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Manfred Gessler

Researcher at University of Würzburg

Publications -  166
Citations -  15165

Manfred Gessler is an academic researcher from University of Würzburg. The author has contributed to research in topics: Wilms' tumor & Gene. The author has an hindex of 56, co-authored 163 publications receiving 13531 citations. Previous affiliations of Manfred Gessler include Boston Children's Hospital & University of Marburg.

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Homozygous deletion in Wilms tumours of a zinc-finger gene identified by chromosome jumping

TL;DR: YTOGENETIC analysis has identified chromosome Ilpl3 as the smallest overlap region for deletions found in individuals with WAGR syndrome, which includes Wilms tumour, anirida, genito-urinary abnormalities and mental retardation.
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A Murine Model of Holt-Oram Syndrome Defines Roles of the T-Box Transcription Factor Tbx5 in Cardiogenesis and Disease

TL;DR: These studies provide one potential explanation for Holt-Oram syndrome conduction system defects, suggest mechanisms for intrafamilial phenotypic variability, and account for related cardiac malformations caused by other transcription factor mutations.
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The landscape of genomic alterations across childhood cancers

Susanne Gröbner, +185 more
- 15 Mar 2018 - 
TL;DR: The data suggest that 7–8% of the children in this cohort carry an unambiguous predisposing germline variant and that nearly 50% of paediatric neoplasms harbour a potentially druggable event, which is highly relevant for the design of future clinical trials.
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The Notch target genes Hey1 and Hey2 are required for embryonic vascular development

TL;DR: Remaining large arteries in both Notch1 and Hey1/Hey2 knockout mice fail to express the arterial endothelial markers CD44, neuropilin1, and ephrin-B2, which indicates that Hey1 /Hey2 are essential transducers of Notch signals in cardiovascular development that may mediate arterial cell fate decision.
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GLI3 zinc-finger gene interrupted by translocations in Greig syndrome families

TL;DR: The results indicate that mutations disturbing normal GLI3 expression may have a causative role in GCPS and three balanced translocations associated with GCPS are shown.