Development through CRISPR-Cas9 Gene Editing

Mary, Laura / Leclerc, Delphine / Labalme, Audrey / Bellaud, Pascale / Mazaud-Guittot, Séverine / Dréano, Stéphane / Evrard, Bertrand / Bigand, Antoine / Cauchoix, Aurélie / Loget, Philippe / Lokchine, Anna / Cluzeau, Laurence / Gilot, David / Belaud-Rotureau, Marc-Antoine / Jaillard, Sylvie

Genes (Basel). 2023 Jan. 20, v. 14, no. 2

2023

Abstract: Sexual development is a complex process relying on numerous genes. Disruptions in some of these genes are known to cause differences of sexual development (DSDs). Advances in genome sequencing allowed the discovery of new genes implicated in sexual ... ...

Abstract	Sexual development is a complex process relying on numerous genes. Disruptions in some of these genes are known to cause differences of sexual development (DSDs). Advances in genome sequencing allowed the discovery of new genes implicated in sexual development, such as PBX1. We present here a fetus with a new PBX1 NM_002585.3: c.320G>A,p.(Arg107Gln) variant, presenting with severe DSD along with renal and lung malformations. Using CRISPR-Cas9 gene editing on HEK293T cells, we generated a KD cell line for PBX1. The KD cell line showed reduced proliferation and adhesion properties compared with HEK293T cells. HEK293T and KD cells were then transfected plasmids coding either PBX1 WT or PBX1-320G>A (mutant). WT or mutant PBX1 overexpression rescued cell proliferation in both cell lines. RNA-seq analyses showed less than 30 differentially expressed genes, in ectopic mutant-PBX1-expressing cells compared with WT-PBX1. Among them, U2AF1, encoding a splicing factor subunit, is an interesting candidate. Overall, mutant PBX1 seems to have modest effects compared with WT PBX1 in our model. However, the recurrence of PBX1 Arg107 substitution in patients with closely related phenotypes calls for its impact in human diseases. Further functional studies are needed to explore its effects on cellular metabolism.
Keywords	CRISPR-Cas systems ; adhesion ; cell lines ; cell proliferation ; fetus ; genes ; humans ; lungs ; metabolism ; models ; mutants ; plasmids ; sequence analysis ; sexual development
Language	English
Dates of publication	2023-0120
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article ; Online
ZDB-ID	2527218-4
ISSN	2073-4425
ISSN	2073-4425
DOI	10.3390/genes14020273
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Functional Assessment of a New PBX1 Variant in a 46,XY Fetus with Severe Syndromic Difference of Sexual Development through CRISPR-Cas9 Gene Editing.

Genes

2023 Volume 14, Issue 2

Abstract	Sexual development is a complex process relying on numerous genes. Disruptions in some of these genes are known to cause differences of sexual development (DSDs). Advances in genome sequencing allowed the discovery of new genes implicated in sexual development, such as PBX1. We present here a fetus with a new PBX1 NM_002585.3: c.320G>A,p.(Arg107Gln) variant, presenting with severe DSD along with renal and lung malformations. Using CRISPR-Cas9 gene editing on HEK293T cells, we generated a KD cell line for PBX1. The KD cell line showed reduced proliferation and adhesion properties compared with HEK293T cells. HEK293T and KD cells were then transfected plasmids coding either PBX1 WT or PBX1-320G>A (mutant). WT or mutant PBX1 overexpression rescued cell proliferation in both cell lines. RNA-seq analyses showed less than 30 differentially expressed genes, in ectopic mutant-PBX1-expressing cells compared with WT-PBX1. Among them,
MeSH term(s)	Humans ; Gene Editing ; CRISPR-Cas Systems ; HEK293 Cells ; Fetus ; Sexual Development ; Pre-B-Cell Leukemia Transcription Factor 1/genetics
Chemical Substances	PBX1 protein, human ; Pre-B-Cell Leukemia Transcription Factor 1
Language	English
Publishing date	2023-01-20
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2527218-4
ISSN	2073-4425 ; 2073-4425
ISSN (online)	2073-4425
ISSN	2073-4425
DOI	10.3390/genes14020273
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Article ; Online: Anatomic and functional mapping of human uterine innervation.

Pinsard, Marion / Mouchet, Nicolas / Dion, Ludivine / Bessede, Thomas / Bertrand, Martin / Darai, Emile / Bellaud, Pascale / Loget, Philippe / Mazaud-Guittot, Séverine / Morandi, Xavier / Leveque, Jean / Lavoué, Vincent / Duraes, Martha / Nyangoh Timoh, Krystel

Fertility and sterility

2022 Volume 117, Issue 6, Page(s) 1279–1288

Abstract: Objective: To better understand the physiology of pain in pelvic pain pathological conditions, such as endometriosis, in which alterations of uterine innervation have been highlighted, we performed an anatomic and functional mapping of the macro- and ... ...

Abstract	Objective: To better understand the physiology of pain in pelvic pain pathological conditions, such as endometriosis, in which alterations of uterine innervation have been highlighted, we performed an anatomic and functional mapping of the macro- and microinnervation of the human uterus. Our aim was to provide a 3-dimensional reconstruction model of uterine innervation. Design: This was an experimental study. We dissected the pelvises of 4 human female fetuses into serial sections, and treated them with hematoxylin and eosin staining before immunostaining. Setting: Academic Research Unit. Patients: None. Interventions: None. Main outcome measures: Detection of nerves (S100 +) and characterization of the types of nerves. The slices obtained were aligned to construct a 3-dimensional model. Results: A 3-dimensional model of uterine innervation was constructed. The nerve fibers appeared to have a centripetal path from the uterine serosa to the endometrium. Within the myometrium, innervation was dense. Endometrial innervation was sparse but present in the functional layer of the endometrium. Overall innervation was richest in the supravaginal cervix and rarer in the body of the uterus. Innervation was rich particularly laterally to the cervix next to the parametrium and paracervix. Four types of nerve fibers were identified: autonomic sympathetic (TH+), parasympathetic (VIP+), and sensitive (NPY+, CGRP1+ and VIP+). They were found in the 3 portions and the 3 layers of the uterus. Conclusions: We constructed a 3-dimensional model of the human uterine innervation. This model could provide a solid base for studying uterine innervation in pathologic situations, in order to find new therapeutic approaches.
MeSH term(s)	Endometriosis/pathology ; Endometrium/pathology ; Female ; Humans ; Myometrium/pathology ; Pelvic Pain/surgery ; Uterus/pathology
Language	English
Publishing date	2022-03-30
Publishing country	United States
Document type	Journal Article
ZDB-ID	80133-1
ISSN	1556-5653 ; 0015-0282
ISSN (online)	1556-5653
ISSN	0015-0282
DOI	10.1016/j.fertnstert.2022.02.013
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Article ; Online: Prenatal phenotype of 22q11 micro-duplications: A systematic review and report on 12 new cases.

Mary, Laura / Lavillaureix, Alinoë / Perrot, Adélie / Loget, Philippe / Launay, Erika / Leborgne, Anne-Sophie / Demurger, Florence / Fradin, Mélanie / Le Bouar, Gwenaelle / Quélin, Chloé / Dubourg, Christèle / Pasquier, Laurent / Odent, Sylvie / Belaud-Rotureau, Marc-Antoine / Jaillard, Sylvie

European journal of medical genetics

2022 Volume 65, Issue 2, Page(s) 104422

Abstract: The 22q11 region is prone to generating recurring Copy Number Variations (CNVs) as a result of the large numbers of Low Copy Repeats (LCRs). Typical duplications encompass the LCR-A-to-D region but atypical duplications of various sizes have also been ... ...

Abstract	The 22q11 region is prone to generating recurring Copy Number Variations (CNVs) as a result of the large numbers of Low Copy Repeats (LCRs). Typical duplications encompass the LCR-A-to-D region but atypical duplications of various sizes have also been reported. These duplications are responsible for highly variable phenotypes with incomplete penetrance and expressivity, which is challenging for adequate genetic counselling, especially in the prenatal period. To better delineate prenatal phenotypes associated with these CNVs, we report here a clinical and molecular description of twelve cases (9 foetuses and 3 deceased new-borns babies) carrying recurrent 22q11 duplications (diagnosed via aCGH), along with a review of the existing literature. 22q11 duplications were inherited from an apparently healthy parent in almost 60% of the cases. Other CNVs were diagnosed for 8% of the cases. Increased nuchal translucency and cardiac anomalies (CHD) were the most prominent phenotypes observed, along with mild renal and skeletal anomalies. Duplications encompassing the LCR-C-to-D region (and the CRKL gene) seemed more likely to generate CHDs and renal malformations. Cleft lip/palate were observed in foetuses with duplications encompassing the LCR-A-to-B region or the SPECC1L gene, as previously suggested. However, genotype-phenotype correlations remain difficult to ascertain. Second-hit point variants, epigenetic or environmental variations could play a role in the phenotypic variability of 22q11 duplications, but remain a challenge for assessment in the short period of pregnancy.
MeSH term(s)	Abnormalities, Multiple/genetics ; Abnormalities, Multiple/pathology ; Adaptor Proteins, Signal Transducing/genetics ; Chromosome Duplication/genetics ; Chromosomes, Human, Pair 22/genetics ; DiGeorge Syndrome/genetics ; DiGeorge Syndrome/pathology ; Female ; Fetus/pathology ; Humans ; Infant, Newborn ; Male ; Phenotype ; Phosphoproteins/genetics
Chemical Substances	Adaptor Proteins, Signal Transducing ; CRKL protein ; Phosphoproteins ; SPECC1L protein, human
Language	English
Publishing date	2022-01-10
Publishing country	Netherlands
Document type	Case Reports ; Journal Article ; Review ; Systematic Review
ZDB-ID	2184135-4
ISSN	1878-0849 ; 1769-7212
ISSN (online)	1878-0849
ISSN	1769-7212
DOI	10.1016/j.ejmg.2022.104422
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Article ; Online: Multicolor-FISH Characterization of a Prenatal Mosaicism for a Chromosomal Rearrangement Undetected by Molecular Cytogenetics.

Mary, Laura / Loget, Philippe / Odent, Sylvie / Aussel, Dominique / Le Bouar, Gwenaelle / Launay, Erika / Henry, Catherine / Belaud-Rotureau, Marc-Antoine / Jaillard, Sylvie

Cytogenetic and genome research

2021 Volume 161, Issue 3-4, Page(s) 143–152

Abstract: Fetal mosaicism for chromosomal rearrangements remains a challenge to diagnose, even in the era of whole-genome sequencing. We present here a case of fetal mosaicism for a chromosomal rearrangement explored in amniocytes and fetal muscle, consisting of a ...

Abstract	Fetal mosaicism for chromosomal rearrangements remains a challenge to diagnose, even in the era of whole-genome sequencing. We present here a case of fetal mosaicism for a chromosomal rearrangement explored in amniocytes and fetal muscle, consisting of a major cell population (95%) with partial monosomy 4q and a minor population (5%) with additional material replacing the 4qter deleted segment. Molecular techniques (MLPA, array-CGH) failed to assess the origin of this material. Only multicolor-FISH identified the additional segment on chromosome 4 as derived from chromosome 17. Due to the poor prognosis, the couple chose to terminate the pregnancy. Because of low-level mosaicism, chromosomal microarray analysis (CMA), now considered as first-tier prenatal genetic analysis, did not allow the identification of the minor cell line. In case of large CNVs (>5 Mb) detected by CMA, karyotyping may be considered to elucidate the mechanism of the underlying rearrangement and eliminate mosaicism.
MeSH term(s)	Adult ; Chromosome Painting/methods ; Chromosomes, Human, Pair 17/genetics ; Chromosomes, Human, Pair 4/genetics ; Comparative Genomic Hybridization ; Cytogenetics/methods ; Female ; Fetus/metabolism ; Humans ; Karyotyping ; Maternal Age ; Mosaicism ; Pregnancy ; Prenatal Diagnosis/methods ; Translocation, Genetic/genetics
Language	English
Publishing date	2021-04-07
Publishing country	Switzerland
Document type	Case Reports
ZDB-ID	2087824-2
ISSN	1424-859X ; 1424-8581
ISSN (online)	1424-859X
ISSN	1424-8581
DOI	10.1159/000514592
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Article ; Online: Elucidating

Belhomme, Nicolas / Lescoat, Alain / Ballerie, Alice / Rouget, Florence / Le Bouar, Gwenaelle / Loget, Philippe / Caillault, Leïla / Jego, Patrick

The journal of maternal-fetal & neonatal medicine : the official journal of the European Association of Perinatal Medicine, the Federation of Asia and Oceania Perinatal Societies, the International Society of Perinatal Obstetricians

2019 Volume 33, Issue 21, Page(s) 3720–3722

MeSH term(s)	Fetal Death ; Humans
Language	English
Publishing date	2019-02-18
Publishing country	England
Document type	Letter
ZDB-ID	2077261-0
ISSN	1476-4954 ; 1057-0802 ; 1476-7058
ISSN (online)	1476-4954
ISSN	1057-0802 ; 1476-7058
DOI	10.1080/14767058.2019.1580262
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Article: Ultrasound Presentation of a Disseminated Fetal and Neonatal Rhabdoid Tumor.

Joueidi, Yolaine / Rousselin, Aline / Rozel, Céline / Loget, Philippe / Ranchere Vince, Dominique / Odent, Sylvie / Bourdeaut, Franck / Lavoue, Vincent / Le Lous, Maela

Case reports in obstetrics and gynecology

2018 Volume 2018, Page(s) 6073204

Abstract: This is a case report of a disseminated fetal rhabdoid tumor discovered at 32 weeks of gestation in a 29-year-old woman on immunosuppressive therapy. The mother consulted for a decrease in fetal movement. Fetal ultrasound showed signs of a disseminated ... ...

Abstract	This is a case report of a disseminated fetal rhabdoid tumor discovered at 32 weeks of gestation in a 29-year-old woman on immunosuppressive therapy. The mother consulted for a decrease in fetal movement. Fetal ultrasound showed signs of a disseminated tumor affecting the left armpit, liver, spleen, and limbs. A caesarian section was performed because of signs of fetal distress. Immunohistochemical analysis of a fetal biopsy showed deletion of the
Language	English
Publishing date	2018-01-31
Publishing country	United States
Document type	Case Reports
ZDB-ID	2627654-9
ISSN	2090-6692 ; 2090-6684
ISSN (online)	2090-6692
ISSN	2090-6684
DOI	10.1155/2018/6073204
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Article ; Online: Chorioamnionitis following preterm premature rupture of membranes and fetal heart rate variability.

Vandenbroucke, Laurent / Doyen, Matthieu / Le Lous, Maëla / Beuchée, Alain / Loget, Philippe / Carrault, Guy / Pladys, Patrick

PloS one

2017 Volume 12, Issue 9, Page(s) e0184924

Abstract: Introduction: The objective of this study was to identify prenatal markers of histological chorioamnionitis (HC) during pPROM using fetal computerized cardiotocography (cCTG).: Materials and methods: Retrospective review of medical records from ... ...

Abstract	Introduction: The objective of this study was to identify prenatal markers of histological chorioamnionitis (HC) during pPROM using fetal computerized cardiotocography (cCTG). Materials and methods: Retrospective review of medical records from pregnant women referred for pPROM between 26 and 34 weeks, in whom placental histology was available, in a tertiary level obstetric service over a 5-year period. Fetal heart rate variability was assessed using cCTG. Patients were included if they were monitored at least six times in the 72 hours preceding delivery. Clinical and biological cCTG parameters during the pPROM latency period were compared between cases with or without HC. Results: In total, 222 pPROM cases were observed, but cCTG data was available in only 23 of these cases (10 with and 13 without HC) after exclusion of co-morbidities which may potentially perturb fetal heart rate variability measures. Groups were comparable for maternal age, parity, gestational age at pPROM, pPROM duration and neonatal characteristics (p>0.1). Baseline fetal heart rate was higher in the HC group [median 147.3 bpm IQR (144.2-149.2) vs. 141.3 bpm (137.1-145.4) in no HC group; p = 0.02]. The number of low variation episodes [6.4, (3.5-15.3) vs. 2.3 (1-5.2); p = 0.04] was also higher in the HC group, whereas short term variations were lower in the HC group [7.1 ms (6-7.4) vs. 8.1 ms (7.4-9); p = 0.01] within 72 hours before delivery. Differences were especially discriminant within 24 hours before delivery, with less short-term variation [5 ms (3.7-5.9) vs. 7.8 ms (5.4-8.7); p = 0.007] and high variation episodes [3.9 (4.9-3.2) vs. 0.8 (1.5-0.2); p < 0.001] in the HC group. Conclusion: These results show differences in fetal heart rate variability, suggesting that cCTG could be used clinically to diagnoses chorioamnionitis during the pPROM latency period.
MeSH term(s)	Adult ; Biomarkers ; Cardiotocography ; Chorioamnionitis/diagnosis ; Chorioamnionitis/etiology ; Female ; Fetal Membranes, Premature Rupture/physiopathology ; Heart Rate, Fetal ; Humans ; Pregnancy ; Retrospective Studies
Chemical Substances	Biomarkers
Language	English
Publishing date	2017
Publishing country	United States
Document type	Journal Article
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0184924
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Article ; Online: Investigating in utero fetal death: outcome of internal medicine consultation.

Belhomme, Nicolas / Le Noir De Carlan, Marine / Lescoat, Alain / Le Gallou, Thomas / Rouget, Florence / Loget, Philippe / Jego, Patrick

International journal of rheumatic diseases

2017 Volume 21, Issue 2, Page(s) 381–386

Abstract: Aim: The objectives were to determine the frequency of in utero fetal death (IUFD) related to placental disorders and to assess the frequency of antiphospholipid antibodies syndrome (APS) among women referred to the internal medicine department.: ... ...

Abstract	Aim: The objectives were to determine the frequency of in utero fetal death (IUFD) related to placental disorders and to assess the frequency of antiphospholipid antibodies syndrome (APS) among women referred to the internal medicine department. Methodology: A retrospective clinical study conducted in Rennes University Hospital, France. From January 2007 to December 2014, 53 women who presented an IUFD at 14 weeks or more of gestational age were included. The main cause for each IUFD was determined by expert agreement. Primary outcome was to analyze the final etiologies diagnosed and the prevalence of IUFD related to placental disorders. Secondary outcomes included the frequency of APS among patients with IUFD of placental origin and the pathological and clinical features associated with APS. Results: IUFD resulted from placental disorders in 36/53 (68%) patients, and remained unexplained in 11 cases (20.8%). Among the 36 patients with placental disorders, APS was diagnosed in five (13.9%) cases, and four (11.1%) patients were considered as having 'non-criteria' APS. History of thrombosis (P = 0.001) and placental infarcts (P = 0.047) were significantly associated with APS. Conclusion: Placental disorders were the major cause for IUFD in patients who were referred to internal medicine specialists. Importantly, APS was seldom found in patients with placental disorders. Venous thromboembolism history and placental infarcts were both significantly associated with APS. Further studies are needed in order to deepen our understanding of the physiopathology of placental disorders and its underlying causes among non-APS women, and to determine the best treatment regimen for future pregnancies.
MeSH term(s)	Adult ; Antibodies, Antiphospholipid/blood ; Antiphospholipid Syndrome/blood ; Antiphospholipid Syndrome/diagnosis ; Antiphospholipid Syndrome/epidemiology ; Antiphospholipid Syndrome/immunology ; Biomarkers/blood ; Female ; Fetal Death ; France/epidemiology ; Hospitals, University ; Humans ; Infarction/diagnosis ; Infarction/epidemiology ; Internal Medicine ; Placenta/blood supply ; Placenta/pathology ; Placenta Diseases/diagnosis ; Placenta Diseases/epidemiology ; Pregnancy ; Prevalence ; Referral and Consultation ; Retrospective Studies ; Risk Factors ; Stillbirth/epidemiology ; Thrombosis/diagnosis ; Thrombosis/epidemiology ; Young Adult
Chemical Substances	Antibodies, Antiphospholipid ; Biomarkers
Language	English
Publishing date	2017-07-27
Publishing country	England
Document type	Journal Article
ZDB-ID	2426924-4
ISSN	1756-185X ; 1756-1841
ISSN (online)	1756-185X
ISSN	1756-1841
DOI	10.1111/1756-185X.13116
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