2018 - Fellow of the American Association for the Advancement of Science (AAAS)
His primary areas of investigation include Genetics, Chromosomal fragile site, Molecular biology, Chromosome Fragile Site and Chromosome. His is doing research in Chromosome 17, Translocation Breakpoint, Nonsense mutation, Breakpoint and Progeroid syndromes, both of which are found in Genetics. His biological study spans a wide range of topics, including Aphidicolin, DNA, DNA repair, DNA replication and X chromosome.
His Molecular biology study incorporates themes from Chromosome breakage, Biochemistry, Gene, cDNA library and Gene product. His research investigates the connection between Chromosome Fragile Site and topics such as Metaphase that intersect with issues in Identification, Genome, Chromosome instability and Mendelian inheritance. In his research on the topic of Chromosome, Chromosome 3 and Chromatid is strongly related with Chromosomal translocation.
Thomas W. Glover mainly investigates Genetics, Molecular biology, Chromosomal fragile site, Gene and Chromosome. Genetics is represented through his Locus, Gene mapping, Breakpoint, X chromosome and Chromosome 17 research. His Chromosome 17 study combines topics in areas such as Loss of heterozygosity and Neurofibromatosis.
His Molecular biology research is multidisciplinary, incorporating perspectives in Amplicon, Chromosome 3, DNA repair, Gene duplication and Fluorescence in situ hybridization. Thomas W. Glover has included themes like Metaphase, Chromosome breakage, Chromosome Fragility and Aphidicolin in his Chromosomal fragile site study. The Chromosome Fragile Site study combines topics in areas such as Tumor suppressor gene, FHIT and Chromosome instability.
Thomas W. Glover mainly focuses on Genetics, Chromosomal fragile site, Molecular biology, Copy-number variation and Cancer research. His work in Genetics is not limited to one particular discipline; it also encompasses Bioinformatics. A large part of his Chromosomal fragile site studies is devoted to Chromosome Fragile Site.
His work in Chromosome Fragile Site covers topics such as Locus which are related to areas like Pathology. The concepts of his Molecular biology study are interwoven with issues in Breakpoint, Gene, Chromosomal translocation and Chromosome 3. His Copy-number variation study combines topics from a wide range of disciplines, such as Aphidicolin, DNA replication, Gene duplication, Penetrance and Gonadoblastoma.
His primary scientific interests are in Genetics, Copy-number variation, DNA replication, DNA repair and DNA repair protein XRCC4. His studies in Chromosome Fragile Site, Chromosome instability, Chromosomal fragile site and Chromosome breakage are all subfields of Genetics research. His Copy-number variation study is concerned with the field of Gene as a whole.
In his research, Mutagen and Breakpoint is intimately related to Genome, which falls under the overarching field of DNA replication. His research integrates issues of DNA polymerase and Proliferating cell nuclear antigen in his study of DNA repair. As part of his studies on Homology directed repair, he frequently links adjacent subjects like Molecular biology.
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Mutations in the p53 gene occur in diverse human tumour types
J M Nigro;S J Baker;A C Preisinger;J M Jessup.
Recurrent de novo point mutations in lamin A cause Hutchinson-Gilford progeria syndrome
Maria Eriksson;W. Ted Brown;Leslie B. Gordon;Leslie B. Gordon;Michael W. Glynn.
Isolation of a partial candidate gene for Menkes disease by positional cloning.
Julian F. B. Mercer;Janie Livingston;Bryan Hall;Jennifer A. Paynter.
Nature Genetics (1993)
Aberrant regulation of ras proteins in malignant tumour cells from type 1 neurofibromatosis patients.
Tanya N. Basu;David H. Gutmann;Jonathan A. Fletcher;Thomas W. Glover.
Chromosome fragile sites.
Sandra G. Durkin;Thomas W. Glover.
Annual Review of Genetics (2007)
Mutations in FOXC2 (MFH-1), a forkhead family transcription factor, are responsible for the hereditary lymphedema-distichiasis syndrome.
Jianming Fang;Susan L. Dagenais;Robert P. Erickson;Martin F. Arlt.
American Journal of Human Genetics (2000)
DNA polymerase α inhibition by aphidicolin induces gaps and breaks at common fragile sites in human chromosomes
Thomas W. Glover;Carol Berger;Jane Coyle;Barbara Echo.
Human Genetics (1984)
ATR Regulates Fragile Site Stability
Anne M. Casper;Paul Nghiem;Paul Nghiem;Martin F. Arlt;Thomas W. Glover.
A de novo Alu insertion results in neurofibromatosis type 1.
Margaret R. Wallace;Margaret R. Wallace;Lone B. Andersen;Ann M. Saulino;Paula E. Gregory.
Somatic deletion of the neurofibromatosis type 1 gene in a neurofibrosarcoma supports a tumour suppressor gene hypothesis.
Eric Legius;Eric Legius;Douglas A. Marchuk;Francis S. Collins;Thomas W. Glover.
Nature Genetics (1993)
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