Thomas W. Laver

2.4k total citations
34 papers, 1.3k citations indexed

About

Thomas W. Laver is a scholar working on Molecular Biology, Genetics and Endocrinology, Diabetes and Metabolism. According to data from OpenAlex, Thomas W. Laver has authored 34 papers receiving a total of 1.3k indexed citations (citations by other indexed papers that have themselves been cited), including 19 papers in Molecular Biology, 18 papers in Genetics and 12 papers in Endocrinology, Diabetes and Metabolism. Recurrent topics in Thomas W. Laver's work include Hyperglycemia and glycemic control in critically ill and hospitalized patients (10 papers), Pancreatic function and diabetes (10 papers) and Genomics and Rare Diseases (7 papers). Thomas W. Laver is often cited by papers focused on Hyperglycemia and glycemic control in critically ill and hospitalized patients (10 papers), Pancreatic function and diabetes (10 papers) and Genomics and Rare Diseases (7 papers). Thomas W. Laver collaborates with scholars based in United Kingdom, Finland and United States. Thomas W. Laver's co-authors include Karen Moore, Konrad Paszkiewicz, David J. Studholme, Jamie Harrison, Paul O’Neill, Audrey Farbos, Sian Ellard, Michael N. Weedon, Andrew T. Hattersley and Sarah E. Flanagan and has published in prestigious journals such as Cell, Nature Communications and SHILAP Revista de lepidopterología.

In The Last Decade

Thomas W. Laver

30 papers receiving 1.3k citations

Peers

Thomas W. Laver
Amit R. Majithia United States
John Brestelli United States
S Cheng United States
John F. Peden United Kingdom
Jinko Graham Canada
Natacha Klages Switzerland
Guido Sauer Germany
James Diggans United States
Irina D. Pokrovskaya United States
Rebecca Ashfield United Kingdom
Amit R. Majithia United States
Thomas W. Laver
Citations per year, relative to Thomas W. Laver Thomas W. Laver (= 1×) peers Amit R. Majithia

Countries citing papers authored by Thomas W. Laver

Since Specialization
Citations

This map shows the geographic impact of Thomas W. Laver's research. It shows the number of citations coming from papers published by authors working in each country. You can also color the map by specialization and compare the number of citations received by Thomas W. Laver with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Thomas W. Laver more than expected).

Fields of papers citing papers by Thomas W. Laver

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by Thomas W. Laver. Nodes represent research fields, and links connect fields that are likely to share authors. Colored nodes show fields that tend to cite the papers produced by Thomas W. Laver. The network helps show where Thomas W. Laver may publish in the future.

Co-authorship network of co-authors of Thomas W. Laver

This figure shows the co-authorship network connecting the top 25 collaborators of Thomas W. Laver. A scholar is included among the top collaborators of Thomas W. Laver based on the total number of citations received by their joint publications. Widths of edges represent the number of papers authors have co-authored together. Node borders signify the number of papers an author published with Thomas W. Laver. Thomas W. Laver is excluded from the visualization to improve readability, since they are connected to all nodes in the network.

All Works

20 of 20 papers shown
1.
Colclough, Kevin, James H. Leech, Thomas W. Laver, et al.. (2025). Population Prevalence, Penetrance, and Mortality for Genetically Confirmed MODY. The Journal of Clinical Endocrinology & Metabolism.
2.
Wakeling, Matthew N., Andrew T. Hattersley, Michael N. Weedon, et al.. (2025). Rare Variants in NEUROD1 and PDX1 Are Low-Penetrance Causes of MODY, Whereas Those in APPL1 and WFS1 Are Not Associated With MODY. Diabetes. 74(11). 2123–2131.
3.
Flanagan, Sarah E., Jonna M. E. Männistö, James T. Bennett, et al.. (2025). Large copy number variants are an important cause of congenital hyperinsulinism that should be screened for during routine testing. Frontiers in Endocrinology. 16. 1514916–1514916.
4.
Laver, Thomas W. & Kashyap Patel. (2025). Maturity onset diabetes of the young and beyond: the changing face of single-gene diabetes. European Journal of Endocrinology. 193(3). R25–R29.
5.
Laver, Thomas W., Matthew N. Wakeling, Richard Caswell, et al.. (2024). Chromosome 20p11.2 deletions cause congenital hyperinsulinism via the loss of FOXA2 or its regulatory elements. European Journal of Human Genetics. 32(7). 813–818. 2 indexed citations
6.
Patel, Kashyap, Thomas W. Laver, Matthew B. Johnson, et al.. (2023). The Role of ONECUT1 Variants in Monogenic and Type 2 Diabetes Mellitus. Diabetes. 72(11). 1729–1734. 8 indexed citations
7.
Laver, Thomas W., Jayne Houghton, Jonna M. E. Männistö, et al.. (2022). Increased referrals for congenital hyperinsulinism genetic testing in children with trisomy 21 reflects the high burden of non‐genetic risk factors in this group. Pediatric Diabetes. 23(4). 457–461. 6 indexed citations
8.
Houghton, Jayne, Navoda Atapattu, Matthew B. Johnson, et al.. (2022). Hyperinsulinemic Hypoglycemia Diagnosed in Childhood Can Be Monogenic. The Journal of Clinical Endocrinology & Metabolism. 108(3). 680–687. 7 indexed citations
9.
Mirshahi, Uyenlinh L., Kevin Colclough, Caroline F. Wright, et al.. (2022). Reduced penetrance of MODY-associated HNF1A/HNF4A variants but not GCK variants in clinically unselected cohorts. The American Journal of Human Genetics. 109(11). 2018–2028. 42 indexed citations
10.
Laver, Thomas W., Matthew N. Wakeling, Olivia Knox, et al.. (2022). Evaluation of Evidence for Pathogenicity Demonstrates That BLK , KLF11 , and PAX4 Should Not Be Included in Diagnostic Testing for MODY. Diabetes. 71(5). 1128–1136. 35 indexed citations
11.
Laver, Thomas W., Elisa De Franco, Matthew B. Johnson, et al.. (2022). SavvyCNV: Genome-wide CNV calling from off-target reads. PLoS Computational Biology. 18(3). e1009940–e1009940. 12 indexed citations
12.
Yau, Daphne, Thomas W. Laver, Jayne Houghton, et al.. (2021). Birth weight and diazoxide unresponsiveness strongly predict the likelihood of congenital hyperinsulinism due to a mutation in ABCC8 or KCNJ11\n. Europe PMC (PubMed Central). 7 indexed citations
13.
Yau, Daphne, Thomas W. Laver, Antonia Dastamani, et al.. (2020). Using referral rates for genetic testing to determine the incidence of a rare disease: The minimal incidence of congenital hyperinsulinism in the UK is 1 in 28,389. PLoS ONE. 15(2). e0228417–e0228417. 38 indexed citations
14.
Wright, Caroline F., Ben C. West, Marcus A. Tuke, et al.. (2019). Assessing the Pathogenicity, Penetrance, and Expressivity of Putative Disease-Causing Variants in a Population Setting. The American Journal of Human Genetics. 104(2). 275–286. 109 indexed citations
15.
Houghton, Jayne, Indraneel Banerjee, Thomas W. Laver, et al.. (2019). Unravelling the genetic causes of mosaic islet morphology in congenital hyperinsulinism. The Journal of Pathology Clinical Research. 6(1). 12–16. 19 indexed citations
16.
Laver, Thomas W., Matthew N. Wakeling, Jayne Houghton, et al.. (2018). Comprehensive screening shows that mutations in the known syndromic genes are rare in infants presenting with hyperinsulinaemic hypoglycaemia. Clinical Endocrinology. 89(5). 621–627. 7 indexed citations
17.
Locke, Jonathan M., Cécile Saint‐Martin, Thomas W. Laver, et al.. (2018). The Common HNF1A Variant I27L Is a Modifier of Age at Diabetes Diagnosis in Individuals With HNF1A-MODY. Diabetes. 67(9). 1903–1907. 19 indexed citations
18.
Patel, Kashyap, Jarno L. T. Kettunen, Markku Laakso, et al.. (2017). Heterozygous RFX6 protein truncating variants are associated with MODY with reduced penetrance. Nature Communications. 8(1). 888–888. 87 indexed citations
19.
Anderson, Courtney, Bingqing Zhang, Xingyong Wu, et al.. (2016). Fully Automated RNAscope In Situ Hybridization Assays for Formalin‐Fixed Paraffin‐Embedded Cells and Tissues. Journal of Cellular Biochemistry. 117(10). 2201–2208. 77 indexed citations
20.
Hickman, Alison B., Hosam E. Ewis, Xianghong Li, et al.. (2014). Structural Basis of hAT Transposon End Recognition by Hermes, an Octameric DNA Transposase from Musca domestica. Cell. 158(2). 353–367. 53 indexed citations

Rankless uses publication and citation data sourced from OpenAlex, an open and comprehensive bibliographic database. While OpenAlex provides broad and valuable coverage of the global research landscape, it—like all bibliographic datasets—has inherent limitations. These include incomplete records, variations in author disambiguation, differences in journal indexing, and delays in data updates. As a result, some metrics and network relationships displayed in Rankless may not fully capture the entirety of a scholar's output or impact.

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