Anke van den Berg
prof. dr.
I work as a clinical molecular biologist in the department of Pathology. In this function I supervise and implement advanced molecular diagnostic techniques. Within my research line, I focus on the molecular pathogenesis of B-cell Hodgkin and non-Hodgkin lymphoma. The specific fields of interest are genomic aberrations, genetic susceptibility, and the role of small and long noncoding RNAs. I have several international collaborations and am PI and co-PI in various projects.
Report of the Sixth International Workshop on Human Chromosome 3 Mapping 1995 – Held on 23-24 October 1995 – Minneapolis, Minnesota
SL Naylor, B Carritt, C Boileau, C Beroud, C Alexander, P Allderdice, A Alimov, T Ashworth, J Bonifas, P Bugert, CHCM Buys, MA Chipperfield, G Deng, H Drabkin, RM Gemmill, M Grompe, T Joensuu, A Jonasdottir, R Gizatullin, L KroisRJ Leach, ST Lott, A Killary, L Messiaen, P OConnell, B Opalka, R Plaetke, EM Sankila, DI Smith, T Strachen, Anke van den Berg, E Zabarovsky
Ordering of polymorphic markers in the chromosome region 3p21
Starting from five markers, with a well-defined order from distal to proximal 3p21, nine other markers could be inserted in this 3p21 map. Five were precisely mapped genetically. The other markers were ordered by FISH and/or deletion hybrid mapping. The overall 3p21 order from distal to proximal is as follows: D3S1298-D3S1260-(D3S966, D3S1448 (= D3S1449))-D3S1029-D3S32-D3S643-D3F15S2 -D3S2968-D3S1235-D3S1289-D3S1447-D3S1295.
Anke van den Berg, RF Kooy, MMF Hulsbeek, D deJong, K Kok, AY vanderVeen, CHCM Buys
Major role for a 3p21 region and lack of involvement of the t(3;8) breakpoint region in the development of renal cell carcinoma suggested by loss of heterozygosity analysis
In a loss of heterozygosity analysis of 3p, we examined 44 sporadic cases of renal cell carcinoma (RCC) and matched normal tissue with 18 markers distributed over the whole p-arm. The majority of these markers clustered in three regions that have been suggested to be involved in the development of RCC, namely the p25 region, where the von Hippel Lindau (VHL) gene is located; the p21 region, which has been identified as a common region of overlap (SRO) of heterozygous deletions; and the p14 region, which is the...
Anke van den Berg, MMF Hulsbeek, D deJong, K Kok, PMJF Veldhuis, J Roche, CHCM Buys
DEFINING THE POSITION OF THE BREAKPOINT OF THE CONSTITUTIONAL T(3-6) OCCURRING IN A FAMILY WITH RENAL-CELL CARCINOMA
In a family with a constitutional translocation t(3;6), the oldest member carrying the translocation had developed multiple nonpapillary renal cell carcinomas (RCCs). The translocation breakpoint was positioned between 3p13 and 3p14.1. This is close to the region in which a t(3;8) breakpoint has been reported in a family with hereditary RCC. We defined the location of the t(3;6) and t(3;8) breakpoints by fluorescence in situ hybridization (FISH) analysis with yeast artificial chromosomes (YACs) from the 3p14-13 region. Both interphase nuclei and metaphase cells from translocation-carrying members of both...
Anke van den Berg, A VANDERVEEN, M HULSBEEK, K KOK, G KOVACS, R GEMMILL, H DRABKIN, C BUYS
SOMATIC MUTATIONS OF THE VON HIPPEL-LINDAU DISEASE TUMOR-SUPPRESSOR GENE IN NONFAMILIAL CLEAR-CELL RENAL-CARCINOMA
Loss of heterozygosity (LOH) studies have suggested that somatic mutations of a tumour suppressor gene or genes on chromosome 3p are a critical event in the pathogenesis of non-familial renal cell carcinoma (RCC). Germline mutations of the von Hippel – Lindau (VHL) disease gene predispose to early onset and multifocal clear cell renal cell carcinoma, and the mechanism of tumorigenesis in VHL disease is consistent with a one-hit mutation model. To investigate the role of somatic VHL gene mutations in non-famitial RCC, we analysed 99 primary RCC for...
K FOSTER, A PROWSE, Anke van den Berg, S FLEMING, MMF HULSBEEK, PA CROSSEY, FM RICHARDS, P CAIRNS, MA FERGUSONSMITH, CHCM BUYS, ER MAHER