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Lehrstuhl für Entwicklungsbiochemie
Ausgewählte Publikationen Nierentumoren

Recurrent intragenic rearrangements of EGFR and BRAF in soft tissue tumors of infants
Wegert, Vokuhl, Collord, Del Castillo Velasco-Herrera, Farndon, Guzzo, Jorgensen, Anderson, Slater, Duncan, Bausenwein, Streitenberger, Ziegler, Furtwängler, Graf, Stratton, Campbell, Jones, Koelsche, Pfister, Mifsud, Sebire, Sparber-Sauer, Koscielniak, Rosenwald, Gessler, Behjati. (2018) Nature Communicaions. DOI: 10.1038/s41467-018-04650-6

TP53 alterations in Wilms tumour represent progression events with strong intratumour heterogeneity that are closely linked but not limited to anaplasia.
Wegert, Vokuhl, Ziegler, Ernestus, Leuschner, Furtwängler, Graf, Gessler. (2014)J Pathol Clin Res. 3(4):234-248. doi: 10.1002/cjp2.77.

Gain of 1q As a Prognostic Biomarker in Wilms Tumors (WTs) Treated With Preoperative Chemotherapy in the International Society of Paediatric Oncology (SIOP) WT 2001 Trial: A SIOP Renal Tumours Biology Consortium Study.Chagtai, Zill, Dainese, Wegert, Savola, Popov, Mifsud, Vujanić, Sebire, Le Bouc, Ambros, Kager, O'Sullivan, Blaise, Bergeron, Mengelbier, Gisselsson, Kool, Tytgat, van den Heuvel-Eibrink, Graf, van Tinteren, Coulomb, Gessler, Williams, Pritchard-Jones. (2016). J Clin Oncol. 34(26):3195-203.

Mutually exclusive BCOR internal tandem duplications and YWHAE-NUTM2 fusions in clear cell sarcoma of kidney: not the full story.
Kenny, Bausenwein, Lazaro, Furtwängler, Gooskens, van den Heuvel Eibrink, Vokuhl, Leuschner, Graf, Gessler, O'Sullivan. (2016). J Pathol. 238(5):617-20.

Multiple mechanisms of MYCN dysregulation in Wilms tumour.
Williams, Chagtai, Alcaide-German, Apps, Wegert, Popov, Vujanic, van Tinteren, van den Heuvel-Eibrink, Kool, de Kraker, Gisselsson, Graf, Gessler, Pritchard-Jones. (2015). Oncotarget. 6(9):7232-43.

Mutations in the SIX1/2 Pathway and the DROSHA/DGCR8 miRNA Microprocessor Complex Underlie High-Risk Blastemal Type Wilms Tumors.
Wegert J, Ishaque N, Vardapour R, Georg C, Gu Z, Bieg M, Ziegler B, Bausenwein S, Nourkami N, Ludwig N, Keller A, Grimm C, Kneitz S, Williams RD, Chagtai T, Pritchard-Jones K, van Sluis P, Volckmann R, Koster J, Versteeg R, Acha T, O'Sullivan MJ, Bode PK, Niggli F, Tytgat GA, van Tinteren H, van den Heuvel-Eibrink MM, Meese E, Vokuhl C, Leuschner I, Graf N, Eils R, Pfister SM, Kool M, Gessler M, Gessler M (2015). Cancer Cell. 27:298.

Multiple mechanisms of MYCN dysregulation in Wilms tumour.
Williams RD, Chagtai T, Alcaide-German M, Apps J, Wegert J, Popov S, Vujanic G, van Tinteren H, van den Heuvel-Eibrink MM, Kool M, de Kraker J, Gisselsson D, Graf N, Gessler M, Pritchard-Jones K (2015). Oncotarget. 6(9):7232-43.

Characterization of primary Wilms tumor cultures as an in vitro model.
Wegert J, Bausenwein S, Roth S, Graf N, Geissinger E, Gessler M (2012). Genes Chromosomes Cancer. 51:92-104.

Retinoic acid pathway activity in Wilms tumors and characterization of biological responses in vitro.

Ausgewählte Publikationen Hey Proteine / Kardiovaskuläre Entwicklung

Hey bHLH Proteins Interact with a FBXO45 Containing SCF Ubiquitin Ligase Complex and Induce Its Translocation into the Nucleus.
Salat D, Winkler A, Urlaub H, Gessler M. (2015). PLoS One. 10(6):e0130288.

Mechanisms of epigenetic and cell-type specific regulation of Hey target genes in ES cells and cardiomyocytes.
Weber D, Heisig J, Kneitz S, Wolf E, Eilers M, Gessler M (2014). J Mol Cell Cardiol. 79: 79-88.

Hey bHLH transcription factors. (review)
Weber D, Wiese C, Gessler M (2014). Current topics in developmental biology. 110: 285-315.

Target gene analysis by microarrays and chromatin immunoprecipitation identifies HEY proteins as highly redundant bHLH repressors.
Heisig J, Weber D, Englberger E, Winkler A, Kneitz S, Sung WK, Wolf E, Eilers M, Wei CL, Gessler M (2012). PLoS Genet. 8:e1002728.

Combined loss of Hey1 and HeyL causes congenital heart defects because of impaired epithelial to mesenchymal transition.
Fischer A, Steidl C, Wagner TU, Lang E, Jakob PM, Friedl P, Knobeloch KP, Gessler M (2007). Circ Res. 100:856-63.

Hypoxia-mediated activation of Dll4-Notch-Hey2 signaling in endothelial progenitor cells and adoption of arterial cell fate.
Diez H, Fischer A, Winkler A, Hu CJ, Hatzopoulos AK, Breier G, Gessler M (2007). Exp Cell Res. 313:1-9.

The Notch target genes Hey1 and Hey2 are required for embryonic vascular development.
Fischer A, Schumacher N, Maier M, Sendtner M, Gessler M (2004). Genes Dev. 18:901-11.


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