Sarah Flanagan

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Associate Professor of Genomic Medicine and Sir Henry Dale Fellow

University of Exeter

United Kingdom

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About

Sarah Flanagan is an Associate Professor of Genomic Medicine and a Sir Henry Dale Fellow at the University of Exeter, UK. Her research focuses on neonatal diabetes and congenital hyperinsulinism, with recent publications investigating genetic causes and outcomes of these conditions. She is actively involved in developing international collaborative research networks aimed at prioritizing research agendas in these areas.

Recent Grants

Grant: Open

Non-coding mutations in congenital hyperinsulinism: deciphering the role of gene dysregulation in human disease

Open Date: 2022-03-31

Close Date: 2027-03-30

Grant: Close

Identifying novel insulin secretion disorders caused by mitochondrial dysfunction to highlight fundamental pathways within the β-cell

Open Date: 2021-10-01

Close Date: 2024-09-01

Grant: Close

Novel insights into autoimmune diabetes

Open Date: 2020-07-01

Close Date: 2021-06-01

Grant: Close

Using state-of-the-art technology to discover novel genetic mechanisms of insulin secretion

Open Date: 2019-06-01

Close Date: 2020-05-01

Grant: Close

Genetic Testing for Congenital Hyperinsulinism

Open Date: 2018-07-01

Close Date: 2021-12-01

Articles (20)

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2021

Collaborators (15)

Julie Raskin

Chief Executive Officer

Congenital Hyperinsulinism International

UNITED STATES

Sarah Flanagan

Research Interests

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About

Recent Grants

Articles (20)

Developing a congenital hyperinsulinism prioritized research agenda: a patient-driven international collaborative research network

Improved Neurodevelopment Following In Utero Sulfonylurea Exposure in a Patient With KCNJ11 Permanent Neonatal Diabetes: Future Implications for Targeted Treatment During Pregnancy

Rare disease gene association discovery in the 100,000 Genomes Project.

Non-coding cis-regulatory variants in HK1 cause congenital hyperinsulinism with variable disease severity

A homozygous TARS2 variant is a novel cause of syndromic neonatal diabetes

Characterization of congenital hyperinsulinism in Argentina: Clinical features, genetic findings, and treatment outcomes

Complete loss of PAX4 causes transient neonatal diabetes in humans

Comprehensive clinical and molecular characterization with long-term outcomes in 40 patients with congenital hyperinsulinism

Large copy number variants are an important cause of congenital hyperinsulinism that should be screened for during routine testing

Neonatal diabetes mellitus is a significant feature of COXPD-24 caused by recessive NARS2 variants

Bringing precision medicine to the management of pregnancy in women with glucokinase-MODY: a study of diagnostic accuracy and feasibility of non-invasive prenatal testing

International Guidelines for the Diagnosis and Management of Hyperinsulinism

Monogenic disease analysis establishes that fetal insulin accounts for half of human fetal growth

Hyperinsulinemic Hypoglycemia Diagnosed in Childhood Can Be Monogenic

A biallelic loss‐of‐function PDIA6 variant in a second patient with polycystic kidney disease, infancy‐onset diabetes, and microcephaly

SavvyCNV: Genome-wide CNV calling from off-target reads

Association of birthweight and penetrance of diabetes in individuals with HNF4A-MODY: a cohort study

Genetic and clinical heterogeneity of permanent neonatal diabetes mellitus: a single tertiary centre experience

Founder mutation in the PMM2 promotor causes hyperinsulinemic hypoglycaemia/polycystic kidney disease (HIPKD)

Sex-biased islet β cell dysfunction is caused by the MODY MAFA S64F variant by inducing premature aging and senescence in males

Collaborators (15)

Julie Raskin

Julius Jacobsen

Kashyap A Patel

James Russ-Silsby

Elisa De Franco

Detlef Bockenhauer

Emma Dempster

Albert C. M. Ong

Pamela Bowman

David A. Jacobson

Diva D. De Leon

Li Chan

Rachel Freathy

Indraneel Banerjee

Andrew Hattersley

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