Evidence map›Paper›PMID 38824260›Full record

Observational studyEuropean journal of human genetics : EJHG2024

Defining the variant-phenotype correlation in patients affected by Noonan syndrome with the RAF1:c.770C>T p.(Ser257Leu) variant.

Andrea Gazzin, Federico Fornari, Marcello Niceta, Chiara Leoni, Maria Lisa Dentici, Diana Carli, Anna Maria Villar, Giulio Calcagni, Elena Banaudi, Stefania Massuras and 12 more

Abstract readObservational Study
In one paragraph

Observational study in European journal of human genetics : EJHG, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

12 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Domain-specific phenotypic profiles in RAF1-related Noonan syndrome.European journal of human genetics : EJHG · 2026
    Article
  8. Noonan Syndrome, Cancer Risk, and Growth Hormone TreatmentJournal of clinical research in pediatric endocrinology · 2025
    Review
  9. World journal of cardiology · 2025
    Article
  10. Article
  11. Summer reading in EJHG.European journal of human genetics : EJHG · 2024
    Article
  12. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

22 authors.

Andrea GazzinDepartment of Molecular Biotechnology and Health Sciences, Molecular Biotechnology Center, University of Turin, Turin, Italy.ORCID 0000-0002-5230-2831
Federico FornariPostgraduate School of Pediatrics, University of Turin, Turin, Italy.
Marcello NicetaMolecular Genetics and Functional Genomics, Bambino Gesù Children's Hospital IRCCS, 00146, Rome, Italy.ORCID 0000-0003-4766-7753
Chiara LeoniCenter for Rare Diseases and Birth Defects, Department of Woman and Child Health and Public Health, Fondazione Policlinico Universitario A. Gemelli, IRCCS, Rome, Italy.ORCID 0000-0002-4089-637X
Maria Lisa DenticiMedical Genetics, Bambino Gesù Children's Hospital, IRCCS, Rome, Italy.
Diana CarliDepartment of Medical Sciences, University of Turin, Turin, Italy.ORCID 0000-0001-5690-6504
Anna Maria VillarCardiology Department, Regina Margherita Children's Hospital, Turin, Italy.
Giulio CalcagniPediatric Cardiology and Cardiac Surgery, Bambino Gesù Children's Hospital, IRCCS, Rome, Italy.
Elena BanaudiCardiology Department, Regina Margherita Children's Hospital, Turin, Italy.
Stefania MassurasDepartment of Public Health and Pediatrics, University of Turin, Turin, Italy.
Simona CardaropoliDepartment of Public Health and Pediatrics, University of Turin, Turin, Italy.ORCID 0000-0002-8927-8900
Elena AiruloDepartment of Public Health and Pediatrics, University of Turin, Turin, Italy.
Paola DanieleMedical Genetics Unit, Fondazione IRCCS-Casa Sollievo della Sofferenza, San Giovanni Rotondo, Italy.
Emanuele MondaInherited and Rare Cardiovascular Diseases, Department of Translational Medical Sciences, University of Campania "Luigi Vanvitelli", Monaldi Hospital, Naples, Italy.
Giuseppe LimongelliInherited and Rare Cardiovascular Diseases, Department of Translational Medical Sciences, University of Campania "Luigi Vanvitelli", Monaldi Hospital, Naples, Italy.
Chiara RiggiCardiology Department, Regina Margherita Children's Hospital, Turin, Italy.
Giuseppe ZampinoCenter for Rare Diseases and Birth Defects, Department of Woman and Child Health and Public Health, Fondazione Policlinico Universitario A. Gemelli, IRCCS, Rome, Italy.
Maria Cristina DigilioMedical Genetics, Bambino Gesù Children's Hospital, IRCCS, Rome, Italy.
Alessandro De LucaMedical Genetics Unit, Fondazione IRCCS-Casa Sollievo della Sofferenza, San Giovanni Rotondo, Italy.ORCID 0000-0002-4408-8062
Marco TartagliaMolecular Genetics and Functional Genomics, Bambino Gesù Children's Hospital IRCCS, 00146, Rome, Italy.ORCID 0000-0001-7736-9672
Giovanni Battista FerreroDepartment of Clinical and Biological Sciences, University of Turin, Orbassano, Italy. giovannibattista.ferrero@unito.it.ORCID 0000-0002-3793-5788
Alessandro MussaDepartment of Public Health and Pediatrics, University of Turin, Turin, Italy. alessandro.mussa@unito.it.ORCID 0000-0003-2795-6013

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hypertrophic cardiomyopathy (HCM) is the major contributor to morbidity and mortality in Noonan syndrome (NS). Gain-of-function variants in RAF1 are associated with high prevalence of HCM. Among these, NM_002880.4:c.770C > T, NP_002871.1:p.(Ser257Leu) accounts for approximately half of cases and has been reported as associated with a particularly severe outcome. Nevertheless, comprehensive studies on cases harboring this variant are missing. To precisely define the phenotype associated to the RAF1:c.770C > T, variant, an observational retrospective analysis on patients carrying the c.770C > T variant was conducted merging 17 unpublished patients and literature-derived ones. Data regarding prenatal findings, clinical features and cardiac phenotypes were collected to provide an exhaustive description of the associated phenotype. Clinical information was collected in 107 patients. Among them, 92% had HCM, mostly diagnosed within the first year of life. Thirty percent of patients were preterm and 47% of the newborns was admitted in a neonatal intensive care unit, mainly due to respiratory complications of HCM and/or pulmonary arterial hypertension. Mortality rate was 13%, mainly secondary to HCM-related complications (62%) at the average age of 7.5 months. Short stature had a prevalence of 91%, while seizures and ID of 6% and 12%, respectively. Two cases out of 75 (3%) developed neoplasms. In conclusion, patients with the RAF1:c.770C > T pathogenic variant show a particularly severe phenotype characterized by rapidly progressive neonatal HCM and high mortality rate suggesting the necessity of careful monitoring and early intervention to prevent or slow down the progression of HCM.

Indexed as

Cardiomyopathy, HypertrophicNoonan SyndromePhenotypeProto-Oncogene Proteins c-rafAdolescentAdultChildChild, PreschoolFemaleGain of Function MutationHumansInfantInfant, NewbornMaleProto-Oncogene Proteins c-rafRaf1 protein, human

Identifiers

PMID38824260
PMCPMC11291835

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