SDH mutations establish a hypermethylator phenotype in paraganglioma.

By E. Letouzé, Cosimo Martinelli, Céline Loriot, N. Burnichon, N. Abermil, C. Ottolenghi, M. Janin, M. Ménara, A. T. Nguyen, P. Bénit and 8 more. Cancer Cell, 2013

729 citations recorded by the source corpus.

Subfields: Cancer Research, Endocrinology, Diabetes and Metabolism, Surgery

View Paper: https://www.semanticscholar.org/paper/12ff63634482848e635a81bd0e943c6b9634ac9a

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cancer Research

1. D. Y. Gui
2. Alba Luengo
3. M. V. Vander Heiden
4. A. Gimenez-Roqueplo
5. Karel Pacak
6. Ralph J. Deberardinis
7. Craig B. Thompson
8. C. V. Dang

In Endocrinology, Diabetes and Metabolism

1. A. Gimenez-Roqueplo
2. Karel Pacak
3. M. V. Vander Heiden

In Surgery

1. A. Gimenez-Roqueplo
2. Karel Pacak
3. M. V. Vander Heiden

Citations in the corpus

• Comprehensive molecular characterization of pheochromocytoma and paraganglioma (2017, result): “…subtype also contained two of the three unsupervised clusters of DNA methylation (hypermethylated and intermediate), confirming earlier reports (Letouze et al., 2013), with most SDHB and SDHD germline mutations occurring in the hypermethylated subtype and nearly all VHL and EPAS1mutations in…”
• Targeting Metabolism for Cancer Therapy (2017, background): “Familial cancer syndromes caused by fumarate hydratase (FH) or succinate dehydrogenase (SDH) deletion suggest that these TCA enzymes can behave as classical tumor suppressors.”