@article{BarnekowGessler1986,
  author    = {Barnekow, Angelika and Gessler, Manfred},
  title     = {Activation of the pp60\(^{c-src}\) kinase during differentiation of monomyelocytic cells in vitro},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-59278},
  year      = {1986},
  abstract  = {Tbe proto-oncogene c-src, the cellular homolog of the Rous sarcoma virus (RSV) transforming gene v-src, is expressed in a tissue-specific and age-dependent manner. Its physiological function, although still unknown, appears to be more closely related to differentiation processes than to proliferation processes. To obtain more information about the physiological role of the c-src gene in cells, we have studied differentiation-dependent alterations using the human HL-60 leukaemia cell line as a model system. Induction of monocytic and granulocytic differentiation of HL-60 cells by 12-0-tetradecanoylphorbol-13-acetate (TPA) and dimethylsulfoxide (DMSO) is associated with an activation of the pp60<sup>c-src</sup> tyrosine kinase, but not with increased c-src gene expression. Control experiments exclude an interaction of TPA and DMSO themselves with the pp60<sup>c-src</sup> kinase.},
  subject      = {Biochemie},
  language  = {en}
}
@article{ChagtaiZillDaineseetal.2016,
  author    = {Chagtai, Tasnim and Zill, Christina and Dainese, Linda and Wegert, Jenny and Savola, Suvi and Popov, Sergey and Mifsud, William and Vujanic, Gordan and Sebire, Neil and Le Bouc, Yves and Ambros, Peter F. and Kager, Leo and O`Sullivan, Maureen J. and Blaise, Annick and Bergeron, Christophe and Holmquist Mengelbier, Linda and Gisselsson, David and Kool, Marcel and Tytgat, Godelieve A.M. and van den Heuvel-Eibrink, Marry M. and Graf, Norbert and van Tinteren, Harm and Coulomb, Aurore and Gessler, Manfred and Williams, Richard Dafydd and Pritchard-Jones, Kathy},
  title     = {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},
  series = {Journal of Clinical Oncology},
  volume    = {34},
  journal   = {Journal of Clinical Oncology},
  number    = {26},
  doi       = {10.1200/JCO.2015.66.0001},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-187478},
  pages     = {3195-3205},
  year      = {2016},
  abstract  = {Purpose Wilms tumor (WT) is the most common pediatric renal tumor. Treatment planning under International Society of Paediatric Oncology (SIOP) protocols is based on staging and histologic assessment of response to preoperative chemotherapy. Despite high overall survival (OS), many relapses occur in patients without specific risk factors, and many successfully treated patients are exposed to treatments with significant risks of late effects. To investigate whether molecular biomarkers could improve risk stratification, we assessed 1q status and other potential copy number biomarkers in a large WT series. Materials and Methods WT nephrectomy samples from 586 SIOP WT 2001 patients were analyzed using a multiplex ligation-dependent probe amplification (MLPA) assay that measured the copy number of 1q and other regions of interest. Results One hundred sixty-seven (28\%) of 586 WTs had 1q gain. Five-year event-free survival (EFS) was 75.0\% in patients with 1q gain (95\% CI, 68.5\% to 82.0\%) and 88.2\% in patients without gain (95\% CI, 85.0\% to 91.4\%). OS was 88.4\% with gain (95\% CI, 83.5\% to 93.6\%) and 94.4\% without gain (95\% CI, 92.1\% to 96.7\%). In univariable analysis, 1q gain was associated with poorer EFS (P<.001; hazard ratio, 2.33) and OS (P=.01; hazard ratio, 2.16). The association of 1q gain with poorer EFS retained significance in multivariable analysis adjusted for 1p and 16q loss, sex, stage, age, and histologic risk group. Gain of 1q remained associated with poorer EFS in tumor subsets limited to either intermediate-risk localized disease or nonanaplastic localized disease. Other notable aberrations associated with poorer EFS included MYCN gain and TP53 loss. Conclusion Gain of 1q is a potentially valuable prognostic biomarker in WT, in addition to histologic response to preoperative chemotherapy and tumor stage.},
  language  = {en}
}
@article{GesslerBarnekow1984,
  author    = {Gessler, Manfred and Barnekow, Angelika},
  title     = {Differential expression of the cellular oncogenes c-src and c-yes in embryonal and adult chicken tissues},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-59289},
  year      = {1984},
  abstract  = {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.},
  subject      = {Biochemie},
  language  = {en}
}
@article{GesslerBruns1989,
  author    = {Gessler, Manfred and Bruns, G. A. P.},
  title     = {A physical map around the WAGR complex on the short arm of chromosome 11},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-59246},
  year      = {1989},
  abstract  = {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.},
  subject      = {Biochemie},
  language  = {en}
}
@misc{GesslerBruns1993,
  author    = {Gessler, Manfred and Bruns, Gail A.},
  title     = {Sequence of the WT1 upstream region including the Wit-1 gene},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-30193},
  year      = {1993},
  abstract  = {No abstract available},
  language  = {en}
}
@article{GesslerBruns1988,
  author    = {Gessler, Manfred and Bruns, Gail A. P.},
  title     = {Molecular mapping and cloning of the breakpoints of a chromosome 11p14.1-p13 deletion associated with the AGR syndrome},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-59264},
  year      = {1988},
  abstract  = {Chromosome 11p13 is frequently rearranged in individuals with the WAGR syndrome (Wilms tumor, aniridia, genitourinary anomalies, and mental retardation) or parts of this syndrome. To map the cytogenetic aberrations molecularly, we screened DNA from cell Unes with known WAGR-related chromosome abnormalities for rearrangements with pulsed fleld gel (PFG) analysis using probes deleted from one chromosome 11 homolog of a WAGR patient. The first alteration was detected in a cell line from an individual with aniridia, genitourinary anomalies, mental retardation, and a deletion described as 11p14.1-p13. We have located one breakpoint close to probe HU11-164B and we have cloned both breakpoint sites as well as the junctional fragment. The breakpoints subdivide current intervals on the genetic map, and the probes for both sides will serve as important additional markers for a long-range restriction map of this region. Further characterization and sequencing of the breakpoints may yield insight into the mechanisms by which these deletions occur.},
  subject      = {Biochemie},
  language  = {en}
}
@article{GesslerGrupeGrzeschiketal.1992,
  author    = {Gessler, Manfred and Grupe, Andrew and Grzeschik, Karl-Heinz and Pongs, Olaf},
  title     = {The potassium channel gene HK1 maps to human chromosome 11p14.1, close to the FSHB gene},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-59184},
  year      = {1992},
  abstract  = {Transiently activating (A-type) potassium (K) channels are important regulators of action potential and action potential firing frequencies. HK1 designates the firsthuman cDNA that is highly homologous to the rat RCK4 cDNA that codes for an A-type K-channel. The HK1 channel is expressed in heart. By somatic cell hybrid analysis, the HK1 gene has been assigned to human chromosome 11p13-pl4, the WAGR deletion region (Wilms tumor, aniridia, genito-urinary abnormalities and mental retardation). Subsequent pulsed field gel (PFG) analysis and comparison with the well-established PFG map of this region localized the gene to 11p14, 200-600 kb telomeric to the FSHB gene.},
  subject      = {Biochemie},
  language  = {en}
}
@article{GesslerHameisterHenryetal.1990,
  author    = {Gessler, Manfred and Hameister, H. and Henry, I. and Junien, C. and Braun, T. and Arnold, H. H.},
  title     = {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},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-59221},
  year      = {1990},
  abstract  = {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.},
  subject      = {Biochemie},
  language  = {en}
}
@article{GesslerKonigMooreetal.1993,
  author    = {Gessler, Manfred and Konig, Anja and Moore, Jay and Qualman, Steven and Arden, Karen and Cavenee, Webster and Bruns, Gail},
  title     = {Homozygous inactivation of WTI in a Wilms' tumor associated with the WAGR syndrome},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-59146},
  year      = {1993},
  abstract  = {Wilms' tumor is a childhood nephroblastoma that is postulated to arise through the inactivation of a tumor suppressor gene by a two-hit mechanism. A candidate II p 13 Wilms' tumor gene, WTI, has been cloned and shown to encode a zinc finger protein. Patients with the WAGR syndrome (Wilms' tumor, aniridia, genitourinary abnormalities, and mental retardation) have a high risk of developing Wilms' tumor and they carry constitutional deletions of one chromosome II allele encompassing the WTI gene. Analysis of the remaining WTI allele in a Wilms' tumor from a WAGR patient revealed the deletion of a single nucleotide in exon 7. This mutation likely played a key role in tumor formation, as it prevents translation of the DNA-binding zinc finger domain that is essential for the function of the WTI polypeptide as a transcriptional regulator.},
  subject      = {Biochemie},
  language  = {en}
}
@article{GesslerKoenigArdenetal.1994,
  author    = {Gessler, Manfred and K{\"o}nig, A. and Arden, K. and Grundy, P. and Orkin, S. H. and Sallan, S. and Peters, C. and Ruyle, S. and Mandell, J. and Li, F. and Cavenee, W. and Bruns, G. A.},
  title     = {Infrequent mutation of the WT1 gene in 77 Wilms' Tumors},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-34308},
  year      = {1994},
  abstract  = {Homozygous deletions in Wilms' tumor DNA have been a key step in the identification and isolation of the WTI gene. Several additional loci are also postulated to contribute to Wilms' tumor formation. To assess the frequency of WTI alterations we have analyzed the WTI locus in a panel of 77 Wilms' tumors. Eight tumors showed evidence for large deletions of several hundred or thousand kilobasepairs of DNA, some of which were also cytogenetically detected. Additional intragenic mutations were detected using more sensitive SSCP analyses to scan all 10 WTI exons. Most of these result in premature stop codons or missense mutations that inactivate the remaining WTI allele. The overall frequency of WTI alterations detected with these methods is less than 15\%. While some mutations may not be detectable with the methods employed, our results suggest that direct alterations of the WTI gene are present in only a small fraction of Wilms' tumors. Thus, mutations at other Wilms' tumor loci or disturbance of interactions between these genes likely play an important role in Wilms' tumor development.},
  language  = {en}
}