A novel member of the WD-repeat gene family, WDR11, maps to the 10q26 region and is disrupted by a chromosome translocation in human glioblastoma cells

WAVE3, an actin-polymerization gene, is truncated and inactivated as a result of a constitutional t(1;13)(q21;q12) chromosome translocation in a patient with ganglioneuroblastoma

“…Since only 1 -2% of the genome codes for genes it is unlikely that this is a random event that involves a coding region by chance. In fact, all of the constitutional chromosome translocation breakpoints we have described to date (Mitchell and Cowell, 1989;Roberts et al, 1998b) as well as tumor-specific translocations (Still and Cowell, 1998;Chernova et al, 1998Chernova et al, , 2001, have involved breakpoints within the coding regions of genes, often on both sides of the breakpoints. From the molecular evidence it seems likely that WAVE3 is inactivated as a result of this translocation but, since it is not normally expressed in hematopoietic cells, we cannot verify this using the only tissue we have available from patient DG, which is a lymphoblastoid cell line.…”

Thyroid cancer GWAS identifies 10q26.12 and 6q14.1 as novel susceptibility loci and reveals genetic heterogeneity among populations

“…Therefore, the disruption of the WDR11 regulation axis may represent a potentially transforming molecular mechanism in DTC etiology. Of note, this locus has been found to be disrupted in cancer by translocation events, 35 and proposed to have a tumor suppressor role. The eQTL analysis Genevar tool (http://www.sanger.ac.uk/resources/software/genevar/) found a significant association between rs10788123 and WDR11 expression in lymphocytes.…”

Identification of novel genomic markers related to progression to glioblastoma through genomic profiling of 25 primary glioma cell lines

“…As shown in Figure 2, three distinct areas emerged in all cell lines by using this algorithm. The three areas on chromosome 10 encompass several candidate tumor suppressor genes, including KLF6, LGI1, PTEN, DMBT1, WDR11 and MXI1, already known to be indeed associated with glioma progression (Chernova et al, 2001;Manni et al, 2002;Kohler et al, 2004). One region spans from 10pter to 10p14, with a peak between clones RP11-89B19 and RP11-80D10 at 10p15.3 telomerically to KLF6; only the ADARB2 gene, a brain-specific adenosine deaminase, resides within this interval.…”