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Article ; Online: eQTL Colocalization Analyses Identify NTN4 as a Candidate Breast Cancer Risk Gene.

Beesley, Jonathan / Sivakumaran, Haran / Moradi Marjaneh, Mahdi / Shi, Wei / Hillman, Kristine M / Kaufmann, Susanne / Hussein, Nehal / Kar, Siddhartha / Lima, Luize G / Ham, Sunyoung / Möller, Andreas / Chenevix-Trench, Georgia / Edwards, Stacey L / French, Juliet D

American journal of human genetics

2020 Volume 107, Issue 4, Page(s) 778–787

Abstract: Breast cancer genome-wide association studies (GWASs) have identified 150 genomic risk regions containing more than 13,000 credible causal variants (CCVs). The CCVs are predominantly noncoding and enriched in regulatory elements. However, the genes ... ...

Abstract	Breast cancer genome-wide association studies (GWASs) have identified 150 genomic risk regions containing more than 13,000 credible causal variants (CCVs). The CCVs are predominantly noncoding and enriched in regulatory elements. However, the genes underlying breast cancer risk associations are largely unknown. Here, we used genetic colocalization analysis to identify loci at which gene expression could potentially explain breast cancer risk phenotypes. Using data from the Breast Cancer Association Consortium (BCAC) and quantitative trait loci (QTL) from the Genotype-Tissue Expression (GTEx) project and The Cancer Genome Project (TCGA), we identify shared genetic relationships and reveal novel associations between cancer phenotypes and effector genes. Seventeen genes, including NTN4, were identified as potential mediators of breast cancer risk. For NTN4, we showed the rs61938093 CCV at this region was located within an enhancer element that physically interacts with the NTN4 promoter, and the risk allele reduced NTN4 promoter activity. Furthermore, knockdown of NTN4 in breast cells increased cell proliferation in vitro and tumor growth in vivo. These data provide evidence linking risk-associated variation to genes that may contribute to breast cancer predisposition.
MeSH term(s)	Alleles ; Animals ; Breast Neoplasms/diagnosis ; Breast Neoplasms/genetics ; Breast Neoplasms/pathology ; Cell Line, Tumor ; Enhancer Elements, Genetic ; Female ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Genetic Predisposition to Disease ; Genome-Wide Association Study ; Genomics/methods ; Heterografts ; Humans ; MCF-7 Cells ; Mice ; Mice, Nude ; Neoplasm Proteins/genetics ; Neoplasm Proteins/metabolism ; Netrins/genetics ; Netrins/metabolism ; Phenotype ; Quantitative Trait Loci ; Risk
Chemical Substances	NTN4 protein, human ; Neoplasm Proteins ; Netrins
Language	English
Publishing date	2020-08-31
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	219384-x
ISSN	1537-6605 ; 0002-9297
ISSN (online)	1537-6605
ISSN	0002-9297
DOI	10.1016/j.ajhg.2020.08.006
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Article ; Online: Porphyromonas loveana sp. nov., isolated from the oral cavity of Australian marsupials.

Bird, Philip S / Trott, Darren J / Mikkelsen, Deirdre / Milinovich, Gabriel J / Hillman, Kristine M / Burrell, Paul C / Blackall, Linda L

International journal of systematic and evolutionary microbiology

2016 Volume 66, Issue 10, Page(s) 3771–3778

Abstract: An obligatory anaerobic, Gram-stain-negative coccobacillus with black-pigmented colonies was isolated from the oral cavity of selected Australian marsupial species. Phenotypic and molecular criteria showed that this bacterium was a distinct species ... ...

Abstract	An obligatory anaerobic, Gram-stain-negative coccobacillus with black-pigmented colonies was isolated from the oral cavity of selected Australian marsupial species. Phenotypic and molecular criteria showed that this bacterium was a distinct species within the genus Porphyromonas, and was closely related to Porphyromonas gingivalis and Porphyromonas gulae. This putative novel species and P. gulae could be differentiated from P. gingivalis by catalase activity. Further characterization by multi-locus enzyme electrophoresis of glutamate dehydrogenase and malate dehydrogenase enzyme mobility and matrix-assisted laser desorption ionization time-of-flight MS showed that this putative novel species could be differentiated phenotypically from P. gingivalis and P. gulae. Definitive identification by 16S rRNA gene sequencing showed that this bacterium belonged to a unique monophyletic lineage, phylogenetically distinct from P. gingivalis (94.9 % similarity) and P. gulae (95.5 %). This also was supported by 16S-23S rRNA intergenic spacer region and glutamate dehydrogenase gene sequencing. A new species epithet, Porphyromonas loveana sp. nov., is proposed for this bacterium, with DSM 28520T (=NCTC 13658T=UQD444T=MRK101T), isolated from a musky rat kangaroo, as the type strain.
MeSH term(s)	Animals ; Australia ; Bacterial Typing Techniques ; Base Composition ; DNA, Bacterial/genetics ; DNA, Ribosomal Spacer/genetics ; Glutamate Dehydrogenase/genetics ; Marsupialia/microbiology ; Mouth/microbiology ; Phylogeny ; Pigmentation ; Porphyromonas/classification ; Porphyromonas/genetics ; Porphyromonas/isolation & purification ; RNA, Ribosomal, 16S/genetics ; Sequence Analysis, DNA
Chemical Substances	DNA, Bacterial ; DNA, Ribosomal Spacer ; RNA, Ribosomal, 16S ; Glutamate Dehydrogenase (EC 1.4.1.2)
Language	English
Publishing date	2016-08-10
Publishing country	England
Document type	Journal Article
ZDB-ID	2002336-4
ISSN	1466-5034 ; 1466-5026
ISSN (online)	1466-5034
ISSN	1466-5026
DOI	10.1099/ijsem.0.000898
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Article: Chromatin interactome mapping at 139 independent breast cancer risk signals

Beesley, Jonathan / Sivakumaran, Haran / Moradi Marjaneh, Mahdi / Lima, Luize G / Hillman, Kristine M / Kaufmann, Susanne / Tuano, Natasha / Hussein, Nehal / Ham, Sunyoung / Mukhopadhyay, Pamela / Kazakoff, Stephen / Lee, Jason S / Michailidou, Kyriaki / Barnes, Daniel R / Antoniou, Antonis C / Fachal, Laura / Dunning, Alison M / Easton, Douglas F / Waddell, Nicola /

Rosenbluh, Joseph / Möller, Andreas / Chenevix-Trench, Georgia / French, Juliet D / Edwards, Stacey L

Genome biology. 2020 Dec., v. 21, no. 1

2020

Abstract: BACKGROUND: Genome-wide association studies have identified 196 high confidence independent signals associated with breast cancer susceptibility. Variants within these signals frequently fall in distal regulatory DNA elements that control gene expression. ...

Abstract	BACKGROUND: Genome-wide association studies have identified 196 high confidence independent signals associated with breast cancer susceptibility. Variants within these signals frequently fall in distal regulatory DNA elements that control gene expression. RESULTS: We designed a Capture Hi-C array to enrich for chromatin interactions between the credible causal variants and target genes in six human mammary epithelial and breast cancer cell lines. We show that interacting regions are enriched for open chromatin, histone marks for active enhancers, and transcription factors relevant to breast biology. We exploit this comprehensive resource to identify candidate target genes at 139 independent breast cancer risk signals and explore the functional mechanism underlying altered risk at the 12q24 risk region. CONCLUSIONS: Our results demonstrate the power of combining genetics, computational genomics, and molecular studies to rationalize the identification of key variants and candidate target genes at breast cancer GWAS signals.
Keywords	DNA ; breast neoplasms ; breasts ; cell lines ; chromatin ; epithelium ; gene expression ; genes ; genome-wide association study ; genomics ; histone code ; humans ; neoplasm cells ; risk ; transcription factors
Language	English
Dates of publication	2020-12
Size	p. 8.
Publishing place	BioMed Central
Document type	Article
ZDB-ID	2040529-7
ISSN	1474-760X ; 1465-6906
ISSN (online)	1474-760X
ISSN	1465-6906
DOI	10.1186/s13059-019-1877-y
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Article ; Online: Chromatin interactome mapping at 139 independent breast cancer risk signals.

Rosenbluh, Joseph / Möller, Andreas / Chenevix-Trench, Georgia / French, Juliet D / Edwards, Stacey L

Genome biology

2020 Volume 21, Issue 1, Page(s) 8

Abstract: Background: Genome-wide association studies have identified 196 high confidence independent signals associated with breast cancer susceptibility. Variants within these signals frequently fall in distal regulatory DNA elements that control gene ... ...

Abstract	Background: Genome-wide association studies have identified 196 high confidence independent signals associated with breast cancer susceptibility. Variants within these signals frequently fall in distal regulatory DNA elements that control gene expression. Results: We designed a Capture Hi-C array to enrich for chromatin interactions between the credible causal variants and target genes in six human mammary epithelial and breast cancer cell lines. We show that interacting regions are enriched for open chromatin, histone marks for active enhancers, and transcription factors relevant to breast biology. We exploit this comprehensive resource to identify candidate target genes at 139 independent breast cancer risk signals and explore the functional mechanism underlying altered risk at the 12q24 risk region. Conclusions: Our results demonstrate the power of combining genetics, computational genomics, and molecular studies to rationalize the identification of key variants and candidate target genes at breast cancer GWAS signals.
MeSH term(s)	Breast Neoplasms/genetics ; Breast Neoplasms/metabolism ; Cell Line, Tumor ; Chromatin/metabolism ; Genome, Human ; Genome-Wide Association Study ; Humans
Chemical Substances	Chromatin
Language	English
Publishing date	2020-01-07
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2040529-7
ISSN	1474-760X ; 1474-760X
ISSN (online)	1474-760X
ISSN	1474-760X
DOI	10.1186/s13059-019-1877-y
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Article: Non-coding RNAs underlie genetic predisposition to breast cancer

Moradi Marjaneh, Mahdi / Beesley, Jonathan / O’Mara, Tracy A / Mukhopadhyay, Pamela / Koufariotis, Lambros T / Kazakoff, Stephen / Hussein, Nehal / Fachal, Laura / Bartonicek, Nenad / Hillman, Kristine M / Kaufmann, Susanne / Sivakumaran, Haran / Smart, Chanel E / McCart Reed, Amy E / Ferguson, Kaltin / Saunus, Jodi M / Lakhani, Sunil R / Barnes, Daniel R / Antoniou, Antonis C /

Dinger, Marcel E / Waddell, Nicola / Easton, Douglas F / Dunning, Alison M / Chenevix-Trench, Georgia / Edwards, Stacey L / French, Juliet D

Genome biology. 2020 Dec., v. 21, no. 1

2020

Abstract: BACKGROUND: Genetic variants identified through genome-wide association studies (GWAS) are predominantly non-coding and typically attributed to altered regulatory elements such as enhancers and promoters. However, the contribution of non-coding RNAs to ... ...

Abstract	BACKGROUND: Genetic variants identified through genome-wide association studies (GWAS) are predominantly non-coding and typically attributed to altered regulatory elements such as enhancers and promoters. However, the contribution of non-coding RNAs to complex traits is not clear. RESULTS: Using targeted RNA sequencing, we systematically annotated multi-exonic non-coding RNA (mencRNA) genes transcribed from 1.5-Mb intervals surrounding 139 breast cancer GWAS signals and assessed their contribution to breast cancer risk. We identify more than 4000 mencRNA genes and show their expression distinguishes normal breast tissue from tumors and different breast cancer subtypes. Importantly, breast cancer risk variants, identified through genetic fine-mapping, are significantly enriched in mencRNA exons, but not the promoters or introns. eQTL analyses identify mencRNAs whose expression is associated with risk variants. Furthermore, chromatin interaction data identify hundreds of mencRNA promoters that loop to regions that contain breast cancer risk variants. CONCLUSIONS: We have compiled the largest catalog of breast cancer-associated mencRNAs to date and provide evidence that modulation of mencRNAs by GWAS variants may provide an alternative mechanism underlying complex traits.
Keywords	breast neoplasms ; chromatin ; exons ; genetic predisposition to disease ; genetic variation ; genome-wide association study ; introns ; non-coding RNA ; regulatory sequences ; risk ; sequence analysis ; transcription (genetics)
Language	English
Dates of publication	2020-12
Size	p. 7.
Publishing place	BioMed Central
Document type	Article
ZDB-ID	2040529-7
ISSN	1474-760X ; 1465-6906
ISSN (online)	1474-760X
ISSN	1465-6906
DOI	10.1186/s13059-019-1876-z
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Article ; Online: Targeting VEGF with LNA-stabilized G-rich oligonucleotide for efficient breast cancer inhibition.

Edwards, Stacey L / Poongavanam, Vasanthanathan / Kanwar, Jagat R / Roy, Kislay / Hillman, Kristine M / Prasad, Neerati / Leth-Larsen, Rikke / Petersen, Michael / Marušič, Maja / Plavec, Janez / Wengel, Jesper / Veedu, Rakesh N

Chemical communications (Cambridge, England)

2015 Volume 51, Issue 46, Page(s) 9499–9502

Abstract: In this study, we investigated the efficacy of an LNA (locked nucleic acid)-modified DNA aptamer named RNV66 targeting VEGF against various breast cancer cell lines. Our results demonstrate that RNV66 efficiently inhibits breast cancer cell proliferation ...

Abstract	In this study, we investigated the efficacy of an LNA (locked nucleic acid)-modified DNA aptamer named RNV66 targeting VEGF against various breast cancer cell lines. Our results demonstrate that RNV66 efficiently inhibits breast cancer cell proliferation both in vitro and in vivo. Introduction of LNA nucleotides were crucial for higher efficacy. Furthermore, the binding interaction of RNV66 with VEGF was investigated using molecular dynamic simulations leading to the first computational model of the LNA aptamer-VEGF complex blocking its interaction with VEGF-receptor.
MeSH term(s)	Animals ; Antineoplastic Agents/chemistry ; Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Aptamers, Nucleotide/chemistry ; Aptamers, Nucleotide/pharmacology ; Aptamers, Nucleotide/therapeutic use ; Breast Neoplasms/drug therapy ; Breast Neoplasms/pathology ; Cell Line, Tumor ; Cell Movement/drug effects ; Cell Proliferation/drug effects ; Female ; Guanine ; Human Umbilical Vein Endothelial Cells/drug effects ; Humans ; Mice, Nude ; Molecular Docking Simulation ; Molecular Dynamics Simulation ; Oligonucleotides/chemistry ; Tumor Burden/drug effects ; Vascular Endothelial Growth Factor A/metabolism
Chemical Substances	Antineoplastic Agents ; Aptamers, Nucleotide ; Oligonucleotides ; RNV66 DNA aptamer ; Vascular Endothelial Growth Factor A ; locked nucleic acid ; Guanine (5Z93L87A1R)
Language	English
Publishing date	2015-06-11
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1472881-3
ISSN	1364-548X ; 1359-7345 ; 0009-241X
ISSN (online)	1364-548X
ISSN	1359-7345 ; 0009-241X
DOI	10.1039/c5cc02756j
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Article ; Online: Long-Range Modulation of PAG1 Expression by 8q21 Allergy Risk Variants.

Vicente, Cristina T / Edwards, Stacey L / Hillman, Kristine M / Kaufmann, Susanne / Mitchell, Hayley / Bain, Lisa / Glubb, Dylan M / Lee, Jason S / French, Juliet D / Ferreira, Manuel A R

American journal of human genetics

2015 Volume 97, Issue 2, Page(s) 329–336

Abstract: The gene(s) whose expression is regulated by allergy risk variants is unknown for many loci identified through genome-wide association studies. Addressing this knowledge gap might point to new therapeutic targets for allergic disease. The aim of this ... ...

Abstract	The gene(s) whose expression is regulated by allergy risk variants is unknown for many loci identified through genome-wide association studies. Addressing this knowledge gap might point to new therapeutic targets for allergic disease. The aim of this study was to identify the target gene(s) and the functional variant(s) underlying the association between rs7009110 on chromosome 8q21 and allergies. Eight genes are located within 1 Mb of rs7009110. Multivariate association analysis of publicly available exon expression levels from lymphoblastoid cell lines (LCLs) identified a significant association between rs7009110 and the expression of a single gene, PAG1 (p = 0.0017), 732 kb away. Analysis of histone modifications and DNase I hypersensitive sites in LCLs identified four putative regulatory elements (PREs) in the region. Chromosome conformation capture confirmed that two PREs interacted with the PAG1 promoter, one in allele-specific fashion. To determine whether these PREs were functional, LCLs were transfected with PAG1 promoter-driven luciferase reporter constructs. PRE3 acted as a transcriptional enhancer for PAG1 exclusively when it carried the rs2370615:C allergy predisposing allele, a variant in complete linkage disequilibrium with rs7009110. As such, rs2370615, which overlaps RelA transcription factor (TF) binding in LCLs and was found to disrupt Foxo3a binding to PRE3, represents the putative functional variant in this locus. Our studies suggest that the risk-associated allele of rs2370615 predisposes to allergic disease by increasing PAG1 expression, which might promote B cell activation and have a pro-inflammatory effect. Inhibition of PAG1 expression or function might have therapeutic potential for allergic diseases.
MeSH term(s)	Adaptor Proteins, Signal Transducing/genetics ; B-Lymphocytes/immunology ; Chromosomes, Human, Pair 8/genetics ; Gene Expression Regulation/genetics ; Genetic Association Studies ; Humans ; Hypersensitivity/genetics ; Hypersensitivity/immunology ; Linkage Disequilibrium ; Luciferases ; Lymphocyte Activation/genetics ; Membrane Proteins/genetics ; Multivariate Analysis ; Nucleic Acid Conformation ; Polymorphism, Single Nucleotide/genetics ; Regulatory Sequences, Nucleic Acid/genetics
Chemical Substances	Adaptor Proteins, Signal Transducing ; Membrane Proteins ; PAG1 protein, human ; Luciferases (EC 1.13.12.-)
Language	English
Publishing date	2015-07-23
Publishing country	United States
Document type	Case Reports ; Journal Article
ZDB-ID	219384-x
ISSN	1537-6605 ; 0002-9297
ISSN (online)	1537-6605
ISSN	0002-9297
DOI	10.1016/j.ajhg.2015.06.010
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Article: Targeting VEGF with LNA-stabilized G-rich oligonucleotide for efficient breast cancer inhibition

Chemical communications. 2015 May 26, v. 51, no. 46

2015

Abstract	In this study, we investigated the efficacy of an LNA (locked nucleic acid)-modified DNA aptamer named RNV66 targeting VEGF against various breast cancer cell lines. Our results demonstrate that RNV66 efficiently inhibits breast cancer cell proliferation both in vitro and in vivo. Introduction of LNA nucleotides were crucial for higher efficacy. Furthermore, the binding interaction of RNV66 with VEGF was investigated using molecular dynamic simulations leading to the first computational model of the LNA aptamer–VEGF complex blocking its interaction with VEGF-receptor.
Keywords	DNA ; breast neoplasms ; cell lines ; cell proliferation ; chemical compounds ; chemical reactions ; models ; neoplasm cells ; oligonucleotides ; vascular endothelial growth factor receptors ; vascular endothelial growth factors
Language	English
Dates of publication	2015-0526
Size	p. 9499-9502.
Publishing place	The Royal Society of Chemistry
Document type	Article
ZDB-ID	1472881-3
ISSN	1364-548X ; 1359-7345 ; 0009-241X
ISSN (online)	1364-548X
ISSN	1359-7345 ; 0009-241X
DOI	10.1039/c5cc02756j
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Article ; Online: Non-coding RNAs underlie genetic predisposition to breast cancer.

Moradi Marjaneh, Mahdi / Beesley, Jonathan / O'Mara, Tracy A / Mukhopadhyay, Pamela / Koufariotis, Lambros T / Kazakoff, Stephen / Hussein, Nehal / Fachal, Laura / Bartonicek, Nenad / Hillman, Kristine M / Kaufmann, Susanne / Sivakumaran, Haran / Smart, Chanel E / McCart Reed, Amy E / Ferguson, Kaltin / Saunus, Jodi M / Lakhani, Sunil R / Barnes, Daniel R / Antoniou, Antonis C /

Dinger, Marcel E / Waddell, Nicola / Easton, Douglas F / Dunning, Alison M / Chenevix-Trench, Georgia / Edwards, Stacey L / French, Juliet D

Genome biology

2020 Volume 21, Issue 1, Page(s) 7

Abstract: Background: Genetic variants identified through genome-wide association studies (GWAS) are predominantly non-coding and typically attributed to altered regulatory elements such as enhancers and promoters. However, the contribution of non-coding RNAs to ... ...

Abstract	Background: Genetic variants identified through genome-wide association studies (GWAS) are predominantly non-coding and typically attributed to altered regulatory elements such as enhancers and promoters. However, the contribution of non-coding RNAs to complex traits is not clear. Results: Using targeted RNA sequencing, we systematically annotated multi-exonic non-coding RNA (mencRNA) genes transcribed from 1.5-Mb intervals surrounding 139 breast cancer GWAS signals and assessed their contribution to breast cancer risk. We identify more than 4000 mencRNA genes and show their expression distinguishes normal breast tissue from tumors and different breast cancer subtypes. Importantly, breast cancer risk variants, identified through genetic fine-mapping, are significantly enriched in mencRNA exons, but not the promoters or introns. eQTL analyses identify mencRNAs whose expression is associated with risk variants. Furthermore, chromatin interaction data identify hundreds of mencRNA promoters that loop to regions that contain breast cancer risk variants. Conclusions: We have compiled the largest catalog of breast cancer-associated mencRNAs to date and provide evidence that modulation of mencRNAs by GWAS variants may provide an alternative mechanism underlying complex traits.
MeSH term(s)	Breast Neoplasms/genetics ; Genome-Wide Association Study ; Humans ; RNA, Untranslated/genetics ; Sequence Analysis, RNA
Chemical Substances	RNA, Untranslated
Language	English
Publishing date	2020-01-07
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2040529-7
ISSN	1474-760X ; 1474-760X
ISSN (online)	1474-760X
ISSN	1474-760X
DOI	10.1186/s13059-019-1876-z
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Article ; Online: A Common Variant at the 14q32 Endometrial Cancer Risk Locus Activates AKT1 through YY1 Binding.

American journal of human genetics

2016 Volume 98, Issue 6, Page(s) 1159–1169

Abstract: A recent meta-analysis of multiple genome-wide association and follow-up endometrial cancer case-control datasets identified a novel genetic risk locus for this disease at chromosome 14q32.33. To prioritize the functional SNP(s) and target gene(s) at ... ...

Abstract	A recent meta-analysis of multiple genome-wide association and follow-up endometrial cancer case-control datasets identified a novel genetic risk locus for this disease at chromosome 14q32.33. To prioritize the functional SNP(s) and target gene(s) at this locus, we employed an in silico fine-mapping approach using genotyped and imputed SNP data for 6,608 endometrial cancer cases and 37,925 controls of European ancestry. Association and functional analyses provide evidence that the best candidate causal SNP is rs2494737. Multiple experimental analyses show that SNP rs2494737 maps to a silencer element located within AKT1, a member of the PI3K/AKT/MTOR intracellular signaling pathway activated in endometrial tumors. The rs2494737 risk A allele creates a YY1 transcription factor-binding site and abrogates the silencer activity in luciferase assays, an effect mimicked by transfection of YY1 siRNA. Our findings suggest YY1 is a positive regulator of AKT1, mediating the stimulatory effects of rs2494737 increasing endometrial cancer risk. Identification of an endometrial cancer risk allele within a member of the PI3K/AKT signaling pathway, more commonly activated in tumors by somatic alterations, raises the possibility that well tolerated inhibitors targeting this pathway could be candidates for evaluation as chemopreventive agents in individuals at high risk of developing endometrial cancer.
MeSH term(s)	Chromosomes, Human, Pair 14/genetics ; Endometrial Neoplasms/genetics ; Endometrial Neoplasms/metabolism ; Endometrial Neoplasms/pathology ; Female ; Genetic Loci ; Genetic Predisposition to Disease ; Genome-Wide Association Study ; Genotype ; Humans ; Phosphatidylinositol 3-Kinases/genetics ; Polymorphism, Single Nucleotide/genetics ; Protein Binding ; Proto-Oncogene Proteins c-akt/genetics ; Proto-Oncogene Proteins c-akt/metabolism ; Risk Factors ; Signal Transduction ; Uterine Neoplasms/genetics ; Uterine Neoplasms/metabolism ; Uterine Neoplasms/pathology ; YY1 Transcription Factor/genetics ; YY1 Transcription Factor/metabolism
Chemical Substances	YY1 Transcription Factor ; YY1 protein, human ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; AKT1 protein, human (EC 2.7.11.1) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1)
Language	English
Publishing date	2016-05-31
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	219384-x
ISSN	1537-6605 ; 0002-9297
ISSN (online)	1537-6605
ISSN	0002-9297
DOI	10.1016/j.ajhg.2016.04.012
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