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1

Tong, Xin, Yang Gao, and Zhongjing Su. "Interaction of CTCF and CTCFL in genome regulation through chromatin architecture during the spermatogenesis and carcinogenesis." PeerJ 12 (October 15, 2024): e18240. http://dx.doi.org/10.7717/peerj.18240.

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The zinc finger protein CTCF is ubiquitously expressed and is integral to the regulation of chromatin architecture through its interaction with cohesin. Conversely, CTCFL expression is predominantly restricted to the adult male testis but is aberrantly expressed in certain cancers. Despite their distinct expression patterns, the cooperative and competitive mechanisms by which CTCF and CTCFL regulate target gene expression in spermatocytes and cancer cells remain inadequately understood. In this review, we comprehensively examine the literature on the divergent amino acid sequences, target site
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2

Yao, Haibo, Qinshu Shao, and Yanfei Shao. "Transcription Factor CTCFL Promotes Cell Proliferation, Migration, and Invasion in Gastric Cancer via Activating DPPA2." Computational and Mathematical Methods in Medicine 2021 (October 19, 2021): 1–11. http://dx.doi.org/10.1155/2021/9097931.

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Objective. To explore the relationship between CTCFL and DPPA2 and validate the positive role of CTCFL/DPPA2 in cell malignant behaviors in gastric cancer. Methods. We predicted gastric cancer-related transcription factors and corresponding target mRNAs through bioinformatics. Levels of CTCFL and DPPA2 were assessed via qRT-PCR and western blot. In vitro experiments were utilized to assay the cell biological behaviors. CHIP was utilized for the assessment of the targeted relationship between CTCFL and DPPA2. Results. CTCFL and DPPA2 were both highly expressed in gastric cancer cells, and high
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3

Debaugny, Roxanne E., and Jane A. Skok. "CTCF and CTCFL in cancer." Current Opinion in Genetics & Development 61 (April 2020): 44–52. http://dx.doi.org/10.1016/j.gde.2020.02.021.

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4

Voutsadakis, Ioannis. "Molecular Lesions of Insulator CTCF and Its Paralogue CTCFL (BORIS) in Cancer: An Analysis from Published Genomic Studies." High-Throughput 7, no. 4 (2018): 30. http://dx.doi.org/10.3390/ht7040030.

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CTCF (CCCTC-binding factor) is a transcription regulator with hundreds of binding sites in the human genome. It has a main function as an insulator protein, defining together with cohesins the boundaries of areas of the genome called topologically associating domains (TADs). TADs contain regulatory elements such as enhancers which function as regulators of the transcription of genes inside the boundaries of the TAD while they are restricted from regulating genes outside these boundaries. This paper will examine the most common genetic lesions of CTCF as well as its related protein CTCFL (CTCF-
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DEL CAMPO, EDUARDO PORTILLO, JOSÉ JORGE TALAMÁS MÁRQUEZ, FRANCIANELLA REYES-VARGAS та ін. "CTCF and CTCFL mRNA expression in 17β-estradiol-treated MCF7 cells". Biomedical Reports 2, № 1 (2013): 101–4. http://dx.doi.org/10.3892/br.2013.200.

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6

Hore, Timothy A., Janine E. Deakin, and Jennifer A. Marshall Graves. "The Evolution of Epigenetic Regulators CTCF and BORIS/CTCFL in Amniotes." PLoS Genetics 4, no. 8 (2008): e1000169. http://dx.doi.org/10.1371/journal.pgen.1000169.

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7

Campbell, Amy E., Selena R. Martinez, and JJ L. Miranda. "Molecular architecture of CTCFL." Biochemical and Biophysical Research Communications 396, no. 3 (2010): 648–50. http://dx.doi.org/10.1016/j.bbrc.2010.04.146.

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8

Pugacheva, Elena M., Naoki Kubo, Dmitri Loukinov, et al. "CTCF mediates chromatin looping via N-terminal domain-dependent cohesin retention." Proceedings of the National Academy of Sciences 117, no. 4 (2020): 2020–31. http://dx.doi.org/10.1073/pnas.1911708117.

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The DNA-binding protein CCCTC-binding factor (CTCF) and the cohesin complex function together to shape chromatin architecture in mammalian cells, but the molecular details of this process remain unclear. Here, we demonstrate that a 79-aa region within the CTCF N terminus is essential for cohesin positioning at CTCF binding sites and chromatin loop formation. However, the N terminus of CTCF fused to artificial zinc fingers was not sufficient to redirect cohesin to non-CTCF binding sites, indicating a lack of an autonomously functioning domain in CTCF responsible for cohesin positioning. BORIS (
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9

Hernandez-Gonzalez, Ignacio, Jair Tenorio-Castano, Nuria Ochoa-Parra, et al. "Novel Genetic and Molecular Pathways in Pulmonary Arterial Hypertension Associated with Connective Tissue Disease." Cells 10, no. 6 (2021): 1488. http://dx.doi.org/10.3390/cells10061488.

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Pulmonary Arterial Hypertension (PAH) is a severe complication of Connective Tissue Disease (CTD), with remarkable morbidity and mortality. However, the molecular and genetic basis of CTD-PAH remains incompletely understood. This study aimed to screen for genetic defects in a cohort of patients with CTD-PAH, using a PAH-specific panel of 35 genes. During recruitment, 79 patients were studied, including 59 Systemic Sclerosis patients (SSc) and 69 females. Disease-associated variants were observed in nine patients: 4 pathogenic/likely pathogenic variants in 4 different genes (TBX4, ABCC8, KCNA5
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10

Soto Reyes Solis, Ernesto, Daniela Morales-Espinosa, David Cantu, et al. "Characterization of DNA methylation of the promoters CTCF and BORIS (CTCFL) in breast and ovarian cancer." Journal of Clinical Oncology 31, no. 15_suppl (2013): e22151-e22151. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.e22151.

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e22151 Background: Genetic and epigenetic alterations may promote the initiation or development of cancer. Global DNA hypomethylation and local hypermethylation have been observed, particularly in cell cycle control-associated genes, such as tumor suppressor genes like CTCF. The dissociation of CTCF is associated with hypermethylation of several promoters; its paralogue gene (BORIS) is normally expressed in testicular tissue during spermatogenesis. BORIS over-expression has been identified in multiple neoplasms such as melanoma, gynecological cancer, glioblastoma and – recently – breast cancer
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11

Sati, Leyla, Bikem Soygur, Ethem Goksu, Cumhur Ibrahim Bassorgun, and James McGrath. "CTCFL expression is associated with cerebral vascular abnormalities." Tissue and Cell 72 (October 2021): 101528. http://dx.doi.org/10.1016/j.tice.2021.101528.

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12

Loukinov, Dmitri. "Targeting CTCFL/BORIS for the immunotherapy of cancer." Cancer Immunology, Immunotherapy 67, no. 12 (2018): 1955–65. http://dx.doi.org/10.1007/s00262-018-2251-8.

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13

Bergmaier, Philipp, Oliver Weth, Sven Dienstbach, et al. "Choice of binding sites for CTCFL compared to CTCF is driven by chromatin and by sequence preference." Nucleic Acids Research 46, no. 14 (2018): 7097–107. http://dx.doi.org/10.1093/nar/gky483.

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14

Jones, Tania A., Babatunji W. Ogunkolade, Jaroslaw Szary, et al. "Widespread Expression of BORIS/CTCFL in Normal and Cancer Cells." PLoS ONE 6, no. 7 (2011): e22399. http://dx.doi.org/10.1371/journal.pone.0022399.

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15

Bai, Jie, Supannika Sorin, Arusyak Ivanyan, et al. "Chromatin Modifier Hmga1 Maintains Hematopoietic Stem Cell Integrity in Stress Conditions." Blood 144, Supplement 1 (2024): 26. https://doi.org/10.1182/blood-2024-212002.

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Hematopoietic stem cells (HSCs) respond to various stresses, such as inflammation, and expand hematopoietic stem and progenitor cells (HSPCs) to produce mature blood cells; however, the mechanisms by which HSCs maintain hematopoiesis in differential responses to homeostatic and stress conditions have yet to be elucidated. High-mobility group AT-hook 1 (Hmga1), a chromatin modifier, opens and closes the chromatin and modulates the transcription. Hmga1 is highly expressed in somatic stem cells including HSC. Hmga1 is shown to promote the development of myeloid malignancies via driving the prolif
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16

Ogunkolade, Babatunji W., Tania A. Jones, Johan Aarum, et al. "BORIS/CTCFL is an RNA-binding protein that associates with polysomes." BMC Cell Biology 14, no. 1 (2013): 52. http://dx.doi.org/10.1186/1471-2121-14-52.

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17

de Necochea-Campion, Rosalia, Anahit Ghochikyan, Steven F. Josephs, et al. "Expression of the Epigenetic factor BORIS (CTCFL) in the Human Genome." Journal of Translational Medicine 9, no. 1 (2011): 213. http://dx.doi.org/10.1186/1479-5876-9-213.

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18

Hoffmann, Michèle J., Mirko Müller, Rainer Engers, and Wolfgang A. Schulz. "Epigenetic control of CTCFL/BORIS and OCT4 expression in urogenital malignancies." Biochemical Pharmacology 72, no. 11 (2006): 1577–88. http://dx.doi.org/10.1016/j.bcp.2006.06.020.

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19

Zampieri, Michele, Fabio Ciccarone, Rocco Palermo, et al. "The epigenetic factor BORIS/CTCFL regulates the NOTCH3 gene expression in cancer cells." Biochimica et Biophysica Acta (BBA) - Gene Regulatory Mechanisms 1839, no. 9 (2014): 813–25. http://dx.doi.org/10.1016/j.bbagrm.2014.06.017.

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20

Zambrano-Galván, Graciela, Miguel Reyes-Romero, Ronell Bologna-Molina, Oscar Eduardo Almeda-Ojeda, and Obed Lemus-Rojero. "CTCFL(BORIS) mRNA Expression in a Peripheral Giant Cell Granuloma of the Oral Cavity." Case Reports in Dentistry 2014 (2014): 1–4. http://dx.doi.org/10.1155/2014/792615.

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Peripheral giant cell granuloma (PGCG) is a relatively common benign reactive lesion of the oral cavity which can occur at any age.CTCFL/BORIS(CTCFlike/Brother of the Regulator of Imprinted Sites) andCTCF(CCCTC-binding factor) are paralogous genes with an important role in the regulation of gene expression, genomic imprinting, and nuclear chromatin insulators regulation.BORISexpression promotes cell immortalization and growth whileCTCFhas tumor suppressor activity; the expression pattern may reflect the reverse transcription silencing ofBORIS. The aim of this work was to describe a histopathol
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21

Chen, M. M., R. C. Zhao, K. F. Chen, et al. "Hypomethylation of CTCFL promoters as a noninvasive biomarker in plasma from patients with hepatocellular carcinoma." Neoplasma 67, no. 04 (2020): 909–15. http://dx.doi.org/10.4149/neo_2020_190819n789.

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22

Loukinov, Dmitri, Amanda Laust Anderson, Mikayel Mkrtichyan, et al. "A Therapeutic Vaccine Targeting Rat BORIS (CTCFL) for the Treatment of Rat Breast Cancer Tumors." International Journal of Molecular Sciences 24, no. 6 (2023): 5976. http://dx.doi.org/10.3390/ijms24065976.

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Cancer testis antigens are ideal for tumor immunotherapy due to their testis-restricted expression. We previously showed that an immunotherapeutic vaccine targeting the germ cell-specific transcription factor BORIS (CTCFL) was highly effective in treating aggressive breast cancer in the 4T1 mouse model. Here, we further tested the therapeutic efficacy of BORIS in a rat 13762 breast cancer model. We generated a recombinant VEE-VRP (Venezuelan Equine Encephalitis-derived replicon particle) vector-expressing modified rat BORIS lacking a DNA-binding domain (VRP-mBORIS). Rats were inoculated with t
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23

Hines, William C., Alexey V. Bazarov, Rituparna Mukhopadhyay, and Paul Yaswen. "BORIS (CTCFL) Is Not Expressed in Most Human Breast Cell Lines and High Grade Breast Carcinomas." PLoS ONE 5, no. 3 (2010): e9738. http://dx.doi.org/10.1371/journal.pone.0009738.

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24

Renaud, S., D. Loukinov, L. Alberti, et al. "BORIS/CTCFL-mediated transcriptional regulation of the hTERT telomerase gene in testicular and ovarian tumor cells." Nucleic Acids Research 39, no. 3 (2010): 862–73. http://dx.doi.org/10.1093/nar/gkq827.

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25

Sati, Leyla, Caroline Zeiss, Krishna Yekkala, Ramazan Demir та James McGrath. "Expression of theCTCFLGene during Mouse Embryogenesis Causes Growth Retardation, Postnatal Lethality, and Dysregulation of the Transforming Growth Factor β Pathway". Molecular and Cellular Biology 35, № 19 (2015): 3436–45. http://dx.doi.org/10.1128/mcb.00381-15.

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CTCFL, a paralog ofCTCF, also known asBORIS(brother of regulator of imprinted sites), is a testis-expressed gene whose function is largely unknown. Its product is a cancer testis antigen (CTA), and it is often expressed in tumor cells and also seen in two benign human vascular malformations, juvenile angiofibromas and infantile hemangiomas. To understand the function ofCtcfl, we created tetracycline-inducibleCtcfltransgenic mice. We show thatCtcflexpression during embryogenesis results in growth retardation, eye malformations, multiorgan pathologies, vascular defects, and neonatal death. This
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26

Camprubí, Cristina, Marta Pladevall, Mark Grossmann, Nicolás Garrido, Maria C. Pons, and Joan Blanco. "Lack of association of MTHFR rs1801133 polymorphism and CTCFL mutations with sperm methylation errors in infertile patients." Journal of Assisted Reproduction and Genetics 30, no. 9 (2013): 1125–31. http://dx.doi.org/10.1007/s10815-013-0013-2.

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27

Jelinic, Petar, Jean-Christophe Stehle, and Phillip Shaw. "The Testis-Specific Factor CTCFL Cooperates with the Protein Methyltransferase PRMT7 in H19 Imprinting Control Region Methylation." PLoS Biology 4, no. 11 (2006): e355. http://dx.doi.org/10.1371/journal.pbio.0040355.

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28

Alberti, Loredana, Stéphanie Renaud, Lorena Losi, Serge Leyvraz, and Jean Benhattar. "High Expression of hTERT and Stemness Genes in BORIS/CTCFL Positive Cells Isolated from Embryonic Cancer Cells." PLoS ONE 9, no. 10 (2014): e109921. http://dx.doi.org/10.1371/journal.pone.0109921.

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29

Nguyen, Phuongmai, Gil Bar-Sela, Lunching Sun, et al. "BAT3 and SET1A Form a Complex with CTCFL/BORIS To Modulate H3K4 Histone Dimethylation and Gene Expression." Molecular and Cellular Biology 28, no. 21 (2008): 6720–29. http://dx.doi.org/10.1128/mcb.00568-08.

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ABSTRACT Chromatin status is characterized in part by covalent posttranslational modifications of histones that regulate chromatin dynamics and direct gene expression. BORIS (brother of the regulator of imprinted sites) is an insulator DNA-binding protein that is thought to play a role in chromatin organization and gene expression. BORIS is a cancer-germ line gene; these are genes normally present in male germ cells (testis) that are also expressed in cancer cell lines as well as primary tumors. This work identifies SET1A, an H3K4 methyltransferase, and BAT3, a cochaperone recruiter, as bindin
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EFTHYMIOU, VISSARION, JEREMY I. CHIMENE-WEISS, LIYUAN ZHOU, SORAVIS OSATAPHAN, LEI SU, and MARY-ELIZABETH PATTI. "280-OR: CTCFL Is a Fasting-Induced Epigenetic Regulator That Modulates Lipid and Cholesterol Metabolism in the Liver." Diabetes 70, Supplement 1 (2021): 280—OR. http://dx.doi.org/10.2337/db21-280-or.

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31

Nguyen, Phuongmai, Hengmi Cui, Kheem S. Bisht, et al. "CTCFL/BORIS Is a Methylation-Independent DNA-Binding Protein That Preferentially Binds to the Paternal H19 Differentially Methylated Region." Cancer Research 68, no. 14 (2008): 5546–51. http://dx.doi.org/10.1158/0008-5472.can-08-1005.

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Alberti, Loredana, Lorena Losi, Serge Leyvraz, and Jean Benhattar. "Different Effects of BORIS/CTCFL on Stemness Gene Expression, Sphere Formation and Cell Survival in Epithelial Cancer Stem Cells." PLOS ONE 10, no. 7 (2015): e0132977. http://dx.doi.org/10.1371/journal.pone.0132977.

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33

Xiao, Kui, Yang Wang, Lihua Zhou, et al. "Construction of ceRNA network to identify the lncRNA and mRNA related to non-small cell lung cancer." PLOS ONE 16, no. 10 (2021): e0259091. http://dx.doi.org/10.1371/journal.pone.0259091.

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Background Non-small cell lung cancer (NSCLC) harms human health, but its pathogenesis remains unclear. We wish to provide more molecular therapeutic targets for NSCLC. Methods The NSCLC tissue and normal tissue samples were screened for genetic comparison in the TCGA database. The predicted lncRNA and mRNA in BEAS2B and A549 cells were detected. Results Volcano plot displayed differentially expressed lncRNAs and mRNAs in adjacent tissues and NSCLC tissues. The survival curve showed that the lncRNA and mRNA had a significant impact on the patient’s survival. The results of GO term enrichment a
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34

Bernier-Latmani, Jeremiah, Alessandra Baumer, and Phillip Shaw. "No Evidence for Mutations of CTCFL/BORIS in Silver-Russell Syndrome Patients with IGF2/H19 Imprinting Control Region 1 Hypomethylation." PLoS ONE 4, no. 8 (2009): e6631. http://dx.doi.org/10.1371/journal.pone.0006631.

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35

Sun, L., L. Huang, P. Nguyen, et al. "DNA Methyltransferase 1 and 3B Activate BAG-1 Expression via Recruitment of CTCFL/BORIS and Modulation of Promoter Histone Methylation." Cancer Research 68, no. 8 (2008): 2726–35. http://dx.doi.org/10.1158/0008-5472.can-07-6654.

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36

Oshchepkova, Evgeniya, Yana Sizentsova, Daniil Wiebe, Victoria Mironova, and Nikolay Kolchanov. "Meta-Analysis of Transcriptome Data Detected New Potential Players in Response to Dioxin Exposure in Humans." International Journal of Molecular Sciences 21, no. 21 (2020): 7858. http://dx.doi.org/10.3390/ijms21217858.

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Dioxins are one of the most potent anthropogenic poisons, causing systemic disorders in embryonic development and pathologies in adults. The mechanism of dioxin action requires an aryl hydrocarbon receptor (AhR), but the downstream mechanisms are not yet precisely clear. Here, we performed a meta-analysis of all available transcriptome datasets taken from human cell cultures exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Differentially expressed genes from different experiments overlapped partially, but there were a number of those genes that were systematically affected by TCDD. Some
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37

Oczkowicz, Maria, Tomasz Szmatoła, and Małgorzata Świątkiewicz. "Source of Dietary Fat in Pig Diet Affects Adipose Expression of Genes Related to Cancer, Cardiovascular, and Neurodegenerative Diseases." Genes 10, no. 12 (2019): 948. http://dx.doi.org/10.3390/genes10120948.

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It has been known for many years that excessive consumption of saturated fats has proatherogenic properties, contrary to unsaturated fats. However, the molecular mechanism covering these effects is not fully understood. In this paper, we aimed to identify differentially expressed genes (DEGs) using RNA-sequencing, following feeding pigs with different sources of fat. After comparison of adipose samples from three dietary groups (rapeseed oil (n = 6), beef tallow (n = 5), coconut oil (n = 5)), we identified 29 DEGs (adjusted p-value < 0.05, fold change > 1.3) between beef tallow and rapes
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38

Hoivik, Erling A., Kanthida Kusonmano, Mari K. Halle, et al. "Hypomethylation of the CTCFL/BORIS promoter and aberrant expression during endometrial cancer progression suggests a role as an Epi-driver gene." Oncotarget 5, no. 4 (2014): 1052–61. http://dx.doi.org/10.18632/oncotarget.1697.

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39

Buoncervello, Maria, Paola Borghi, Giulia Romagnoli, et al. "Apicidin and Docetaxel Combination Treatment Drives CTCFL Expression and HMGB1 Release Acting as Potential Antitumor Immune Response Inducers in Metastatic Breast Cancer Cells." Neoplasia 14, no. 9 (2012): 855—IN19. http://dx.doi.org/10.1593/neo.121020.

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40

Garikapati, Koteswara Rao, Nibedita Patel, Venkata Krishna Kanth Makani, Priyanka Cilamkoti, Utpal Bhadra та Manika Pal Bhadra. "Down-regulation of BORIS/CTCFL efficiently regulates cancer stemness and metastasis in MYCN amplified neuroblastoma cell line by modulating Wnt/β-catenin signaling pathway". Biochemical and Biophysical Research Communications 484, № 1 (2017): 93–99. http://dx.doi.org/10.1016/j.bbrc.2017.01.066.

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41

Teplyakov, Evgeny, Qiongfang Wu, Jian Liu, et al. "The downregulation of putative anticancer target BORIS/CTCFL in an addicted myeloid cancer cell line modulates the expression of multiple protein coding and ncRNA genes." Oncotarget 8, no. 43 (2017): 73448–68. http://dx.doi.org/10.18632/oncotarget.20627.

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42

Creemers, S. G., P. M. van Koetsveld, F. J. van Kemenade, et al. "Methylation of IGF2 regulatory regions to diagnose adrenocortical carcinomas." Endocrine-Related Cancer 23, no. 9 (2016): 727–37. http://dx.doi.org/10.1530/erc-16-0266.

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Adrenocortical carcinoma (ACC) is a rare malignancy with a poor prognosis. Discrimination of ACCs from adrenocortical adenomas (ACAs) is challenging on both imaging and histopathological grounds. High IGF2 expression is associated with malignancy, but shows large variability. In this study, we investigate whether specific methylation patterns of IGF2 regulatory regions could serve as a valuable biomarker in distinguishing ACCs from ACAs. Pyrosequencing was used to analyse methylation percentages in DMR0, DMR2, imprinting control region (ICR) (consisting of CTCF3 and CTCF6) and the H19 promoter
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43

Frederico, Stephen, Itay Raphael, Michal Nisnboym, et al. "IMMU-07. THE IMMUNE LANDSCAPE OF PEDIATRIC BRAIN TUMORS: A TRANSCRIPTOMIC ANALYSIS." Neuro-Oncology 26, Supplement_8 (2024): viii153. http://dx.doi.org/10.1093/neuonc/noae165.0600.

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Abstract Despite standard-of-care therapy, pediatric brain tumors are now the leading cause of cancer-related death in children, highlighting an urgent need for the development of new treatments. Immunotherapy is actively being evaluated as a therapeutic approach to pediatric brain tumors, however, more research is needed to reveal additional antigenic targets that exist in these malignancies. In this study, our team performed a transcriptomic analysis of pediatric brain tumor RNA sequencing data within the Children’s Brain Tumor Network (CBTN) to identify intra and extracellular antigens that
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44

Kulaeva, E. D., E. S. Muzlaeva, and E. V. Mashkina. "mRNA-lncRNA gene expression signature in HPV-associated neoplasia and cervical cancer." Vavilov Journal of Genetics and Breeding 28, no. 3 (2024): 342–50. http://dx.doi.org/10.18699/vjgb-24-39.

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Cervical cancer is one of the most frequent cancers in women and is associated with human papillomavirus (HPV) in 70 % of cases. Cervical cancer occurs because of progression of low-differentiated cervical intraepithelial neoplasia through grade 2 and 3 lesions. Along with the protein-coding genes, long noncoding RNAs (lncRNAs) play an important role in the development of malignant cell transformation. Although human papillomavirus is widespread, there is currently no well-characterized transcriptomic signature to predict whether this tumor will develop in the presence of HPV-associated neopla
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45

Heimbruch, Katelyn E., and Sridhar Rao. "Genetic Interactions between Cohesin Mutations and Core-Binding Factor Driver Oncogenes." Blood 134, Supplement_1 (2019): 2540. http://dx.doi.org/10.1182/blood-2019-125893.

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Introduction: AML is a genetically heterogeneous disease, with an average 5-year survival of 50%. The core-binding factor complex is essential for normal hematopoiesis and is composed of two subunits, AML1 (aka RUNX1) and CBFB. Both AML1 and CBFB are involved in distinct chromosomal translocations in AML, t(8;21) and inv(16), which generate the fusion oncoproteins AML1-ETO or CBFB-MYH11 (Speck 2002). Heterozygous mutations in one of four members of the cohesin complex (RAD21, SMC3, STAG2, and SMC1A) are commonly found in patients with AML, and frequently (up to 25%) co-occur with AML1-ETO, but
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46

Thangavel, Hariprasad, Carmine De Angelis, Suhas Vasaikar, et al. "A CTC-Cluster-Specific Signature Derived from OMICS Analysis of Patient-Derived Xenograft Tumors Predicts Outcomes in Basal-Like Breast Cancer." Journal of Clinical Medicine 8, no. 11 (2019): 1772. http://dx.doi.org/10.3390/jcm8111772.

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Circulating tumor cell clusters (CTCcl) have a higher metastatic potential compared to single CTCs and predict long-term outcomes in breast cancer (BC) patients. Because of the rarity of CTCcls, molecular characterization of primary tumors that give rise to CTCcl hold significant promise for better diagnosis and target discovery to combat metastatic BC. In our study, we utilized the reverse-phase protein array (RPPA) and transcriptomic (RNA-Seq) data of 10 triple-negative BC patient-derived xenograft (TNBC PDX) transplantable models with CTCs and evaluated expression of upregulated candidate p
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47

Cannarella, Rossella, Andrea Crafa, Laura M. Mongioì, et al. "DNA Methylation in Offspring Conceived after Assisted Reproductive Techniques: A Systematic Review and Meta-Analysis." Journal of Clinical Medicine 11, no. 17 (2022): 5056. http://dx.doi.org/10.3390/jcm11175056.

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Background: In the last 40 years, assisted reproductive techniques (ARTs) have emerged as potentially resolving procedures for couple infertility. This study aims to evaluate whether ART is associated with epigenetic dysregulation in the offspring. Methods. To accomplish this, we collected all available data on methylation patterns in offspring conceived after ART and in spontaneously conceived (SC) offspring. Results. We extracted 949 records. Of these, 50 were considered eligible; 12 were included in the quantitative synthesis. Methylation levels of H19 CCCTC-binding factor 3 (CTCF3) were si
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Hu, Gongcheng, Xiaotao Dong, Shixin Gong, Yawei Song, Andrew P. Hutchins, and Hongjie Yao. "Systematic screening of CTCF binding partners identifies that BHLHE40 regulates CTCF genome-wide distribution and long-range chromatin interactions." Nucleic Acids Research 48, no. 17 (2020): 9606–20. http://dx.doi.org/10.1093/nar/gkaa705.

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Abstract:
Abstract CTCF plays a pivotal role in mediating chromatin interactions, but it does not do so alone. A number of factors have been reported to co-localize with CTCF and regulate CTCF loops, but no comprehensive analysis of binding partners has been performed. This prompted us to identify CTCF loop participants and regulators by co-localization analysis with CTCF. We screened all factors that had ChIP-seq data in humans by co-localization analysis with human super conserved CTCF (hscCTCF) binding sites, and identified many new factors that overlapped with hscCTCF binding sites. Combined with CT
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Bailey, Charles, Cynthia Metierre, Yue Feng, et al. "CTCF Expression is Essential for Somatic Cell Viability and Protection Against Cancer." International Journal of Molecular Sciences 19, no. 12 (2018): 3832. http://dx.doi.org/10.3390/ijms19123832.

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CCCTC-binding factor (CTCF) is a conserved transcription factor that performs diverse roles in transcriptional regulation and chromatin architecture. Cancer genome sequencing reveals diverse acquired mutations in CTCF, which we have shown functions as a tumour suppressor gene. While CTCF is essential for embryonic development, little is known of its absolute requirement in somatic cells and the consequences of CTCF haploinsufficiency. We examined the consequences of CTCF depletion in immortalised human and mouse cells using shRNA knockdown and CRISPR/Cas9 genome editing as well as examined the
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Chernukhin, Igor, Shaharum Shamsuddin, Sung Yun Kang, et al. "CTCF Interacts with and Recruits the Largest Subunit of RNA Polymerase II to CTCF Target Sites Genome-Wide." Molecular and Cellular Biology 27, no. 5 (2007): 1631–48. http://dx.doi.org/10.1128/mcb.01993-06.

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ABSTRACT CTCF is a transcription factor with highly versatile functions ranging from gene activation and repression to the regulation of insulator function and imprinting. Although many of these functions rely on CTCF-DNA interactions, it is an emerging realization that CTCF-dependent molecular processes involve CTCF interactions with other proteins. In this study, we report the association of a subpopulation of CTCF with the RNA polymerase II (Pol II) protein complex. We identified the largest subunit of Pol II (LS Pol II) as a protein significantly colocalizing with CTCF in the nucleus and s
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