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Article ; Online: Dermatological manifestations, management, and care in RASopathies.

Kavamura, Maria Ines / Leoni, Chiara / Neri, Giovanni

American journal of medical genetics. Part C, Seminars in medical genetics

2022 Volume 190, Issue 4, Page(s) 452–458

Abstract: RASopathies are rare genetic disorders caused by germline pathogenic variants in genes belonging to the RAS/MAPK pathway, which signals cell proliferation, differentiation, survival and death. The dysfunction of such signaling pathway causes syndromes ... ...

Abstract	RASopathies are rare genetic disorders caused by germline pathogenic variants in genes belonging to the RAS/MAPK pathway, which signals cell proliferation, differentiation, survival and death. The dysfunction of such signaling pathway causes syndromes with overlapping clinical manifestations. Skin and adnexal lesions are the cardinal clinical signs of RASopathies, such as cardiofaciocutaneous syndrome, Noonan syndrome with multiple lentigines, formerly known as LEOPARD syndrome, Costello syndrome, neurofibromatosis (NF1), Legius syndrome, Noonan-like syndrome with loose anagen hair (NSLH) and Noonan syndrome. As NF1, one of the most common RASopathies, described in 1882, has its clinical features well delineated, we will focus on the dermatological diagnosis, management and care of non-NF1 RASopathies, which are less known and more recently described. Dermatological manifestations are important clinical diagnostic elements that can aid differential diagnosis among RASopathies. They can affect dermis and epidermis, causing pigmented lesions (melanocytic nevi, café-au-lait spots, and lentigines), hyperkeratosis (keratosis pilaris, ulerythema ophryogenes, and palmoplantar keratosis) or hyperplasia. To date there are rare known links to malignancy, but oftentimes skin lesions require close attention because they can highly affect quality of life.
MeSH term(s)	Humans ; Quality of Life ; ras Proteins/genetics ; Noonan Syndrome/diagnosis ; Noonan Syndrome/genetics ; Noonan Syndrome/therapy ; Costello Syndrome/diagnosis ; Costello Syndrome/genetics ; Costello Syndrome/therapy ; Darier Disease ; Mutation
Chemical Substances	ras Proteins (EC 3.6.5.2)
Language	English
Publishing date	2022-12-21
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2108622-9
ISSN	1552-4876 ; 0148-7299 ; 1552-4868
ISSN (online)	1552-4876
ISSN	0148-7299 ; 1552-4868
DOI	10.1002/ajmg.c.32027
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Article ; Online: My memories of Professor Giovanni Neri: the cardiofaciocutaneous syndrome (CFC).

Kavamura, Maria Ines

American journal of medical genetics. Part A

2013 Volume 161A, Issue 11, Page(s) 2707–2709

MeSH term(s)	Ectodermal Dysplasia/history ; Facies ; Failure to Thrive/history ; Heart Defects, Congenital/history ; History, 20th Century ; History, 21st Century ; Humans
Language	English
Publishing date	2013-10-27
Publishing country	United States
Document type	Biography ; Historical Article ; Letter ; Portrait
ZDB-ID	1493479-6
ISSN	1552-4833 ; 1552-4825
ISSN (online)	1552-4833
ISSN	1552-4825
DOI	10.1002/ajmg.a.36263
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Article: CFC syndrome.

Neri, Giovanni / Kavamura, Maria Ines / Zollino, Marcella / Opitz, John M

American journal of medical genetics. Part A

2003 Volume 116A, Issue 4, Page(s) 410

MeSH term(s)	Abnormalities, Multiple/genetics ; Chromosomes, Human, Pair 12 ; Heart Defects, Congenital/genetics ; Humans ; Intellectual Disability/genetics ; Syndrome
Language	English
Publishing date	2003-01-09
Publishing country	United States
Document type	Comment ; Letter
ZDB-ID	2108614-X
ISSN	1552-4825
ISSN	1552-4825
DOI	10.1002/ajmg.a.10012
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Article ; Online: Cardio-facio-cutaneous syndrome: clinical features, diagnosis, and management guidelines.

Pierpont, Mary Ella M / Magoulas, Pilar L / Adi, Saleh / Kavamura, Maria Ines / Neri, Giovanni / Noonan, Jacqueline / Pierpont, Elizabeth I / Reinker, Kent / Roberts, Amy E / Shankar, Suma / Sullivan, Joseph / Wolford, Melinda / Conger, Brenda / Santa Cruz, Molly / Rauen, Katherine A

Pediatrics

2014 Volume 134, Issue 4, Page(s) e1149–62

Abstract: Cardio-facio-cutaneous syndrome (CFC) is one of the RASopathies that bears many clinical features in common with the other syndromes in this group, most notably Noonan syndrome and Costello syndrome. CFC is genetically heterogeneous and caused by gene ... ...

Abstract	Cardio-facio-cutaneous syndrome (CFC) is one of the RASopathies that bears many clinical features in common with the other syndromes in this group, most notably Noonan syndrome and Costello syndrome. CFC is genetically heterogeneous and caused by gene mutations in the Ras/mitogen-activated protein kinase pathway. The major features of CFC include characteristic craniofacial dysmorphology, congenital heart disease, dermatologic abnormalities, growth retardation, and intellectual disability. It is essential that this condition be differentiated from other RASopathies, as a correct diagnosis is important for appropriate medical management and determining recurrence risk. Children and adults with CFC require multidisciplinary care from specialists, and the need for comprehensive management has been apparent to families and health care professionals caring for affected individuals. To address this need, CFC International, a nonprofit family support organization that provides a forum for information, support, and facilitation of research in basic medical and social issues affecting individuals with CFC, organized a consensus conference. Experts in multiple medical specialties provided clinical management guidelines for pediatricians and other care providers. These guidelines will assist in an accurate diagnosis of individuals with CFC, provide best practice recommendations, and facilitate long-term medical care.
MeSH term(s)	Diagnosis, Differential ; Disease Management ; Ectodermal Dysplasia/diagnosis ; Ectodermal Dysplasia/genetics ; Ectodermal Dysplasia/therapy ; Facies ; Failure to Thrive/diagnosis ; Failure to Thrive/genetics ; Failure to Thrive/therapy ; Genetic Testing/methods ; Heart Defects, Congenital/diagnosis ; Heart Defects, Congenital/genetics ; Heart Defects, Congenital/therapy ; Humans ; Practice Guidelines as Topic/standards
Language	English
Publishing date	2014-09-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	207677-9
ISSN	1098-4275 ; 0031-4005
ISSN (online)	1098-4275
ISSN	0031-4005
DOI	10.1542/peds.2013-3189
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Article: Miliary osteoma of the face: a report of 4 cases and review of the literature.

Bergonse, Fabiane N / Nico, Marcello Menta S / Kavamura, Maria Ines / Sotto, Miriam N

Cutis

2002 Volume 69, Issue 5, Page(s) 383–386

Abstract: Osteoma cutis (OC) is a rare disorder characterized by compact bone formation in the dermis and subcutaneous tissue. It is classified in primary and secondary forms according to the presence or absence of previous cutaneous lesions. Miliary osteoma of ... ...

Abstract	Osteoma cutis (OC) is a rare disorder characterized by compact bone formation in the dermis and subcutaneous tissue. It is classified in primary and secondary forms according to the presence or absence of previous cutaneous lesions. Miliary osteoma of the face (MOF) is a form of primary OC that generally occurs in middle-aged and older adult women. We report 3 cases of typical MOF and one additional case in a black patient, which to our knowledge has not been described previously.
MeSH term(s)	Aged ; Facial Dermatoses/pathology ; Female ; Humans ; Middle Aged ; Ossification, Heterotopic/pathology ; Osteoma/pathology ; Skin Neoplasms/pathology
Language	English
Publishing date	2002-05
Publishing country	United States
Document type	Case Reports ; Journal Article
ZDB-ID	391840-3
ISSN	0011-4162 ; 0151-9522
ISSN	0011-4162 ; 0151-9522
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Article ; Online: SOS1 mutations in Noonan syndrome: molecular spectrum, structural insights on pathogenic effects, and genotype-phenotype correlations.

Lepri, Francesca / De Luca, Alessandro / Stella, Lorenzo / Rossi, Cesare / Baldassarre, Giuseppina / Pantaleoni, Francesca / Cordeddu, Viviana / Williams, Bradley J / Dentici, Maria L / Caputo, Viviana / Venanzi, Serenella / Bonaguro, Michela / Kavamura, Ines / Faienza, Maria F / Pilotta, Alba / Stanzial, Franco / Faravelli, Francesca / Gabrielli, Orazio / Marino, Bruno /

Neri, Giovanni / Silengo, Margherita Cirillo / Ferrero, Giovanni B / Torrrente, Isabella / Selicorni, Angelo / Mazzanti, Laura / Digilio, Maria C / Zampino, Giuseppe / Dallapiccola, Bruno / Gelb, Bruce D / Tartaglia, Marco

Human mutation

2011 Volume 32, Issue 7, Page(s) 760–772

Abstract: Noonan syndrome (NS) is among the most common nonchromosomal disorders affecting development and growth. NS is caused by aberrant RAS-MAPK signaling and is genetically heterogeneous, which explains, in part, the marked clinical variability documented for ...

Abstract	Noonan syndrome (NS) is among the most common nonchromosomal disorders affecting development and growth. NS is caused by aberrant RAS-MAPK signaling and is genetically heterogeneous, which explains, in part, the marked clinical variability documented for this Mendelian trait. Recently, we and others identified SOS1 as a major gene underlying NS. Here, we explored further the spectrum of SOS1 mutations and their associated phenotypic features. Mutation scanning of the entire SOS1 coding sequence allowed the identification of 33 different variants deemed to be of pathological significance, including 16 novel missense changes and in-frame indels. Various mutation clusters destabilizing or altering orientation of regions of the protein predicted to contribute structurally to the maintenance of autoinhibition were identified. Two previously unappreciated clusters predicted to enhance SOS1's recruitment to the plasma membrane, thus promoting a spatial reorientation of domains contributing to inhibition, were also recognized. Genotype-phenotype analysis confirmed our previous observations, establishing a high frequency of ectodermal anomalies and a low prevalence of cognitive impairment and reduced growth. Finally, mutation analysis performed on cohorts of individuals with nonsyndromic pulmonic stenosis, atrial septal defects, and ventricular septal defects excluded a major contribution of germline SOS1 lesions to the isolated occurrence of these cardiac anomalies.
MeSH term(s)	Adolescent ; Adult ; Child ; Exons ; Female ; Genetic Association Studies ; Heart Septal Defects, Atrial/genetics ; Heart Septal Defects, Ventricular/genetics ; Humans ; INDEL Mutation/genetics ; Introns ; Male ; Mitogen-Activated Protein Kinase Kinases/genetics ; Mutation ; Mutation, Missense/genetics ; Noonan Syndrome/diagnosis ; Noonan Syndrome/genetics ; Protein Conformation ; Pulmonary Valve Stenosis/genetics ; SOS1 Protein/chemistry ; SOS1 Protein/genetics
Chemical Substances	SOS1 Protein ; Mitogen-Activated Protein Kinase Kinases (EC 2.7.12.2)
Language	English
Publishing date	2011-04-28
Publishing country	United States
Document type	Journal Article
ZDB-ID	1126646-6
ISSN	1098-1004 ; 1059-7794
ISSN (online)	1098-1004
ISSN	1059-7794
DOI	10.1002/humu.21492
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Article ; Online: Multiple giant cell lesions in patients with Noonan syndrome and cardio-facio-cutaneous syndrome.

European journal of human genetics : EJHG

2008 Volume 17, Issue 4, Page(s) 420–425

Abstract: Noonan syndrome (NS) and cardio-facio-cutaneous syndrome (CFCS) are related developmental disorders caused by mutations in genes encoding various components of the RAS-MAPK signaling cascade. NS is associated with mutations in the genes PTPN11, SOS1, ... ...

Abstract	Noonan syndrome (NS) and cardio-facio-cutaneous syndrome (CFCS) are related developmental disorders caused by mutations in genes encoding various components of the RAS-MAPK signaling cascade. NS is associated with mutations in the genes PTPN11, SOS1, RAF1, or KRAS, whereas CFCS can be caused by mutations in BRAF, MEK1, MEK2, or KRAS. The NS phenotype is rarely accompanied by multiple giant cell lesions (MGCL) of the jaw (Noonan-like/MGCL syndrome (NL/MGCLS)). PTPN11 mutations are the only genetic abnormalities reported so far in some patients with NL/MGCLS and in one individual with LEOPARD syndrome and MGCL. In a cohort of 75 NS patients previously tested negative for mutations in PTPN11 and KRAS, we detected SOS1 mutations in 11 individuals, four of whom had MGCL. To explore further the relevance of aberrant RAS-MAPK signaling in syndromic MGCL, we analyzed the established genes causing CFCS in three subjects with MGCL associated with a phenotype fitting CFCS. Mutations in BRAF or MEK1 were identified in these patients. All mutations detected in these seven patients with syndromic MGCL had previously been described in NS or CFCS without apparent MGCL. This study demonstrates that MGCL may occur in NS and CFCS with various underlying genetic alterations and no obvious genotype-phenotype correlation. This suggests that dysregulation of the RAS-MAPK pathway represents the common and basic molecular event predisposing to giant cell lesion formation in patients with NS and CFCS rather than specific mutation effects.
MeSH term(s)	Abnormalities, Multiple/diagnosis ; Abnormalities, Multiple/genetics ; Abnormalities, Multiple/pathology ; Adolescent ; Adult ; Child ; Cohort Studies ; Female ; Giant Cells/pathology ; Heart Diseases/congenital ; Heart Diseases/pathology ; Humans ; MAP Kinase Signaling System/genetics ; Male ; Mutation ; Noonan Syndrome/diagnosis ; Noonan Syndrome/genetics ; Noonan Syndrome/pathology ; Phenotype ; Skin Diseases/pathology ; Syndrome ; ras Proteins/genetics ; ras Proteins/metabolism
Chemical Substances	ras Proteins (EC 3.6.5.2)
Language	English
Publishing date	2008-10-15
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1141470-4
ISSN	1476-5438 ; 1018-4813
ISSN (online)	1476-5438
ISSN	1018-4813
DOI	10.1038/ejhg.2008.188
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Article: Molecular and clinical characterization of cardio-facio-cutaneous (CFC) syndrome: overlapping clinical manifestations with Costello syndrome.

Narumi, Yoko / Aoki, Yoko / Niihori, Tetsuya / Neri, Giovanni / Cavé, Hélène / Verloes, Alain / Nava, Caroline / Kavamura, Maria Ines / Okamoto, Nobuhiko / Kurosawa, Kenji / Hennekam, Raoul C M / Wilson, Louise C / Gillessen-Kaesbach, Gabriele / Wieczorek, Dagmar / Lapunzina, Pablo / Ohashi, Hirofumi / Makita, Yoshio / Kondo, Ikuko / Tsuchiya, Shigeru /

Ito, Etsuro / Sameshima, Kiyoko / Kato, Kumi / Kure, Shigeo / Matsubara, Yoichi

American journal of medical genetics. Part A

2007 Volume 143A, Issue 8, Page(s) 799–807

Abstract: Cardio-facio-cutaneous (CFC) syndrome is a multiple congenital anomaly/mental retardation syndrome characterized by heart defects, a distinctive facial appearance, ectodermal abnormalities and mental retardation. Clinically, it overlaps with both Noonan ... ...

Abstract	Cardio-facio-cutaneous (CFC) syndrome is a multiple congenital anomaly/mental retardation syndrome characterized by heart defects, a distinctive facial appearance, ectodermal abnormalities and mental retardation. Clinically, it overlaps with both Noonan syndrome and Costello syndrome, which are caused by mutations in two genes, PTPN11 and HRAS, respectively. Recently, we identified mutations in KRAS and BRAF in 19 of 43 individuals with CFC syndrome, suggesting that dysregulation of the RAS/RAF/MEK/ERK pathway is a molecular basis for CFC syndrome. The purpose of this study was to perform comprehensive mutation analysis in 56 patients with CFC syndrome and to investigate genotype-phenotype correlation. We analyzed KRAS, BRAF, and MAP2K1/2 (MEK1/2) in 13 new CFC patients and identified five BRAF and one MAP2K1 mutations in nine patients. We detected one MAP2K1 mutation in three patients and four new MAP2K2 mutations in four patients out of 24 patients without KRAS or BRAF mutations in the previous study [Niihori et al., 2006]. No mutations were identified in MAPK3/1 (ERK1/2) in 21 patients without any mutations. In total, 35 of 56 (62.5%) patients with CFC syndrome had mutations (3 in KRAS, 24 in BRAF, and 8 in MAP2K1/2). No significant differences in clinical manifestations were found among 3 KRAS-positive patients, 16 BRAF-positive patients, and 6 MAP2K1/2-positive patients. Wrinkled palms and soles, hyperpigmentation and joint hyperextension, which have been commonly reported in Costello syndrome but not in CFC syndrome, were observed in 30-40% of the mutation-positive CFC patients, suggesting a significant clinical overlap between these two syndromes.
MeSH term(s)	Abnormalities, Multiple/diagnosis ; Abnormalities, Multiple/epidemiology ; Abnormalities, Multiple/genetics ; Case-Control Studies ; Craniofacial Abnormalities/diagnosis ; Craniofacial Abnormalities/epidemiology ; Craniofacial Abnormalities/genetics ; DNA Mutational Analysis ; Diagnosis, Differential ; Genotype ; Heart Defects, Congenital/diagnosis ; Heart Defects, Congenital/epidemiology ; Heart Defects, Congenital/genetics ; Humans ; Intellectual Disability/diagnosis ; Intellectual Disability/epidemiology ; Intellectual Disability/genetics ; MAP Kinase Kinase 1/genetics ; MAP Kinase Kinase 2/genetics ; Molecular Epidemiology ; Phenotype ; Proto-Oncogene Proteins B-raf/genetics ; Signal Transduction ; Skin Abnormalities/diagnosis ; Skin Abnormalities/epidemiology ; Skin Abnormalities/genetics ; Syndrome ; ras Proteins/metabolism
Chemical Substances	MAP2K2 protein, human (EC 2.7.1.-) ; BRAF protein, human (EC 2.7.11.1) ; Proto-Oncogene Proteins B-raf (EC 2.7.11.1) ; MAP Kinase Kinase 1 (EC 2.7.12.2) ; MAP Kinase Kinase 2 (EC 2.7.12.2) ; MAP2K1 protein, human (EC 2.7.12.2) ; ras Proteins (EC 3.6.5.2)
Language	English
Publishing date	2007-03-16
Publishing country	United States
Document type	Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2108614-X
ISSN	1552-4825
ISSN	1552-4825
DOI	10.1002/ajmg.a.31658
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Article: Germline KRAS and BRAF mutations in cardio-facio-cutaneous syndrome.

Niihori, Tetsuya / Aoki, Yoko / Narumi, Yoko / Neri, Giovanni / Cavé, Hélène / Verloes, Alain / Okamoto, Nobuhiko / Hennekam, Raoul C M / Gillessen-Kaesbach, Gabriele / Wieczorek, Dagmar / Kavamura, Maria Ines / Kurosawa, Kenji / Ohashi, Hirofumi / Wilson, Louise / Heron, Delphine / Bonneau, Dominique / Corona, Giuseppina / Kaname, Tadashi / Naritomi, Kenji /

Baumann, Clarisse / Matsumoto, Naomichi / Kato, Kumi / Kure, Shigeo / Matsubara, Yoichi

Nature genetics

2006 Volume 38, Issue 3, Page(s) 294–296

Abstract: Cardio-facio-cutaneous (CFC) syndrome is characterized by a distinctive facial appearance, heart defects and mental retardation. It phenotypically overlaps with Noonan and Costello syndrome, which are caused by mutations in PTPN11 and HRAS, respectively. ...

Abstract	Cardio-facio-cutaneous (CFC) syndrome is characterized by a distinctive facial appearance, heart defects and mental retardation. It phenotypically overlaps with Noonan and Costello syndrome, which are caused by mutations in PTPN11 and HRAS, respectively. In 43 individuals with CFC, we identified two heterozygous KRAS mutations in three individuals and eight BRAF mutations in 16 individuals, suggesting that dysregulation of the RAS-RAF-ERK pathway is a common molecular basis for the three related disorders.
MeSH term(s)	Amino Acid Sequence ; Face/abnormalities ; Heart Defects, Congenital/genetics ; Humans ; Intellectual Disability/genetics ; Molecular Sequence Data ; Proto-Oncogene Proteins/genetics ; Proto-Oncogene Proteins B-raf/genetics ; Proto-Oncogene Proteins p21(ras) ; Reference Values ; Skin Abnormalities/genetics ; Syndrome ; ras Proteins
Chemical Substances	KRAS protein, human ; Proto-Oncogene Proteins ; BRAF protein, human (EC 2.7.11.1) ; Proto-Oncogene Proteins B-raf (EC 2.7.11.1) ; Proto-Oncogene Proteins p21(ras) (EC 3.6.5.2) ; ras Proteins (EC 3.6.5.2)
Language	English
Publishing date	2006-03
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1108734-1
ISSN	1546-1718 ; 1061-4036
ISSN (online)	1546-1718
ISSN	1061-4036
DOI	10.1038/ng1749
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