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• W2984831652 abstract "Postzygotic mutations in the genes GNAQ/GNA11 encoding heterotrimeric G protein alpha subunits account for skin mosaic conditions with vascular or pigmentary anomalies (Couto et al., 2017Couto J.A. Ayturk U.M. Konczyk D.J. Goss J.A. Huang A.Y. Hann S. et al.A somatic GNA11 mutation is associated with extremity capillary malformation and overgrowth.Angiogenesis. 2017; 20: 303-306Crossref PubMed Scopus (82) Google Scholar; Shirley et al., 2013Shirley M.D. Tang H. Gallione C.J. Baugher J.D. Frelin L.P. Cohen B. et al.Sturge–Weber syndrome and port-wine stains caused by somatic mutation in GNAQ.N Engl J Med. 2013; 368: 1971-1979Crossref PubMed Scopus (637) Google Scholar, Siegel et al., 2018Siegel D.H. Cottrell C.E. Streicher J.L. Schilter K.F. Basel D.G. Baselga E. et al.Analyzing the genetic spectrum of vascular anomalies with overgrowth via cancer genomics.J Invest Dermatol. 2018; 138: 957-967Abstract Full Text Full Text PDF PubMed Scopus (29) Google Scholar, Thomas et al., 2016Thomas A.C. Zeng Z. Rivière J.B. O’Shaughnessy R. Al-Olabi L. St-Onge J. et al.Mosaic activating mutations in GNA11 and GNAQ are associated with phakomatosis Pigmentovascularis and extensive dermal melanocytosis.J Invest Dermatol. 2016; 136: 770-778Abstract Full Text Full Text PDF PubMed Scopus (116) Google Scholar). We sought to delineate the phenotype of 32 patients with skin capillary malformations (CMs) harboring an activating postzygotic mutation in GNA11 or GNAQ in affected skin. Nevus flammeus, ipsilateral segmental overgrowth, varicose veins, and macrocephaly were associated with GNAQ mutations, whereas cutis marmorata, nevus anemicus, and ipsilateral hypotrophy were associated with GNA11 mutations. Pigmentary anomalies were only associated with pigment skin type. Additional extracutaneous features included ocular and neurological anomalies of Sturge-Weber syndrome, varicose veins with deep vein thrombosis, and hypertension with renal anomalies, encompassing a wide clinical spectrum. All 32 patients (19 females, 13 males) aged 3 months to 67 years (median, 14 years) were referred for genetic testing because of cutaneous CMs suggesting involvement of GNA11 or GNAQ and were included in the Mosaic Undiagnosed Skin Traits And Related Disorders (NCT01950975) cohort, approved by our regional institutional review board and ethics committee. Five patients with phakomatosis pigmentovascularis (PPV) were previously reported (Thomas et al., 2016Thomas A.C. Zeng Z. Rivière J.B. O’Shaughnessy R. Al-Olabi L. St-Onge J. et al.Mosaic activating mutations in GNA11 and GNAQ are associated with phakomatosis Pigmentovascularis and extensive dermal melanocytosis.J Invest Dermatol. 2016; 136: 770-778Abstract Full Text Full Text PDF PubMed Scopus (116) Google Scholar). Written informed consent from all participants or their parents was obtained. Ultradeep next generation sequencing of the whole coding sequence of GNAQ/GNA11 (600× to 6,700×) was performed on DNA from affected skin and venous blood on a MiSeq (Illumina, San Diego, CA) according to standard protocol. Patients were phenotypically classified based on clinical charts and photographs from referring clinicians, with additional data from a standardized questionnaire addressing vascular, pigmentary, neurological, and ocular involvement or overgrowth. Cutaneous CMs were subclassified as suggested by Happle: nevus flammeus (port wine stain), nevus roseus (pale pink nevus), cutis marmorata/reticulate CM, and nevus anemicus (Figure 1) (Happle, 2015Happle R. Capillary malformations: a classification using specific names for specific skin disorders.J Eur Acad Dermatol Venereol. 2015; 29: 2295-2305Crossref PubMed Scopus (46) Google Scholar). Patients with vascular and pigmentary manifestations were diagnosed with PPV and classified into one of the three types defined by Happle, 2005Happle R. Phacomatosis pigmentovascularis revisited and reclassified.Arch Dermatol. 2005; 141: 385-388Crossref PubMed Scopus (175) Google Scholar. Patients with vascular anomalies and segmental asymmetry (overgrowth or hypotrophy) were assigned to one of the six types defined by Oduber et al (2011). Association between phenotypes and GNAQ or GNA11 mutations was analyzed using two-tailed Fisher’s exact test. Most patients (n = 19) carried a postzygotic p.Arg183Gln GNAQ mutation in their CMs, and only one had a p.Arg183Gly GNAQ mutation (Supplementary Table S1). Twelve patients carried one of the following GNA11 mutations: p.Arg183Cys (n = 10), p.Arg183His (n = 1), or p.Gln209His (n = 1). A postzygotic PIK3CA mutation was excluded in nine patients, two initially referred for suspicion of macrocephaly–capillary malformation–polymicrogyria syndrome (OMIM#602501) and seven with Klippel-Trénaunay syndrome. Variant allele fraction in affected tissue ranged from 1% to 17% (median, 5%). Cutaneous CMs (Figure 2a) involved the face in 21 patients and multiple body segments in 23 patients. Nevus flammeus was associated with GNAQ rather than GNA11 mutations, but not significantly (P = 0.069). In contrast, nevus anemicus and cutis marmorata were associated with GNA11 mutations (P = 0.030 and P = 0.042, respectively). Nevus roseus did not show any association with either GNAQ or GNA11 mutations. Nevus anemicus was always associated with other CMs (resulting in nevus vascularis mixtus), mainly cutis marmorata (10 patients). Pigmentary anomalies associated with CMs (Figure 2b) consisted of extensive dermal melanocytosis, scleral melanocytosis, or café-au-lait macules and led to a diagnosis of PPV in 11 patients. They were not preferentially associated with either GNAQ or GNA11 mutations but instead with pigment skin types III–V (11 of 20 patients) and were absent in skin types I–II (P = 0.006). Similar findings had previously been reported (Polubothu and Kinsler, 2017Polubothu S. Kinsler V.A. The ethnic profile of patients with birthmarks reveals interaction of germline and postzygotic genetics.Br J Dermatol. 2017; 176: 1385-1387Crossref PubMed Scopus (3) Google Scholar). All patients with PPV cesioflammea carried GNAQ mutations, whereas all patients with PPV cesiomarmorata carried GNA11 mutations. No patients had PPV spilorosea. Three patients with PPV could not be classified. In patients with facial CMs (Figure 2c), macrocephaly or hemifacial overgrowth were associated with a GNAQ mutation. Thirteen patients had Sturge-Weber syndrome, with seizures, brain MRI anomalies (leptomeningeal angiomatosis and cortical atrophy with calcifications), or glaucoma, without preferential GNAQ or GNA11 genotype. In patients with extracephalic CMs (Figure 2d), proportionate ipsilateral segmental overgrowth was found in 50%, mainly with nevus flammeus–type CMs and GNAQ mutations. In contrast, all patients with ipsilateral segmental hypotrophy (inverse Klippel-Trénaunay syndrome) (Danarti et al., 2007Danarti R. König A. Bittar M. Happle R. Inverse Klippel-Trenaunay syndrome: review of cases showing deficient growth.Dermatology. 2007; 214: 130-132Crossref PubMed Scopus (23) Google Scholar) carried a GNA11 mutation. Varicose veins were present in seven patients with GNAQ mutations. Three of them experienced deep vein thrombosis. Most patients with overgrowth could be clinically classified as type 1 (CM type) or 2 (CM-venous malformation type), but types 3 (Klippel-Trénaunay type) and 6 (reticular CM type) were also found. Two patients could not be classified. Six patients had arterial hypertension, associated with renal artery dysplasia in two patients and renal hypoplasia in two patients. No preferential association with either GNAQ or GNA11 mutations was found. Our results suggest that clinical features in patients with CM may differentiate between GNAQ and GNA11 mutations, although more patients need to be studied to corroborate our findings. A limitation to our study is the absence of information on evolution. CMs may be classified differently at birth than later in life, particularly cutis marmorata/reticulate CM, which may evolve into a homogeneous CM with time. Likewise, with age, nevus roseus may darken and extensive dermal melanocytosis may fade away. Also, extensive skin involvement in most patients and high frequency of extracutaneous manifestations reflect ascertainment bias, as only severe forms were referred. Yet, posterior phenotyping has allowed us to better define the highly variable mosaic GNAQ/GNA11-related clinical spectrum. Association of overgrowth with a slow flow vascular anomaly can be diagnosed as Klippel-Trénaunay syndrome (Vahidnezhad et al., 2016Vahidnezhad H. Youssefian L. Uitto J. Klippel-Trenaunay syndrome belongs to the PIK3CA-related overgrowth spectrum (PROS).Exp Dermatol. 2016; 25: 17-19Crossref PubMed Scopus (107) Google Scholar). However, GNAQ/GNA11-related overgrowth, previously reported (Couto et al., 2017Couto J.A. Ayturk U.M. Konczyk D.J. Goss J.A. Huang A.Y. Hann S. et al.A somatic GNA11 mutation is associated with extremity capillary malformation and overgrowth.Angiogenesis. 2017; 20: 303-306Crossref PubMed Scopus (82) Google Scholar), was proportionate and milder than in PIK3CA-related Klippel-Trénaunay syndrome (Keppler-Noreuil et al., 2015Keppler-Noreuil K.M. Rios J.J. Parker V.E.R. Semple R.K. Lindhurst M.J. Sapp J.C. et al.PIK3CA-related overgrowth spectrum (PROS): diagnostic and testing eligibility criteria, differential diagnosis, and evaluation.Am J Med Genet A. 2015; 167A: 287-295Crossref PubMed Scopus (304) Google Scholar, Keppler-Noreuil et al., 2014Keppler-Noreuil K.M. Sapp J.C. Lindhurst M.J. Parker V.E.R. Blumhorst C. Darling T. et al.Clinical delineation and natural history of the PIK3CA-related overgrowth spectrum.Am J Med Genet A. 2014; 164A: 1713-1733Crossref PubMed Scopus (191) Google Scholar). The term ‘‘diffuse capillary malformation with overgrowth’’ has been suggested for extensive reticular/homogeneous CMs with proportionate overgrowth (Lee et al., 2013Lee M.S. Liang M.G. Mulliken J.B. Diffuse capillary malformation with overgrowth: A clinical subtype of vascular anomalies with hypertrophy.J Am Acad Dermatol. 2013; 69: 589-594Abstract Full Text Full Text PDF PubMed Scopus (54) Google Scholar) and may apply to many patients in our series. No correlation was found between GNAQ/GNA11 mutations and the classification of vascular anomalies associated with deregulated growth by Oduber et al., because our patients belonged to four of the six subtypes or could not be classified at all (Oduber et al., 2011Oduber C.E.U. van der Horst C.M.A.M. Sillevis Smitt J.H. Smeulders M.J.C. Mendiratta V. Harper J.I. et al.A proposal for classification of entities combining vascular malformations and deregulated growth.Eur J Med Genet. 2011; 54: 262-271Crossref PubMed Scopus (18) Google Scholar). Varicose veins and thrombosis may be associated with overgrowth. To our knowledge, hypertension and renal anomalies had not previously been reported in association with GNAQ/GNA11 mutations. They are reminiscent of the vascular manifestations of neurofibromatosis type I, caused by loss-of-function mutations in a GTPase activating protein that normally switches off small G proteins, and should be considered in the clinical assessment and follow-up of GNAQ/GNA11 patients. No data sets were generated. Maud, Jordan: https://orcid.org/0000-0001-9259-5643 Virginie, Carmignac: https://orcid.org/0000-0001-8802-6448 Arthur, Sorlin: https://orcid.org/0000-0001-8008-9145 Paul, Kuentz: https://orcid.org/0000-0003-2814-6303 Juliette, Albuisson: https://orcid.org/0000-0002-8947-6499 Luca, Borradori: https://orcid.org/0000-0003-0424-6297 Emmanuelle, Bourrat: https://orcid.org/0000-0001-5375-738X Odile, Boute: https://orcid.org/0000-0002-7766-381X Nenad, Bukvic: https://orcid.org/0000-0002-9235-8987 Anne-Claire, Bursztejn: https://orcid.org/0000-0002-3281-7299 Christine, Chiaverini: https://orcid.org/0000-0002-6063-5409 Bruno, Delobel: https://orcid.org/0000-0002-0444-4763 Marine, Fournet: https://orcid.org/0000-0002-2873-532X Jéhanne, Martel: https://orcid.org/0000-0003-4393-5239 Alice, Goldenberg: https://orcid.org/0000-0002-5864-9182 Smail, Hadj-Rabia: https://orcid.org/0000-0001-6801-7106 Antoine, Mahé: https://orcid.org/0000-0003-1228-2220 Annabel, Maruani: https://orcid.org/0000-0003-3734-810X Juliette, Mazereeuw-Hautier: https://orcid.org/0000-0001-6259-9790 Cyril, Mignot: https://orcid.org/0000-0002-3462-3463 Fanny, Morice-Picard: https://orcid.org/0000-0002-4316-916X Marie Laure, Moutard: https://orcid.org/0000-0002-1570-8605 florence, petit: https://orcid.org/0000-0002-1368-1023 Justine, Pasteur: https://orcid.org/0000-0002-4766-0693 Alice, Phan: https://orcid.org/0000-0003-4246-5853 sandra, whalen: https://orcid.org/0000-0001-9156-5047 Marjolaine, Willems: https://orcid.org/0000-0002-2959-0935 Christophe, Philippe: https://orcid.org/0000-0001-7098-6520 Pierre, Vabres: https://orcid.org/0000-0001-8693-3183 The authors state no conflict of interest. The authors thank subjects and their families involved in the study and the Centre de Calcul from Burgundy university (https://haydn2005.u-bourgogne.fr/dsi-ccub/) for technical support and management of the information technology platform. This work was funded by Société Française de Dermatologie, Conseil Régional de Bourgogne, Centre Hospitalier Universitaire Dijon-Bourgogne, Ministère des Affaires Sociales et de la Santé, and Direction Générale de l’offre de Soins through the National Programme Hospitalier de Recherche Clinique. Conceptualization: PV; Data Curation: JA, LB, EB, OB, NB, ACB, CC, BD, MF, JMartel, AG, SH-R, AMahé, AMaruani, JMazereeuw, CM, FM-P, M-LM, FP, JP, AP, SW, MW, PV, MJ; Formal Analysis: MJ, VC, PV; Funding Acquisition: PV; Supervision: PV; Validation: VC, AS, PK, CP; Writing - Original Draft Preparation: MJ; Writing - Review and Editing: VC, PV. Supplementary Table S1Genotype and Phenotype from the 32 Affected IndividualsPatientGeneVariation (amino acids)Allelic fraction, %Pigment skin typeCutaneous capillary malformationOvergrowthHypotrophyNeurological anomaliesGlaucomaVenous anomaliesPigmentary anomaliesOther featuresPED1064GNAQp.(Arg183Gln)6.0IVNevus flammeus: extensive, F, L; anemic nevus: F, LL,Macrocephaly——+—EDM, SMArterial hypertension, renal artery dysplasiaPED1153GNAQp.(Arg183Gln)3.0IINevus flammeus: L; cutis marmorata: F, extensiveMacrocephaly—Seizures,ID, LA, brain atrophy+———PED1500GNAQp.(Arg183Gln)5.0IVNevus flammeus: extensive, F, LLips—ID——EDMDental anomaliesPED1991GNAQp.(Arg183Gln)6.5IVNevus flammeus: extensive, extrafacialL, mild———VV, partial agenesia——PED2333GNAQp.(Arg183Gln)3.0IIINevus flammeus: extensive, F, LL, mild—Seizures,LA, brain atrophy+VV, thrombosis—Arterial hypertension, renal atrophyPED2355GNAQp.(Arg183Gln)6.0IIINevus flammeus: extensive F, L—————SM—PED2360GNAQp.(Arg183Gln)8.0IIINevus flammeus: LLL, mild———VV——PED2379GNAQp.(Arg183Gln)4.8IINevus flammeus: LLL, mild———VV, thrombosis——PED2586GNAQp.(Arg183Gln)10.0IIINevus flammeus: LL, mild———VV, partial agenesia, thrombosis——PED2613GNAQp.(Arg183Gln)4.0IIINevus flammeus: F, UL; cutis marmorata: LLL + F, mild—————ScoliosisPED2824GNAQp.(Arg183Gln)4.0IINevus flammeus: LLL, mild—————ScoliosisPED3248GNAQp.(Arg183Gln)7.0VNevus flammeus: ULUL, mild————EDM—PED3396GNAQp.(Arg183Gln)5.0IINevus flammeus: F, ULMacrocephaly—LA————PED3886GNAQp.(Arg183Gln)7.1IIINevus flammeus: extensive F, T, L; anemic nevus: TL, mild——————PED4046GNAQp.(Arg183Gln)17.0IINevus flammeus: FF——————PED4110GNAQp.(Arg183Gln)4.0IICutis marmorata: extensive F + L; anemic nevus: FL, mild——+———PED4396GNAQp.(Arg183Gln)4.0IVNevus flammeus: F; nevus roseus: L; anemic nevus: FMacrocephaly——+—EDM—PED4720GNAQp.(Arg183Gly)5.0IVNevus flammeus: F—MicrocephalySeizures, ID, LA+———PED4849GNAQp.(Arg183Gln)3.8IIINevus flammeus: LL, mild———VV, partial agenesia—Arterial hypertensionPED4965GNAQp.(Arg183Gln)6.0IINevus flammeus: mild limb————VV——PED1077GNA11p.(Arg183Cys)4.9IICutis marmorata + anemic nevus: F, L—LID,LA———Iris heterochromiaPED1085GNA11p.(Gln209His)4.0IIICutis marmorata + anemic nevus: T——————Arterial hypertension, renal artery dysplasiaPED1494GNA11p.(Arg183Cys)5.0IVNevus roseus + anemic nevus: F; cutis marmorata: T, L—FSeizures+—SM, self-resoluting EDMEpidermal nevusPED2082GNA11p.(Arg183Cys)5.5IIINevus flammeus: F; nevus roseus + anemic nevus: F, T, L——LA+—Nevus spilus—PED2363GNA11p.(Arg183Cys)3.0IINevus flammeus: F, L; cutis marmorata + anemic nevus: T, L—mild LL—————PED2579GNA11p.(Arg183His)3.0IICutis marmorata + anemic nevus: T, LL—mild LL—————PED2846GNA11p.(Arg183Cys)4.0IINevus roseus: F; cutis marmorata + anemic nevus: T, L———————PED3078GNA11p.(Arg183Cys)6.0IINevus flammeus: F, T, LL, mild—Seizures,LA brain atrophy—VV—Scoliosis, lipoma, arterial hypertension, renal atrophyPED3577GNA11p.(Arg183Cys)7.1IIINevus roseus + anemic nevus: F; cutis marmorata: T, L——Seizures,ID,LA+—SM—PED3767GNA11p.(Arg183Cys)3.7IIICutis marmorata + anemic nevus: LL—————CALM—PED4037GNA11p.(Arg183Cys)3.5IIINevus roseus: F; cutis marmorata + anemic nevus: F, T, L—————EDM—PED4729GNA11p.(Arg183Cys)14.0NANALL, mild————Bilateral SM—Abbreviations: CALM, Café-au-lait macules; EDM, extensive dermal melanocytosis; F, face; ID, intellectual disability; L, limbs; LA: leptomeningeal angiomatosis; LL, lower limb; NA, not available; SM, scleral melanocytosis; T, torso; UL, upper limb; VV, varicose vein. Open table in a new tab Abbreviations: CALM, Café-au-lait macules; EDM, extensive dermal melanocytosis; F, face; ID, intellectual disability; L, limbs; LA: leptomeningeal angiomatosis; LL, lower limb; NA, not available; SM, scleral melanocytosis; T, torso; UL, upper limb; VV, varicose vein." @default.
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• W2984831652 date "2020-05-01" @default.
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• W2984831652 title "Reverse Phenotyping in Patients with Skin Capillary Malformations and Mosaic GNAQ or GNA11 Mutations Defines a Clinical Spectrum with Genotype-Phenotype Correlation" @default.
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