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Richard J. Allen

Researcher at University of Leicester

Publications -  49
Citations -  1820

Richard J. Allen is an academic researcher from University of Leicester. The author has contributed to research in topics: Medicine & Idiopathic pulmonary fibrosis. The author has an hindex of 11, co-authored 26 publications receiving 1045 citations. Previous affiliations of Richard J. Allen include University of York.

Papers
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Journal ArticleDOI

Novel insights into the genetics of smoking behaviour, lung function, and chronic obstructive pulmonary disease (UK BiLEVE): a genetic association study in UK Biobank

TL;DR: By sampling from the extremes of the lung function distribution in UK Biobank, novel genetic causes of lung function and smoking behaviour are identified and substantial shared genetic architecture underlying airflow obstruction is shown across individuals, irrespective of smoking behaviour and other airway disease.
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New genetic signals for lung function highlight pathways and chronic obstructive pulmonary disease associations across multiple ancestries

Nick Shrine, +115 more
- 25 Feb 2019 - 
TL;DR: In this paper, a genome-wide association study in 400,102 individuals of European ancestry was conducted to define 279 lung function signals, 139 of which are new and the combined effect of these variants showed generalizability across smokers and never smokers, and across ancestral groups.
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Genome-wide association analyses for lung function and chronic obstructive pulmonary disease identify new loci and potential druggable targets

Louise V. Wain, +116 more
- 06 Feb 2017 - 
TL;DR: In this article, a genetic risk score was associated with COPD susceptibility (odds ratio per 1 s.d. of the risk score (∼6 alleles) (95% confidence interval) = 1.24 (1.20-1.27), P = 5.05 × 10(-49)), and they observed a 3.7-fold difference in COPD risk between individuals in the highest and lowest GA risk score deciles in UK Biobank.
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Genetic variants associated with susceptibility to idiopathic pulmonary fibrosis in people of European ancestry: a genome-wide association study

TL;DR: The identification of AKAP13 as a susceptibility gene for IPF increases the prospect of successfully targeting RhoA pathway inhibitors in patients with IPF.
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Genome-Wide Association Study of Susceptibility to Idiopathic Pulmonary Fibrosis.

Richard J. Allen, +77 more
TL;DR: The observation that decreased DEPTOR expression associates with increased susceptibility to IPF supports recent studies demonstrating the importance of mTOR signaling in lung fibrosis, and new signals of association implicating KIF15 and MAD1L1 suggest a possible role of mitotic spindle-assembly genes in IPF susceptibility.