Evidence map›Paper›PMID 40730740›Full record

ArticleJournal of inherited metabolic disease2025

Personalized Genotype-Based Approach for Treatment of Phenylketonuria.

Polina Gundorova, Behnam Yousefi, Mathias Woidy, Malcolm Summer Rose-Heine, Robin Khatri, Viviane Kasten, Stefan Bonn, Ania Carolina Muntau, Soeren Waldemar Gersting

Abstract read
In one paragraph

Article in Journal of inherited metabolic disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–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

4 citing papers in PubMed.

  1. Observational
  2. Article
  3. Article
  4. Article
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

9 authors.

Polina GundorovaUniversity Children's Research, University Medical Center Hamburg-Eppendorf (UKE), Hamburg, Germany.ORCID https://orcid.org/0000-0001-8703-7997
Behnam YousefiGerman Center for Child and Adolescent Health (DZKJ), Partner Site Hamburg, University Medical Center Hamburg-Eppendorf (UKE), Hamburg, Germany.
Mathias WoidyUniversity Children's Hospital, University Medical Center Hamburg-Eppendorf (UKE), Hamburg, Germany.
Malcolm Summer Rose-HeineUniversity Children's Research, University Medical Center Hamburg-Eppendorf (UKE), Hamburg, Germany.
Robin KhatriInstitute of Medical Systems Bioinformatics, Center for Biomedical AI (bAIome), Center for Molecular Neurobiology (ZMNH), University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Viviane KastenUniversity Children's Research, University Medical Center Hamburg-Eppendorf (UKE), Hamburg, Germany.
Stefan BonnGerman Center for Child and Adolescent Health (DZKJ), Partner Site Hamburg, University Medical Center Hamburg-Eppendorf (UKE), Hamburg, Germany.
Ania Carolina MuntauGerman Center for Child and Adolescent Health (DZKJ), Partner Site Hamburg, University Medical Center Hamburg-Eppendorf (UKE), Hamburg, Germany.
Soeren Waldemar GerstingUniversity Children's Research, University Medical Center Hamburg-Eppendorf (UKE), Hamburg, Germany.

Funding

Alexander von Humboldt-StiftungBioMarin PharmaceuticalDeutsche Forschungsgemeinschaft FOR 5068 P9Federal Ministry of Education and Research (BMBF), German Center for Child and Adolescent Health (DZKJ) 01GL2404AGerman Academic Exchange ServiceHamburg Macht Kinder Gesund foundation
6 · The paper itself

Abstract

Extensive studies have examined the clinical manifestations, pathogenic mechanisms, and genetic variations of phenylketonuria (PKU) across different populations, resulting in a substantial collection of molecular genetic data on the phenylalanine hydroxylase (PAH) gene and its variants. However, many genotypes are associated with a range of clinical phenotypes, as well as variable responsiveness to sapropterin, presenting ongoing challenges for effective treatment. To address this, we enhanced the PAH activity landscapes method by incorporating high-throughput techniques, including automated pipetting, integrated data processing via Gaussian modeling of 3D surfaces, and bioinformatics analyses with robust quality control. Using PAH activity landscapes, we visualized PAH enzymatic function across 99 common PAH genotypes under varying metabolic and therapeutic conditions. This deep functional phenotyping approach enabled us to identify distinct genotype subpopulations by using consensus clustering, correlate them with clinical phenotypes, and propose subpopulation-specific treatment protocols. Our findings suggest that clinical phenotypes can be predicted and treatment regimens can be adjusted based on residual PAH function profiles. To further support personalized treatment strategies, we revised our publicly accessible PAH genotype & activity landscapes database to share the latest insights into PAH function and patient phenotypes-namely residual enzyme activity and responsiveness to sapropterin as conveyed by two alleles. This resource underscores the translational significance of functional research in PKU and offers a practical tool to support personalized treatment in clinical settings.

Indexed as

Phenylalanine HydroxylasePhenylketonuriasPrecision MedicineBiopterinsGenotypeHumansPhenotypeBiopterinsPhenylalanine Hydroxylasesapropterinmisfoldingphenylalanine hydroxylasephenylketonuriasapropterin dihydrochloridetetrahydrobiopterin

Identifiers

PMID40730740
PMCPMC12307255

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.