ArticleFrontiers in pharmacology2013
Genetic influences on cystic fibrosis lung disease severity.
Article in Frontiers in pharmacology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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.
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.
Who cites it
25 citing papers in PubMed.
- The redefined identity ofJournal of bacteriology · 2026Review
- Transcriptomic and functional responses of the cystic fibrosis airway epithelium to CFTR modulator therapy.JCI insight · 2025Article
- Clinical and Imaging Features of Cystic Fibrosis in Korean Children.Journal of the Korean Society of Radiology · 2023Review
- ATP12A Proton Pump as an Emerging Therapeutic Target in Cystic Fibrosis and Other Respiratory Diseases.Biomolecules · 2023Review
- Forskolin-induced organoid swelling is associated with long-term cystic fibrosis disease progression.The European respiratory journal · 2022Article
- Genetic Modifying Factors of Cystic Fibrosis Phenotype: A Challenge for Modern Medicine.Journal of clinical medicine · 2021Review
- Tensin 1 (TNS1) is a modifier gene for low body mass index (BMI) in homozygous [F508del]CFTR patients.Physiological reports · 2021Article
- Article
- Liposomes Loaded With Phosphatidylinositol 5-Phosphate Improve the Antimicrobial Response toFrontiers in immunology · 2020Article
- Epithelial vectorial ion transport in cystic fibrosis: Dysfunction, measurement, and pharmacotherapy to target the primary deficit.SAGE open medicine · 2020Review
- Efficient protocols and methods for high-throughput utilization of the Collaborative Cross mouse model for dissecting the genetic basis of complex traits.Animal models and experimental medicine · 2019Review
- The impact of host genetic background in the Pseudomonas aeruginosa respiratory infections.Mammalian genome : official journal of the International Mammalian Genome Society · 2018Review
- The Collaborative Cross mouse model for dissecting genetic susceptibility to infectious diseases.Mammalian genome : official journal of the International Mammalian Genome Society · 2018Review
- Variation in Cilia Protein Genes and Progression of Lung Disease in Cystic Fibrosis.Annals of the American Thoracic Society · 2018Observational
- Spontaneous preterm birth: advances toward the discovery of genetic predisposition.American journal of obstetrics and gynecology · 2018Review
- Recent Progress in CFTR Interactome Mapping and Its Importance for Cystic Fibrosis.Frontiers in pharmacology · 2017Review
- Predictors of deterioration of lung function in Polish children with cystic fibrosis.Archives of medical science : AMS · 2016Article
- Cystic Fibrosis Lung Immunity: The Role of the Macrophage.Journal of innate immunity · 2016Review
- Host genetic diversity influences the severity of Pseudomonas aeruginosa pneumonia in the Collaborative Cross mice.BMC genetics · 2015Article
- Cystic fibrosis.Nature reviews. Disease primers · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
Understanding the causes of variation in clinical manifestations of disease should allow for design of new or improved therapeutic strategies to treat the disease. If variation is caused by genetic differences between individuals, identifying the genes involved should present therapeutic targets, either in the proteins encoded by those genes or the pathways in which they function. The technology to identify and genotype the millions of variants present in the human genome has evolved rapidly over the past two decades. Originally only a small number of polymorphisms in a small number of subjects could be studied realistically, but speed and scope have increased nearly as dramatically as cost has decreased, making it feasible to determine genotypes of hundreds of thousands of polymorphisms in thousands of subjects. The use of such genetic technology has been applied to cystic fibrosis (CF) to identify genetic variation that alters the outcome of this single gene disorder. Candidate gene strategies to identify these variants, referred to as "modifier genes," has yielded several genes that act in pathways known to be important in CF and for these the clinical implications are relatively clear. More recently, whole-genome surveys that probe hundreds of thousands of variants have been carried out and have identified genes and chromosomal regions for which a role in CF is not at all clear. Identification of these genes is exciting, as it provides the possibility for new areas of therapeutic development.
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Registered trials
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.