Evidence map›Paper›PMID 25489051›Full record

ArticleHuman molecular genetics2015

Missense variants in CFTR nucleotide-binding domains predict quantitative phenotypes associated with cystic fibrosis disease severity.

David L Masica, Patrick R Sosnay, Karen S Raraigh, Garry R Cutting, Rachel Karchin

Abstract read
In one paragraph

Article in Human molecular genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing 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

10 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Variation benchmark datasets: update, criteria, quality and applications.Database : the journal of biological databases and curation · 2020
    Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. 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

5 authors.

David L MasicaDepartment of Biomedical Engineering and Institute for Computational Medicine, The Johns Hopkins University, Baltimore, MD, USA.
Patrick R SosnayMcKusick-Nathans Institute of Genetic Medicine.
Karen S RaraighMcKusick-Nathans Institute of Genetic Medicine.
Garry R CuttingMcKusick-Nathans Institute of Genetic Medicine.
Rachel KarchinDepartment of Biomedical Engineering and Institute for Computational Medicine, The Johns Hopkins University, Baltimore, MD, USA, Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, MD, USA karchin@jhu.edu.

Funding

Translational Research Central ServicesP30CA006973 · NCI · JOHNS HOPKINS UNIVERSITY · PI Rosalie Wollett · 1985 to 2026
$208.6M
MOLECULAR GENETICS OF CYSTIC FIBROSISR01DK044003 · NIDDK · JOHNS HOPKINS UNIVERSITY · PI Garry R Cutting · 1991 to 2026
$6.7M
NCI NIH HHS P30 CA006973NIDDK NIH HHS R01 DK044003
6 · The paper itself

Abstract

Predicting the impact of genetic variation on human health remains an important and difficult challenge. Often, algorithmic classifiers are tasked with predicting binary traits (e.g. positive or negative for a disease) from missense variation. Though useful, this arrangement is limiting and contrived, because human diseases often comprise a spectrum of severities, rather than a discrete partitioning of patient populations. Furthermore, labeling variants as causal or benign can be error prone, which is problematic for training supervised learning algorithms (the so-called garbage in, garbage out phenomenon). We explore the potential value of training classifiers using continuous-valued quantitative measurements, rather than binary traits. Using 20 variants from cystic fibrosis transmembrane conductance regulator (CFTR) nucleotide-binding domains and six quantitative measures of cystic fibrosis (CF) severity, we trained classifiers to predict CF severity from CFTR variants. Employing cross validation, classifier prediction and measured clinical/functional values were significantly correlated for four of six quantitative traits (correlation P-values from 1.35 × 10(-4) to 4.15 × 10(-3)). Classifiers were also able to stratify variants by three clinically relevant risk categories with 85-100% accuracy, depending on which of the six quantitative traits was used for training. Finally, we characterized 11 additional CFTR variants using clinical sweat chloride testing, two functional assays, or all three diagnostics, and validated our classifier using blind prediction. Predictions were within the measured sweat chloride range for seven of eight variants, and captured the differential impact of specific variants on the two functional assays. This work demonstrates a promising and novel framework for assessing the impact of genetic variation.

Indexed as

Mutation, MissenseCystic FibrosisCystic Fibrosis Transmembrane Conductance RegulatorGenetic VariationHumansPhenotypeProtein Structure, TertiaryTrauma Severity IndicesCystic Fibrosis Transmembrane Conductance Regulator

Identifiers

PMID25489051
PMCPMC4366609

What OpenQuestion holds

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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.