ReviewPharmacology & therapeutics2010
Cystic fibrosis: exploiting its genetic basis in the hunt for new therapies.
Review in Pharmacology & therapeutics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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
22 citing papers in PubMed, 67 citations in OpenAlex.
- Vanzacaftor-tezacaftor-deutivacaftor for children aged 6-11 years with cystic fibrosis (RIDGELINE Trial VX21-121-105): an analysis from a single-arm, phase 3 trial.The Lancet. Respiratory medicine · 2025Trial
- Next-Generation Sequencing for Molecular Diagnosis of Cystic Fibrosis in a Brazilian Cohort.Disease markers · 2021Article
- Chitosan in Non-Viral Gene Delivery: Role of Structure, Characterization Methods, and Insights in Cancer and Rare Diseases Therapies.Polymers · 2018Review
- The potential of antisense oligonucleotide therapies for inherited childhood lung diseases.Molecular and cellular pediatrics · 2018Review
- Cystic fibrosis carriership and tuberculosis: hints toward an evolutionary selective advantage based on data from the Brazilian territory.BMC infectious diseases · 2017Article
- Pancreatic pathophysiology in cystic fibrosis.The Journal of pathology · 2016Review
- The road for survival improvement of cystic fibrosis patients in Arab countries.International journal of pediatrics & adolescent medicine · 2015Review
- Nanotechnology approaches for inhalation treatment of fibrosis.Journal of drug targeting · 2013Review
- Targeting protein-protein interactions to rescue Δf508-cftr: a novel corrector approach to treat cystic fibrosis.EMBO molecular medicine · 2013Article
- Self-reactive CFTR T cells in humans: implications for gene therapy.Human gene therapy. Clinical development · 2013Article
- Liver disease in cystic fibrosis: an update.Hepatitis monthly · 2013Review
- RACK1 interacts with filamin-A to regulate plasma membrane levels of the cystic fibrosis transmembrane conductance regulator.American journal of physiology. Cell physiology · 2013Article
- First cystic fibrosis drug advances towards approval.Nature biotechnology · 2011Article
- Genetic testing: predictive value of genotyping for diagnosis and management of disease.The EPMA journal · 2011Article
- Paraoxonases as potential antibiofilm agents: their relationship with quorum-sensing signals in Gram-negative bacteria.Antimicrobial agents and chemotherapy · 2011Review
- Alpha7 nicotinic receptors as novel therapeutic targets for inflammation-based diseases.Cellular and molecular life sciences : CMLS · 2011Review
- Emergent properties of proteostasis in managing cystic fibrosis.Cold Spring Harbor perspectives in biology · 2011Review
- Stimulation of Wild-Type, F508del- and G551D-CFTR Chloride Channels by Non-Toxic Modified pyrrolo[2,3-b]pyrazine Derivatives.Frontiers in pharmacology · 2011Article
- Article
- MicroRNAs in inflammatory lung disease--master regulators or target practice?Respiratory research · 2010Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Cystic fibrosis (CF) is caused by mutations in the gene encoding the cystic fibrosis transmembrane conductance regulator (CFTR), an anion channel expressed in epithelial cells throughout the body. In the lungs, absence or dysfunction of CFTR results in altered epithelial salt and water transport eventuating in impaired mucociliary clearance, chronic infection and inflammation, and tissue damage. CF lung disease is the major cause of morbidity and mortality in CF despite the many therapies aimed at reducing it. However, recent technological advances combined with two decades of research driven by the discovery of the CFTR gene have resulted in the development and clinical testing of novel therapies aimed at the principal underlying defect in CF, thereby ushering in a new age of therapy for CF.
Indexed as
Identifiers
What OpenQuestion holds
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.