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MYCN and MAX alterations in Wilms tumor and identification of novel N-MYC interaction partners as biomarker candidates (2021)
Martín, Ovidio Jiménez ; Schlosser, Andreas ; Furtwängler, Rhoikos ; Wegert, Jenny ; Gessler, Manfred
Background Wilms tumor (WT) is the most common renal tumor in childhood. Among others, MYCN copy number gain and MYCN P44L and MAX R60Q mutations have been identified in WT. MYCN encodes a transcription factor that requires dimerization with MAX to activate transcription of numerous target genes. MYCN gain has been associated with adverse prognosis in different childhood tumors including WT. The MYCN P44L and MAX R60Q mutations, located in either the transactivating or basic helix-loop-helix domain, respectively, are predicted to be damaging by different pathogenicity prediction tools, but the functional consequences remain to be characterized. Methods We screened a large cohort of unselected WTs for MYCN and MAX alterations. Wild-type and mutant protein function were characterized biochemically, and we analyzed the N-MYC protein interactome by mass spectrometric analysis of N-MYC containing protein complexes. Results Mutation screening revealed mutation frequencies of 3% for MYCN P44L and 0.9% for MAX R60Q that are associated with a higher risk of relapse. Biochemical characterization identified a reduced transcriptional activation potential for MAX R60Q, while the MYCN P44L mutation did not change activation potential or protein stability. The protein interactome of N-MYC-P44L was likewise not altered as shown by mass spectrometric analyses of purified N-MYC complexes. Nevertheless, we could identify a number of novel N-MYC partner proteins, e.g. PEG10, YEATS2, FOXK1, CBLL1 and MCRS1, whose expression is correlated with MYCN in WT samples and several of these are known for their own oncogenic potential. Conclusions The strongly elevated risk of relapse associated with mutant MYCN and MAX or elevated MYCN expression corroborates their role in WT oncogenesis. Together with the newly identified co-expressed interactors they expand the range of potential biomarkers for WT stratification and targeting, especially for high-risk WT.
Differential expression of the cellular oncogenes c-src and c-yes in embryonal and adult chicken tissues (1984)
Gessler, Manfred ; Barnekow, Angelika
The cellular onc-genes c-src and c-yes are expressed very differently during chicken embryonic development. The c-src mRNA and its translational product are detectable at high levels in brain extracts of chicken embryos and adult chickens, whereas muscle extracts show an age-dependent decrease in the amounts of c-src-specific mRNA and pp60<sup>c-src</sup> kinase activity. In contrast, the Ievels of c-yes mRNA in brain, heart, and muscle are relatively low in early embryonic stages and increase later on to values comparable to those found for liver, while in adult animals the pattern of c-yes expression is similar to that of the c-src gene. From the close correlation between the Ievels of pp60<sup>c-src</sup>, its enzymatic activity, and its corresponding mRNA at a given stage of development and in given tissues, it appears that the expression of pp60<sup>c-src</sup> is primarily controlled at the level of transcription. It is suggested that because of the different patterns of expression, the two cellular oncogenes, c-src and c-yes, play different roles in cell proliferation during early embryonic stages as weil as in ensuing differentiation processes.
A somatic cell hybrid panel and DNA probes for physical mapping of human chromosome 7p (1991)
Vortkamp, A. ; Thias, U. ; Gessler, Manfred ; Rosenkranz, W. ; Kroisel, P. M. ; Tommerup, N. ; Kruger, G. ; Gotz, J. ; Pelz, L. ; Grzeschik, Karl-Heinz
No abstract available
The human MyoD1 (MYF3) gene maps on the short arm of chromosome 11 but is not associated with the WAGR locus or the region for the Beckwith-Wiedemann syndrome (1990)
Gessler, Manfred ; Hameister, H. ; Henry, I. ; Junien, C. ; Braun, T. ; Arnold, H. H.
The human gene encoding the myogenic determination factor myf3 (mouse MyoD1) has been mapped to the short arm of chromosome 11. Analysis of several somatic cell hybrids containing various derivatives with deletions or translocations revealed that the human MyoD (MYF3) gene is not associated with the WAGR locus at chromosomal band 11pl3 nor with the loss of the heterozygosity region at 11p15.5 related to the Beckwith-Wiedemann syndrome. Subregional mapping by in situ hybridization with an myf3 specific probe shows that the gene resides at the chromosomal band llp14, possibly at llp14.3.
Role for the Wilms tumor gene in genital development? (1990)
van Heyningen, V. ; Bickmore, W. A. ; Seawright, A. ; Fletcher, J. M. ; Maule, J. ; Fekete, G. ; Gessler, Manfred ; Bruns, G. A. ; Huerre-Jeanpierre, C. ; Junien, C.
No abstract available
A physical map around the WAGR complex on the short arm of chromosome 11 (1989)
Gessler, Manfred ; Bruns, G. A. P.
A long-range restriction map of part of the short arm of ehromosome 11 including the WAGR region has been constructed using pulsed-field gel electrophoresis and a number of infrequently cutting restriction enzymes. A total of 15.4 Mbp has been mapped in detall, extending from proximal 11p14 to the distal part of 11p12. The map localizes 35 different DNA probes and reveals at least nine areas with features eharaeteristle of BTF islands, some of which may be candidates for the different loci underlying the phenotype of the WAGR syndrome. This map will furthermore allow screening of DNA from individuals with WAGR-related phenotypes and from Wilms tumors for associated chromosomal rearrangements.
GLI3 zinc-finger gene interrupted by translocations in Greig syndrome families (1991)
Vortkamp, Andrea ; Gessler, Manfred ; Grzeschik, Karl-Heinz
No abstract available
Homozygous deletion in Wilms tumours of a zinc-finger gene identified by chromosome jumping (1990)
Gessler, Manfred ; Poustka, Annemarie ; Cavenee, Webster ; Neve, Rachael L. ; Orkin, Stuart H. ; Bruns, Gail A.
No abstract available
Sequence of the WT1 upstream region including the Wit-1 gene (1993)
Gessler, Manfred ; Bruns, Gail A.
No abstract available
Deletion of GLI3 supports the homology of the human Greig cephalopolysyndactyly syndrome (GCPS) and the mouse mutant extra toes (Xt) (1992)
Vortkamp, Andrea ; Franz, Thomas ; Gessler, Manfred ; Grzeschik, Karl-Heinz
No abstract available
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