Physical mapping of 3 candidate tumor suppressor genes relative to Beckwith-Wiedemann syndrome associated chromosomal breakpoints at 11p15.3

Redeker, E.; Alders, Mariëlle; Hoovers, J. M. N.; Richard, Charles W.; Westerveld, A.; Mannens, Marcel

doi:10.1159/000133917

Cited by 19 publications

(14 citation statements)

References 7 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Current maps in the databases are still controversial on the order of 11p15.3 genes. The mapping data presented here settles the debate whether LMO1 is more centromeric compared to WEE1 as proposed by Redeker et al (1995), or more telomeric as proposed by Higgins et al (1994) and confirmed by our results.…”

Section: Resultssupporting

confidence: 89%

“…It probably functions as a transcriptional regulator because of its conserved cysteine-rich region homologous to the LIM domains (Boehm et al, 1990). Although all three genes are involved in important cellular functions and are located in the BWSCR3, none of the genes was directly implicated in BWS (Redeker et al, 1995). Furthermore, 11p allelotyping in different lung cancer cell lines revealed frequent allele loss in the discussed 11p15.3 region, with exception of the ST5 gene (Bepler and Koehler, 1995), supporting the location of a potential tumor suppressor region in 11p15.3.…”

confidence: 90%

“…Physical mapping determined the critical regions on 11p15.5 (BWSCR1), 11p15.4 (BWSCR2) and 11p15.3 (BWSCR3). The latter region ranges from D11S738 to D11S778 and contains at least three known tumor suppressor genes WEE1, ST5 and LMO1 (Redeker et al, 1995). WEE1, the human homologue of yeast wee1+, encodes a mitotic inhibitor functioning at the G 2 to M transition in the cell cycle (Igarashi et al, 1991).…”

confidence: 99%

See 2 more Smart Citations

Comparative architectural aspects of regions of conserved synteny on human chromosome 11p15.3 and mouse chromosome 7 (including genes WEE1 and LMO1)

Cichutek

Brueckmann²,

Seipel³

et al. 2001

Cytogenet Genome Res

View full text Add to dashboard Cite

Human chromosome 11p15.3 is associated with chromosome aberrations in the Beckwith Wiedemann Syndrome and implicated in the pathogenesis of different tumor types including lung cancer and leukemias. To date, only single tumor-relevant genes with linkage to this region (e.g. LMO1) have been found suggesting that this region may harbor additional potential disease associated genes. Although this genomic area has been studied for years, the exact order of genes/chromosome markers between D11S572 and the WEE1 gene locus remained unclear. Using the FISH technique and PAC clones of the flanking markers we determined the order of the genomic markers. Based on these clones we established a PAC contig of the respective region. To analyse the chromosome area in detail the synteny of the orthologous region on distal mouse chromosome 7 was determined and a corresponding mouse clone contig established, proving the conserved order of the genes and markers in both species: “cen–WEE1–D11S2043–ZNF143–RANBP7–CEGF1– ST5–D11S932–LMO1–D11S572–TUB–tel”, with inverted order of the murine genes with respect to the telomere/centromere orientation. The region covered by these contigs comprises roughly 1.6 MB in human as well as in mouse. The genomic sequence of the two subregions (around WEE1 and LMO1) in both species was determined using a shotgun sequencing strategy. Comparative sequence analysis techniques demonstrate that the content of repetitive elements seems to decline from centromere to telomere (52.6% to 34.5%) in human and in the corresponding murine region from telomere to centromere (41.87% to 27.82%). Genomic organisation of the regions around WEE1 and LMO1 was conserved, although the length of gene regions varied between the species in an unpredictable ratio. CpG islands were found conserved in putative promoter regions of the known genes but also in regions which so far have not been described as harboring expressed sequences.

show abstract

Section: Resultssupporting

confidence: 89%

confidence: 90%

confidence: 99%

See 1 more Smart Citation

Comparative architectural aspects of regions of conserved synteny on human chromosome 11p15.3 and mouse chromosome 7 (including genes WEE1 and LMO1)

Cichutek

Brueckmann²,

Seipel³

et al. 2001

Cytogenet Genome Res

View full text Add to dashboard Cite

show abstract

“…The CTR9 gene has been localized to chromosome 11p15 (Figure 3d). The 11p15.3 locus contains chromosomal aberrations associated with the pathogenesis of different tumor types including lung cancer and leukemia (Redeker et al, 1995). Interestingly, the Ctr9 gene locus is found to be deleted in pancreatic cancer (Bashyam et al, 2005) (Table 3).…”

Section: Leo1: Interacts With B-catenin During Wnt Signaling Cascadementioning

confidence: 99%

Human RNA polymerase II-associated factor complex: dysregulation in cancer

et al. 2007

View full text Add to dashboard Cite

Genetic instabilities are believed to be one of the major causes of developing a cancer phenotype in humans. During the progression of cancer, aberrant expression of proteins, either owing to genetic (amplification, mutation and deletion) or epigenetic modifications (DNA methylation and histone deacetylation), contributes in different ways to the development of cancer. By differential screening analysis, an amplification of the 19q13 locus containing a novel pancreatic differentiation 2 (PD2) gene was identified. PD2 is the human homolog of the yeast RNA polymerase II-associated factor 1 (yPaf1) and is part of the human RNA polymerase II-associated factor (hPAF) complex. hPAF is comprised of five subunits that include PD2/hPaf1, parafibromin, hLeo1, hCtr9 and hSki8. This multifaceted complex was first identified in yeast (yPAF) and subsequently in Drosophila and human. Recent advances in the study on PAF have revealed various functions of the complex in human, which are similar to yPAF, including efficient transcription elongation, mRNA quality control and cell-cycle regulation. Although the precise function of this complex in cancer is not clearly known, some of its subunits have been linked to a malignant phenotype. Its core subunit, PD2/hPaf1, is amplified and overexpressed in many cancers. Further, an overexpression of PD2/hPaf1 results in the induction of a transformed phenotype, suggesting its possible involvement in tumorigenesis. The parafibromin subunit of the hPAF complex is a product of the HRPT-2 (hereditary hyperparathyroidism type 2) tumor suppressor gene, which is mutated in the germ line of hyperparathyroidismjaw tumor patients. This review focuses on the functions of the PAF complex and its individual subunits, the interaction of the subunits with each other and/or with other molecules, and dysregulation of the complex, providing an insight into its potential involvement in the development of cancer.

show abstract

“…All tumor components were analyzed for LOH at the polymorphic markers DllS922, DllS988, and TH (Tyrosine Hydroxylase), which lie within or near the boundaries of a previously identified minimal region of overlap at 1 lp15.5, 4 ' 6 and DllS837, which maps within a group of potentially growth regulatory genes at 1 lp 15.3, a region that might represent a distinct SRO in breast cancer. [25][26][27] Six additional markers taken from the Genethon panel were used to characterize the SRO in cases with LOH. The order assigned (Fig.…”

Section: Methodsmentioning

confidence: 99%

Characterization of Breast Cancer Progression by Analysis of Genetic Markers.

Lichy¹

1996

View full text Add to dashboard Cite

Physical mapping of 3 candidate tumor suppressor genes relative to Beckwith-Wiedemann syndrome associated chromosomal breakpoints at 11p15.3

Cited by 19 publications

References 7 publications

Comparative architectural aspects of regions of conserved synteny on human chromosome 11p15.3 and mouse chromosome 7 (including genes WEE1 and LMO1)

Comparative architectural aspects of regions of conserved synteny on human chromosome 11p15.3 and mouse chromosome 7 (including genes WEE1 and LMO1)

Human RNA polymerase II-associated factor complex: dysregulation in cancer

Characterization of Breast Cancer Progression by Analysis of Genetic Markers.

Contact Info

Product

Resources

About