It was the aim of this study to examine the IGF-II locus and its surrounding chromosomal environment for such lesions in a large number of WBS patients.
In Wiedemann-Beckwith syndrome (WBS) a putative disease gene resides at the tip of the short arm of chromosome 11 in the region of the insulin growth like factor II (IGF-II) gene.
The WBS gene has been assigned to the locus 11p15 and there appear to be several different genetic mechanisms involving this locus which all give rise to WBS.
The WBS gene has been assigned to the locus 11p15 and there appear to be several different genetic mechanisms involving this locus which all give rise to WBS.
The WBS gene has been assigned to the locus 11p15 and there appear to be several different genetic mechanisms involving this locus which all give rise to WBS.
The WBS gene has been assigned to the locus 11p15 and there appear to be several different genetic mechanisms involving this locus which all give rise to WBS.
The locus for the human parathyroid hormone gene (PTH) was assigned to a region proximal to 11p15.4 using restriction fragment length polymorphisms and gene dose studies performed on a patient with the Beckwith-Wiedemann syndrome accompanied with a chromosome abnormality [46,XX,-14,+der(14),t(14;11)(q32.3;p15.3)pat].
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 11p13 nor with the loss of the heterozygosity region at 11p15.5 related to the Beckwith-Wiedemann syndrome.
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 11p13 nor with the loss of the heterozygosity region at 11p15.5 related to the Beckwith-Wiedemann syndrome.
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 11p13 nor with the loss of the heterozygosity region at 11p15.5 related to the Beckwith-Wiedemann syndrome.
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 11p13 nor with the loss of the heterozygosity region at 11p15.5 related to the Beckwith-Wiedemann syndrome.
Molecular characterization of Beckwith-Wiedemann syndrome (BWS) patients with partial duplication of chromosome 11p excludes the gene MYOD1 from the BWS region.
In support of this hypothesis, we have recently reported generation of homozygosity for the c-Ha-ras-1 protooncogene in an adrenal adenoma from an adult BWS patient.