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  • 1
    Keywords: carcinoma ; POPULATION ; GENE-EXPRESSION ; MARKER ; OVARIAN-CANCER ; PROSTATE-CANCER ; METAANALYSIS ; susceptibility loci ; GENOME-WIDE ASSOCIATION ; PLATFORM
    Abstract: Common variants in the hepatocyte nuclear factor 1 homeobox B (HNF1B) gene are associated with the risk of Type II diabetes and multiple cancers. Evidence to date indicates that cancer risk may be mediated via genetic or epigenetic effects on HNF1B gene expression. We previously found single-nucleotide polymorphisms (SNPs) at the HNF1B locus to be associated with endometrial cancer, and now report extensive fine-mapping and in silico and laboratory analyses of this locus. Analysis of 1184 genotyped and imputed SNPs in 6608 Caucasian cases and 37 925 controls, and 895 Asian cases and 1968 controls, revealed the best signal of association for SNP rs11263763 (P = 8.4 x 10(-14), odds ratio = 0.86, 95% confidence interval = 0.82-0.89), located within HNF1B intron 1. Haplotype analysis and conditional analyses provide no evidence of further independent endometrial cancer risk variants at this locus. SNP rs11263763 genotype was associated with HNF1B mRNA expression but not with HNF1B methylation in endometrial tumor samples from The Cancer Genome Atlas. Genetic analyses prioritized rs11263763 and four other SNPs in high-to-moderate linkage disequilibrium as the most likely causal SNPs. Three of these SNPs map to the extended HNF1B promoter based on chromatin marks extending from the minimal promoter region. Reporter assays demonstrated that this extended region reduces activity in combination with the minimal HNF1B promoter, and that the minor alleles of rs11263763 or rs8064454 are associated with decreased HNF1B promoter activity. Our findings provide evidence for a single signal associated with endometrial cancer risk at the HNF1B locus, and that risk is likely mediated via altered HNF1B gene expression.
    Type of Publication: Journal article published
    PubMed ID: 25378557
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  • 2
    Keywords: APOPTOSIS ; CANCER ; Germany ; THERAPY ; imaging ; TOOL ; GENE-EXPRESSION ; TUMORS ; computed tomography ; MICE ; DYNAMICS ; MR ; MRI ; BIOLOGY ; MOLECULAR-BIOLOGY ; MAGNETIC-RESONANCE ; molecular imaging ; magnetic resonance imaging ; IN-SITU ; positron emission tomography ; POSITRON-EMISSION-TOMOGRAPHY ; tomography ; SPECT ; COMPUTED-TOMOGRAPHY ; PET ; ultrasound ; SINGLE ; molecular biology ; molecular ; SOFTWARE ; genomics ; REPORTER GENE ; development ; PART ; technique ; magnetic resonance (MR) ; in vivo diagnostics ; IRON-OXIDE PARTICLES ; NANOPARTICLES ; near IR fluorescence imaging (NIRF) ; optical imaging ; positron emission tomography (PET) ; single photon emission computed tomography (SPECT) ; small-animal imaging (SAI) ; targeted contrast agents ; TELOMERASE ACTIVITY ; USA
    Abstract: Molecular imaging, as applied to clinical practice today, is in its early stages. Encouraging advances achieved in clinical positron emission tomography (PET) and small-animal imaging indicate that this technique is evolving into an indispensable diagnostic. c tool. When employed with complementary morphological imaging procedures, molecular imaging results in substantial diagnostic capability. It will enable the physician to unveil topographic biochemistry in situ and reduce invasive testing. While this is at least in part futuristic, it is clear already today that a comprehensive set of imaging modalities will be required. Imaging modalities most appropriate for molecular imaging are PET single photon emission computed tomography (SPECT), magnetic resonance imaging (MRI), optical imaging, and ultrasound. The foundation for advances in molecular imaging, however is not primarily imaging hardware development but scientific advancements in molecular biology and progress in probe development. Other factors to consider are postprocessing software and, inevitably, market dynamics. Thus. it implies efficient collaborations across disciplines, agencies, and industries to develop molecular imaging tools for the clinic
    Type of Publication: Journal article published
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  • 3
    Keywords: GENE ; GENE-EXPRESSION ; RETINOIC ACID ; CELL CARCINOMA ; PARATHYROID-HORMONE ; HORMONE-RELATED PROTEIN ; CONFER SUSCEPTIBILITY ; COMMON VARIANTS ; DEVELOPMENTAL REGULATORY MOLECULE ; NEGATIVE-FEEDBACK ; ULNAR-MAMMARY SYNDROME
    Abstract: Breast cancer is the most common cancer among women. To date, 22 common breast cancer susceptibility loci have been identified accounting for similar to 8% of the heritability of the disease. We attempted to replicate 72 promising associations from two independent genome-wide association studies (GWAS) in similar to 70,000 cases and similar to 68,000 controls from 41 case-control studies and 9 breast cancer GWAS. We identified three new breast cancer risk loci at 12p11 (rs10771399; P = 2.7 x 10(-35)), 12q24 (rs1292011; P = 4.3 x 10(-19)) and 21q21 (rs2823093; P = 1.1 x 10(-12)). rs10771399 was associated with similar relative risks for both estrogen receptor (ER)-negative and ER-positive breast cancer, whereas the other two loci were associated only with ER-positive disease. Two of the loci lie in regions that contain strong plausible candidate genes: PTHLH (12p11) has a crucial role in mammary gland development and the establishment of bone metastasis in breast cancer, and NRIP1 (21q21) encodes an ER cofactor and has a role in the regulation of breast cancer cell growth
    Type of Publication: Journal article published
    PubMed ID: 22267197
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  • 4
    Keywords: GENE-EXPRESSION ; CELL-CYCLE ; DOWN-REGULATION ; PROSTATE-CANCER ; ESTROGEN-RECEPTOR ; MAMMARY-GLAND ; susceptibility loci ; GENOME-WIDE ASSOCIATION ; GROWTH-FACTOR RECEPTOR-2 ; MULTIPLE LOCI
    Abstract: Analysis of 4,405 variants in 89,050 European subjects from 41 case-control studies identified three independent association signals for estrogen-receptor-positive tumors at 11q13. The strongest signal maps to a transcriptional enhancer element in which the G allele of the best candidate causative variant rs554219 increases risk of breast cancer, reduces both binding of ELK4 transcription factor and luciferase activity in reporter assays, and may be associated with low cyclin D1 protein levels in tumors. Another candidate variant, rs78540526, lies in the same enhancer element. Risk association signal 2, rs75915166, creates a GATA3 binding site within a silencer element. Chromatin conformation studies demonstrate that these enhancer and silencer elements interact with each other and with their likely target gene, CCND1.
    Type of Publication: Journal article published
    PubMed ID: 23540573
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