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Henri J L M Timmers

Researcher at Radboud University Nijmegen

Publications -  174
Citations -  9567

Henri J L M Timmers is an academic researcher from Radboud University Nijmegen. The author has contributed to research in topics: Paraganglioma & Pheochromocytoma. The author has an hindex of 44, co-authored 150 publications receiving 6955 citations. Previous affiliations of Henri J L M Timmers include University Medical Center Groningen & Radboud University Nijmegen Medical Centre.

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Cell-of-Origin Patterns Dominate the Molecular Classification of 10,000 Tumors from 33 Types of Cancer.

Katherine A Hoadley, +738 more
- 05 Apr 2018 - 
TL;DR: Molecular similarities among histologically or anatomically related cancer types provide a basis for focused pan-cancer analyses, such as pan-gastrointestinal, Pan-gynecological, pan-kidney, and pan-squamous cancers, and those related by stemness features, which may inform strategies for future therapeutic development.
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Genomic and Functional Approaches to Understanding Cancer Aneuploidy

Alison M. Taylor, +732 more
- 09 Apr 2018 - 
TL;DR: The genomic and phenotypic correlates of cancer aneuploidy are defined and genome engineering is applied to delete 3p in lung cells, causing decreased proliferation rescued in part by chromosome 3 duplication.
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MAX Mutations Cause Hereditary and Sporadic Pheochromocytoma and Paraganglioma

Nelly Burnichon, +60 more
- 15 May 2012 - 
TL;DR: Germline mutations in MAX are responsible for 1.12% of PCC/PGL in patients without evidence of other known mutations and should be considered in the genetic work-up of these patients.
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Measurements of Plasma Methoxytyramine, Normetanephrine, and Metanephrine as Discriminators of Different Hereditary Forms of Pheochromocytoma

Graeme Eisenhofer, +11 more
- 01 Mar 2011 - 
TL;DR: The distinct patterns of plasma catecholamine O-methylated metabolites in patients with hereditary pheochromocytoma provide an easily used tool to guide cost-effective genotyping of underlying disease-causing mutations.
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Clinical presentations, biochemical phenotypes, and genotype-phenotype correlations in patients with succinate dehydrogenase subunit B-associated pheochromocytomas and paragangliomas.

Henri J L M Timmers, +7 more
- 01 Mar 2007 - 
TL;DR: SDHB-related PGL often presents as apparently sporadic PGL with symptoms related to tumor mass effect rather than to catecholamine excess, whereas 10% of tumors are biochemically silent, and the clinical expression of these tumors cannot be predicted by the genotype.