Relevant bibliographies by topics / Cancer transcription

Academic literature on the topic 'Cancer transcription'

Author: Grafiati
Published: 11 March 2023

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Journal articles on the topic "Cancer transcription"

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Otálora-Otálora, Beatriz Andrea, Liliana López-Kleine, and Adriana Rojas. "Lung Cancer Gene Regulatory Network of Transcription Factors Related to the Hallmarks of Cancer." Current Issues in Molecular Biology 45, no. 1 (January 5, 2023): 434–64. http://dx.doi.org/10.3390/cimb45010029.

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The transcriptomic analysis of microarray and RNA-Seq datasets followed our own bioinformatic pipeline to identify a transcriptional regulatory network of lung cancer. Twenty-six transcription factors are dysregulated and co-expressed in most of the lung cancer and pulmonary arterial hypertension datasets, which makes them the most frequently dysregulated transcription factors. Co-expression, gene regulatory, coregulatory, and transcriptional regulatory networks, along with fibration symmetries, were constructed to identify common connection patterns, alignments, main regulators, and target genes in order to analyze transcription factor complex formation, as well as its synchronized co-expression patterns in every type of lung cancer. The regulatory function of the most frequently dysregulated transcription factors over lung cancer deregulated genes was validated with ChEA3 enrichment analysis. A Kaplan–Meier plotter analysis linked the dysregulation of the top transcription factors with lung cancer patients' survival. Our results indicate that lung cancer has unique and common deregulated genes and transcription factors with pulmonary arterial hypertension, co-expressed and regulated in a coordinated and cooperative manner by the transcriptional regulatory network that might be associated with critical biological processes and signaling pathways related to the acquisition of the hallmarks of cancer, making them potentially relevant tumor biomarkers for lung cancer early diagnosis and targets for the development of personalized therapies against lung cancer.
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Chen, Chia-Chun, Kai Song, Wendy Tran, Matthew Obusan, Tyler Sugimoto, Katherine Sheu, Donghui Cheng, et al. "Abstract 789: Elucidating transcriptional dynamics in neuroendocrine differentiation of advanced prostate cancer." Cancer Research 82, no. 12_Supplement (June 15, 2022): 789. http://dx.doi.org/10.1158/1538-7445.am2022-789.

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Abstract Small cell carcinomas of the lung, bladder, and prostate share similar transcription patterns and drug sensitivities. Due to their high cellular plasticity, these cancers often escape treatment through a trans-differentiation from adenocarcinoma to the neuroendocrine state. We previously developed a pan small cell cancer in vitro/in vivo model named PARCB that can recapitulate this transition from primary patient tissues. To understand which transcription factors may be important in this transition, we conducted bulk and single cell RNA sequencing over time. We identified a developmental trajectory that is shared among all samples and is defined by stage-specific transcription factors. We plan to interrogate the role that these transcription factors play in the PARCB transformation assay. We performed ATAC sequencing to investigate how these transcription factors regulate these transitional states. Our study will provide a basic understanding of the transcriptional changes that occur during neuroendocrine differentiation and provide new potential therapeutic targets for small cell cancers. Citation Format: Chia-Chun Chen, Kai Song, Wendy Tran, Matthew Obusan, Tyler Sugimoto, Katherine Sheu, Donghui Cheng, Grigor Varuzhanyan, Liang Wang, Lisa Ta, Zhiyuan Mao, Nathanael Bangayan, Jung-Wook Park, Thomas Graerber, Owen Witte. Elucidating transcriptional dynamics in neuroendocrine differentiation of advanced prostate cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 789.
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Tsai, Jessica W., Paloma Cejas, Dayle K. Wang, Smruti Patel, David W. Wu, Phonepasong Arounleut, Xin Wei, et al. "FOXR2 Is an Epigenetically Regulated Pan-Cancer Oncogene That Activates ETS Transcriptional Circuits." Cancer Research 82, no. 17 (July 8, 2022): 2980–3001. http://dx.doi.org/10.1158/0008-5472.can-22-0671.

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Abstract Forkhead box R2 (FOXR2) is a forkhead transcription factor located on the X chromosome whose expression is normally restricted to the testis. In this study, we performed a pan-cancer analysis of FOXR2 activation across more than 10,000 adult and pediatric cancer samples and found FOXR2 to be aberrantly upregulated in 70% of all cancer types and 8% of all individual tumors. The majority of tumors (78%) aberrantly expressed FOXR2 through a previously undescribed epigenetic mechanism that involves hypomethylation of a novel promoter, which was functionally validated as necessary for FOXR2 expression and proliferation in FOXR2-expressing cancer cells. FOXR2 promoted tumor growth across multiple cancer lineages and co-opted ETS family transcription circuits across cancers. Taken together, this study identifies FOXR2 as a potent and ubiquitous oncogene that is epigenetically activated across the majority of human cancers. The identification of hijacking of ETS transcription circuits by FOXR2 extends the mechanisms known to active ETS transcription factors and highlights how transcription factor families cooperate to enhance tumorigenesis. Significance: This work identifies a novel promoter that drives aberrant FOXR2 expression and delineates FOXR2 as a pan-cancer oncogene that specifically activates ETS transcriptional circuits across human cancers. See related commentary by Liu and Northcott, p. 2977
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Rosado-Tristani, Diego A., Carlos S. Morales, Esther A. Peterson, and Jose A. Rodríguez-Martínez. "Abstract 2275: Transcription factor landscape cataloguing highlights key insights in inflammatory breast cancer (IBC)." Cancer Research 82, no. 12_Supplement (June 15, 2022): 2275. http://dx.doi.org/10.1158/1538-7445.am2022-2275.

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Abstract Transcription factors are proteins that bind to DNA in a sequence-specific manner to regulate gene expression for normal cellular functions. Cancers have been shown to have aberrant transcriptional regulation. Therefore, identifying transcription factor landscapes will aid in characterizing complex diseases. As an example, breast cancer has many subtypes that are phenotypically and molecularly distinct. Inflammatory Breast Cancer (IBC) is rare, and the most aggressive form of breast cancer currently known. It is a poorly characterized subtype, and diagnosis often results in poor prognosis for patients. As such, we decided to explore the transcription factor landscape in IBC. This was accomplished employing the following strategy: 1) We assembled de novo transcriptomes for SUM149, an IBC cancer line and MCF7, a non-IBC cancer line using Trinity; 2) We translated the assembled transcriptomes using getORF from EMBOSS; 3) We identified putative transcription factors in the translated transcriptomes using CREPE. We then identified differentially expressed genes between SUM-149 and MCF-7 using DEseq2. Our results highlight differences in the transcription factor catalogues between IBC and non-IBC cancers. Of interest in SUM-149 is the gene BNC1, a member of the C2H2 zinc finger family of transcription factors. Dysregulation of this gene is associated with brain metastasis in breast cancers which is a common phenotype in IBC. BNC1-associated genes are linked to GO terms such as, epithelial cell differentiation, and regulation of alternative mRNA splicing, via spliceosome; however, BNC1 functions in IBC are yet to be determined. This analysis will bridge the gap in knowledge of key transcriptional regulators in IBC. Citation Format: Diego A. Rosado-Tristani, Carlos S. Morales, Esther A. Peterson, Jose A. Rodríguez-Martínez. Transcription factor landscape cataloguing highlights key insights in inflammatory breast cancer (IBC) [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 2275.
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Ishihara, Seiichiro, and Hisashi Haga. "Matrix Stiffness Contributes to Cancer Progression by Regulating Transcription Factors." Cancers 14, no. 4 (February 18, 2022): 1049. http://dx.doi.org/10.3390/cancers14041049.

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Matrix stiffness is critical for the progression of various types of cancers. In solid cancers such as mammary and pancreatic cancers, tumors often contain abnormally stiff tissues, mainly caused by stiff extracellular matrices due to accumulation, contraction, and crosslinking. Stiff extracellular matrices trigger mechanotransduction, the conversion of mechanical cues such as stiffness of the matrix to biochemical signaling in the cells, and as a result determine the cellular phenotypes of cancer and stromal cells in tumors. Transcription factors are key molecules for these processes, as they respond to matrix stiffness and are crucial for cellular behaviors. The Yes-associated protein (YAP)/transcriptional coactivator with PDZ-binding motif (TAZ) is one of the most studied transcription factors that is regulated by matrix stiffness. The YAP/TAZ are activated by a stiff matrix and promotes malignant phenotypes in cancer and stromal cells, including cancer-associated fibroblasts. In addition, other transcription factors such as β-catenin and nuclear factor kappa B (NF-κB) also play key roles in mechanotransduction in cancer tissues. In this review, the mechanisms of stiffening cancer tissues are introduced, and the transcription factors regulated by matrix stiffness in cancer and stromal cells and their roles in cancer progression are shown.
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Cox, PM, and CR Goding. "Transcription and cancer." British Journal of Cancer 63, no. 5 (May 1991): 651–62. http://dx.doi.org/10.1038/bjc.1991.151.

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Arancio, Walter, and Claudia Coronnello. "Repetitive Sequence Transcription in Breast Cancer." Cells 11, no. 16 (August 14, 2022): 2522. http://dx.doi.org/10.3390/cells11162522.

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Repetitive sequences represent about half of the human genome. They are actively transcribed and play a role during development and in epigenetic regulation. The altered activity of repetitive sequences can lead to genomic instability and they can contribute to the establishment or the progression of degenerative diseases and cancer transformation. In this work, we analyzed the expression profiles of DNA repetitive sequences in the breast cancer specimens of the HMUCC cohort. Satellite expression is generally upregulated in breast cancers, with specific families upregulated per histotype: in HER2-enriched cancers, they are the human satellite II (HSATII), in luminal A and B, they are part of the ALR family and in triple-negative, they are part of SAR and GSAT families, together with a perturbation in the transcription from endogenous retroviruses and their LTR sequences. We report that the background expression of repetitive sequences in healthy tissues of cancer patients differs from the tissues of non-cancerous controls. To conclude, peculiar patterns of expression of repetitive sequences are reported in each specimen, especially in the case of transcripts arising from satellite repeats.
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Lai, Trang Huyen, Mahmoud Ahmed, Jin Seok Hwang, Sahib Zada, Trang Minh Pham, Omar Elashkar, and Deok Ryong Kim. "Transcriptional Repression of Raf Kinase Inhibitory Protein Gene by Metadherin during Cancer Progression." International Journal of Molecular Sciences 22, no. 6 (March 17, 2021): 3052. http://dx.doi.org/10.3390/ijms22063052.

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Raf kinase inhibitory protein (RKIP), also known as a phosphatidylethanolamine-binding protein 1 (PEBP1), functions as a tumor suppressor and regulates several signaling pathways, including ERK and NF-κκB. RKIP is severely downregulated in human malignant cancers, indicating a functional association with cancer metastasis and poor prognosis. The transcription regulation of RKIP gene in human cancers is not well understood. In this study, we suggested a possible transcription mechanism for the regulation of RKIP in human cancer cells. We found that Metadherin (MTDH) significantly repressed the transcriptional activity of RKIP gene. An analysis of publicly available datasets showed that the knockdown of MTDH in breast and endometrial cancer cell lines induced the expression RKIP. In addition, the results obtained from qRT-PCR and ChIP analyses showed that MTDH considerably inhibited RKIP expression. In addition, the RKIP transcript levels in MTDH-knockdown or MTDH-overexpressing MCF-7 cells were likely correlated to the protein levels, suggesting that MTDH regulates RKIP expression. In conclusion, we suggest that MTDH is a novel factor that controls the RKIP transcription, which is essential for cancer progression.
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Moparthi, Lavanya, Giulia Pizzolato, and Stefan Koch. "Wnt activator FOXB2 drives the neuroendocrine differentiation of prostate cancer." Proceedings of the National Academy of Sciences 116, no. 44 (October 14, 2019): 22189–95. http://dx.doi.org/10.1073/pnas.1906484116.

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The Wnt signaling pathway is of paramount importance for development and disease. However, the tissue-specific regulation of Wnt pathway activity remains incompletely understood. Here we identify FOXB2, an uncharacterized forkhead box family transcription factor, as a potent activator of Wnt signaling in normal and cancer cells. Mechanistically, FOXB2 induces multiple Wnt ligands, including WNT7B, which increases TCF/LEF-dependent transcription without activating Wnt coreceptor LRP6 or β-catenin. Proximity ligation and functional complementation assays identified several transcription regulators, including YY1, JUN, and DDX5, as cofactors required for FOXB2-dependent pathway activation. Although FOXB2 expression is limited in adults, it is induced in select cancers, particularly advanced prostate cancer. RNA-seq data analysis suggests that FOXB2/WNT7B expression in prostate cancer is associated with a transcriptional program that favors neuronal differentiation and decreases recurrence-free survival. Consistently, FOXB2 controls Wnt signaling and neuroendocrine differentiation of prostate cancer cell lines. Our results suggest that FOXB2 is a tissue-specific Wnt activator that promotes the malignant transformation of prostate cancer.
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Barrera, Giuseppina, Marie Angele Cucci, Margherita Grattarola, Chiara Dianzani, Giuliana Muzio, and Stefania Pizzimenti. "Control of Oxidative Stress in Cancer Chemoresistance: Spotlight on Nrf2 Role." Antioxidants 10, no. 4 (March 25, 2021): 510. http://dx.doi.org/10.3390/antiox10040510.

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Chemoresistance represents the main obstacle to cancer treatment with both conventional and targeted therapy. Beyond specific molecular alterations, which can lead to targeted therapy, metabolic remodeling, including the control of redox status, plays an important role in cancer cell survival following therapy. Although cancer cells generally have a high basal reactive oxygen species (ROS) level, which makes them more susceptible than normal cells to a further increase of ROS, chemoresistant cancer cells become highly adapted to intrinsic or drug-induced oxidative stress by upregulating their antioxidant systems. The antioxidant response is principally mediated by the transcription factor Nrf2, which has been considered the master regulator of antioxidant and cytoprotective genes. Nrf2 expression is often increased in several types of chemoresistant cancer cells, and its expression is mediated by diverse mechanisms. In addition to Nrf2, other transcription factors and transcriptional coactivators can participate to maintain the high antioxidant levels in chemo and radio-resistant cancer cells. The control of expression and function of these molecules has been recently deepened to identify which of these could be used as a new therapeutic target in the treatment of tumors resistant to conventional therapy. In this review, we report the more recent advances in the study of Nrf2 regulation in chemoresistant cancers and the role played by other transcription factors and transcriptional coactivators in the control of antioxidant responses in chemoresistant cancer cells.
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Dissertations / Theses on the topic "Cancer transcription"

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Rheinheimer, Brenna Ann. "Alternative Transcription Of The SLIT2/Mir-218-1 Transcriptional Axis Mediates Pancreatic Cancer Invasion." Diss., The University of Arizona, 2016. http://hdl.handle.net/10150/605118.

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The development of several organ systems through modeling and shaping of the tissue structure occurs from signaling through axon guidance molecules. The Slit family of ligands has been shown to regulate branching morphogenesis in mammary gland duct development and loss of Slit gene expression during this time leads to the formation of hyperplastic, disorganized lesions suggesting a potential role for Slits in cancer formation. Characterization of human pancreatic ductal adenocarcinoma cell lines showed a loss of SLIT2 expression in cells that contain activated Kras. Loss of SLIT2 expression was associated with DNA methylation of CpG sites within the SLIT2 core promoter and chromatin enrichment of repressive histone modifications at the SLIT2 transcriptional start site. Additionally, treatment of pancreatic ductal adenocarcinoma cell lines with demethylating agent 5-aza-2'-deoxycytidine led to SLIT2 re-expression while treatment with histone deacetylase inhibitor Trichostatin A did not. Mir-218-1 is an intronic microRNA encoded within intron 15 of the SLIT2 gene. Expression of mir-218-1 does not correlate with SLIT2 mRNA expression suggesting that it is transcribed from a promoter independent of the SLIT2 gene promoter. Pancreatic ductal adenocarcinoma cell lines showed a peak of H3K4me3 chromatin enrichment localized to a 1kb region within intron 4 of the SLIT2 gene denoting a candidate alternative promoter for mir-218-1. A concordant peak of H4ac chromatin enrichment overlapped the peak of H3K4me3 enrichment and transcriptional activity was measured from the 1kb region in all pancreatic ductal adenocarcinoma cell lines. A NF-κB binding site was also predicted to exist within the 1kb region. Transfection with two independent siRNAs to NF-κB led to an increase in both pre-mir-218-1 and mature mir-218-1 while treatment with an inhibitor to IκB kinase led to an increase in pre-mir-218-1 expression. Additionally, the p65 subunit of NF-κB was found to bind to the candidate mir-218-1 alternative promoter in pancreatic ductal adenocarcinoma cell lines that do not contain DNA CpG methylation at the predicted NF-κB binding site. It was discovered that miR-218 is a modulator of ARF6 expression suggesting a role in the inhibition of pancreatic ductal adenocarcinoma cell invasion through modulation of the actin cytoskeleton. Overexpression with a miR-218 precursor showed that miR-218 is an inhibitor of pancreatic ductal adenocarcinoma cell invasion in two dimensions. Additionally, it was found that while miR-218 does not have an affect on the ability of pancreatic ductal adenocarcinoma cells to form functional invadopodia, miR-218 is an inhibitor of the extracellular matrix degradation properties of mature invadopodia. Interestingly, the effect of miR-218 on pancreatic ductal adenocarcinoma cell invasion or extracellular matrix degradation is not reliant on the cell's dependency on Kras signaling for growth and survival. Collectively, these observations indicate that understanding the transcriptional regulation of SLIT2 and mir-218-1 expression as well as their signaling properties may provide a step toward the development of diagnostic tests and therapeutic treatments for patients with invasive or metastatic pancreatic ductal adenocarcinoma.
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Vance, Keith. "Cell type specific regulation of papillomavirus transcription." Thesis, University of Glasgow, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.340281.

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Pomeranz, Karen M. "Regulation of FoxO transcription factors in breast cancer." Thesis, Imperial College London, 2008. http://hdl.handle.net/10044/1/4253.

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Breast cancer is the world's most prevalent cancer. Although several drugs and chemotherapeutic strategies have been developed to tackle breast cancer, to date most patients eventually acquire resistance to these anticancer therapies. Therefore, identifying ways to increase the efficiency of currently used chemotherapeutic drugs and the development of new drugs for breast cancer treatment is essential. One way to achieve this goal is by identifying cellular targets which play a pivotal role in tumourigenesis and tumour progression. Paclitaxel belongs to a class of naturally occurring anti microtubule agents used for the treatment of malignancies such as breast cancer. Previous work has shown that FoxO3a, a transcription factor downstream of the phosphotidylinsitol-3-kinase/Akt signalling pathway, mediates apoptosis and cell cycle arrest in breast cancer cells in response to paclitaxel treatment. In order to elucidate the significance of FoxO expression and activation in response to paclitaxel treatment and oxidative stress (which is caused by paclitaxel treatment), I investigated the regulation of FoxO in endometrial and breast cancer cells. Both paclitaxel and oxidative stress were found to upregulate FoxO expression at the protein, mRNA and gene-promoter levels. Moreover, treatment with paclitaxel and hydrogen peroxide were shown to increase FoxO3a protein stability. Paclitaxel treatment resulted in JNK mediated nuclear accumulation of FoxO3a with a corresponding reduction in Akt activity. JNK was also shown to induce FoxO3a gene-promoter activity and to phosphorylate FoxO3a at two sites. These phosphorylation events may be important in the regulation of FoxO3a stability and activity. I also investigated the function of FoxO3a, by studying the role of BTG1, a downstream target of FoxO3a. I found that BTG1 expression was induced at the gene-promoter level by FoxO3a in MCF-7 cells. The use of a BTG1 inducible MCF-7 cell line revealed that over-expression of BTG1 results in changes in the expression levels of cell cycle regulators, reduction in cell growth and accumulation of cells in the G2/M phase of the cell cycle. Taken together, these results show that FoxO expression and activity are upregulated following paclitaxel treatment and demonstrate that the PI3K/Akt/FoxO and JNK signalling pathways cross-talk at least at two levels. Furthermore, these results indicate that FoxO expression levels may serve as bio-marker for determining the effectiveness of paclitaxel treatment of breast cancer patients and that FoxOs may serve as a potential target for anti-cancer chemotherapeutic intervention.
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Smith, Richard LeRoy. "Cis-regulatory Sequence and Co-regulatory Transcription Factor Functions in ERα-Mediated Transcriptional Repression." BYU ScholarsArchive, 2009. https://scholarsarchive.byu.edu/etd/2261.

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Estrogens exert numerous actions throughout the human body, targeting healthy tissue while also enhancing the proliferative capacity of breast cancers. Estrogen signaling is mediated by the estrogen receptor (ER), which binds DNA and ultimately affects the expression of adjacent genes. Current understanding of ER-mediated transcriptional regulation is mostly limited to genes whose transcript levels increase following estrogen exposure, though recent studies demonstrate that direct down-regulation of estrogen-responsive genes is also a significant feature of ER action. We hypothesized that differences in cis-regulatory DNA was a factor in determining target gene expression and performed computational and experimental studies to test this hypothesis. From our in silico analyses, we show that the binding motifs for certain transcription factors are enriched in cis-regulatory sequences adjacent to repressed target genes compared to induced target genes, including the motif for RUNX1. In silico analyses were tested experimentally using dual luciferase reporter assays, which indicate that several ER binding sites are estrogen responsive. Mutagenesis of transcription factor motifs (for ER and RUNX1) reduced the response of reporter gene. Further experiments demonstrated that co-recruitment of ER and RUNX1 is necessary for repression of gene expression at some target genes. These findings highlight a novel interaction between ER and RUNX1 and their role in transcriptional repression in breast cancer.
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Tse, Yuen-yu Belinda, and 謝宛余. "Expression of FOXP1 in breast cancer." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2013. http://hdl.handle.net/10722/193527.

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Objectives: Forkhead box protein P1 (FOXP1) is a transcription factor, and a member of the P-subfamily of forkhead box transcription factor and regulate transcription of a subset of genes that involved in various cellular events. It plays a critical role in regulating cell growth and proliferation, differentiation, embryogenesis, adult tissue homeostasis, and possibly tumorigenesis. Predominant nuclear localisation of FOXP1 protein is commonly expressed at low level in normal tissues and upregulated in proliferative cells. Studies have demonstrated that the loss of FOXP1 expression and cytoplasmic mis-localisation is significantly associated with various malignant cancers, including breast cancer. FOXP1 can act either as a tumor suppressor or as an oncogenic protein in cell-type specific functions. It has been shown to be a co-regulator of estrogen receptor alpha and can modify a specific subset of forkhead box transcription factor class O (FOXO)-target genes. We hypothesise that there is association between FOXP1 expression and patient survival, and explore the potential role of FOXP1 expression as a prognostic marker in breast cancer. Methods: One hundred and twenty breast cancer samples in tissue microarray blocks were examined for FOXP1 expression by immuno-histochemistry. Nuclear and cytoplasmic FOXP1 expression patterns were analysed with clinico-pathological parameters. Statistical analysis was performed using SPSS software to determine the correlation between FOXP1 expression and clinico-pathological parameters. The correlation between subcellular FOXP1 expression and survival was evaluated by COX regression analysis. Results: Nuclear or cytoplasmic FOXP1 expression showed no association with clinico-pathological parameters. However, our results showed that there was significant association with estrogen receptor and progesterone receptor when nuclear and cytoplasmic scores were combined as total FOXP1 score (p=0.022 and p=0.028 respectively). In univariate analysis, high nuclear and cytoplasmic FOXP1 expression had no significant correlation with poor survival, while high total FOXP1 expression was associated with poor overall and disease-specific survival (p=0.045). Tumor stage and lymph-node involvement were significantly related to poorer overall and disease-specific survival, while other clinico-pathological parameters did not. In breast cancer with advanced tumor grade and lymph-node involvement, overall and disease-specific survival are significantly associated with high FOXP1 expression (p=0.041 and p=0.015 respectively). Conclusion: Unlike previous reports, our findings show that increased nuclear and cytoplasmic FOXP1 expression were both observed and high total FOXP1 expression was associated with poorer survival, particularly in cases of advance tumor grade and with lymph node metastases. These finding are supported by a recent report that showed that FOXP1 can up-regulate its own expression by binding to the promoter of FOXP1 and promote cell survival of breast cancer cells by suppressing FOXO-induced apoptosis. It may be possible that FOXP1 expression is up-regulated in a positive feedback loop in breast cancer cells such that there is both increased nuclear transcriptional activity and cytoplasm localisation of FOXP1. Further investigation is necessary to understand the role of FOXP1 in the progression of breast cancer and determine its potential use as a prognostic marker.
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Pathology
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Master of Medical Sciences
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Essack, Magbubah. "Transcription Regulation and Candidate Diagnostic Markers of Esophageal Cancer." Thesis, University of the Western Cape, 2009. http://etd.uwc.ac.za/index.php?module=etd&action=viewtitle&id=gen8Srv25Nme4_5306_1267148426.

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This thesis reports on the development of a novel comprehensive database (Dragon Database of Genes Implicated in Esophageal Cancer, DDEC) as an integrated knowledge database aimed at representing a gateway to esophageal cancer related data. More importantly, it illustrates how the biocurated genes in the database may represent a reliable starting point for divulging transcriptional regulation, diagnostic markers and the biology related to esophageal cancer.

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Williams, Christopher M. J. "Transcription factor AP-2 regulatory signatures in breast cancer." Thesis, Queen Mary, University of London, 2007. http://qmro.qmul.ac.uk/xmlui/handle/123456789/1644.

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AP-2 transcription factors are highly conserved basic helix-span-helix proteins whose members ((x, ß, y, S and c) are crucial regulators of bryonic development. They also play an important role in human neoplasia. uohis ochemical studies have detected high levels of AP-2y expression in primary tumo of breast cancer patients. This high expression has been correlated with reduced survival in all patients and reduced survival in an ERa positive subset treated with hormone therapy. In breast cancer cell lines, AP- 2 factors have been implicated in the regulation of the ERBB2 proto-oncogene and ERa. In an effort to further understand the role of AP-2y in breast carcinoma, this study has sought to identify additional AP-2 activated cellular pathways and ultimately novel transcriptional targets for AP-2 through the use of gene expression profiling. RNAi using three independent AP-2y targeting sequences, has been used to deplete AP- 2y levels in the ERa positive MCF-7 breast carcinoma cell line, chosen as it exclusively expresses the AP-2y family member. Microarrays were then utilised to create an AP-2y dependent transcription profile. Statistical comparisons between non-silencing control siRNA and AP-2y targeting siRNA groups identified a total of 162 gene expression changes (p<0.01). These changes implicate AP-2y in the control of cell cycle progression and developmental signalling. Indeed a role for AP-2y in the control of cell cycle, in particular at the GUS transition, has been verified using flow cytometry. Several of these gene expression changes, including IGFBP3, Transgelin and KIAA1324, have been confirmed using qPCR and immunoblotting. Finally, elevated levels of p21 mRNA and protein have been observed following AP-2y silencing in MCF-7 cells. Additionally, the activity of a p21 promoter reporter is repressed following transfection with an AP-2y expression construct in HepG2 cells. These results coupled with ChIP experiments showing AP-2y occupancy at the proximal promoter region of p21 in cycling MCF-7 cells, implicate AP-2y in the repression of p21 transcription and suggest a role for AP2y in- the, control of cell cycle in breast carcinoma in part through the transcriptional repression of p21.
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Wiseman, Elizabeth Fiona. "Novel FOXM1 transcription factor target genes in oesophageal cancer." Thesis, University of Manchester, 2014. https://www.research.manchester.ac.uk/portal/en/theses/novel-foxm1-transcription-factor-target-genes-in-oesophageal-cancer(24278706-fa41-41b9-bf59-1902b1c4ba3d).html.

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The prognosis of oesophageal cancer remains poor, with <10% 5-year survival. Delineating the molecular pathogenesis of oesophageal cancer could inform future research into targeted therapies and may uncover novel biomarkers to aid management decisions. As a transcription factor with important roles in the control of cell cycle transcription, FOXM1 regulates cellular proliferation and chromosome stability. FOXM1 is frequently overexpressed in human cancers and this has recently been described in oesophageal adenocarcinoma (OAC) tissues. We have sought to identify novel gene targets of FOXM1 to better understand the molecular pathogenesis of OAC. Using chromatin immunoprecipitation coupled with high-throughput sequencing (ChIP-seq) in OE33 OAC cells we investigated the genome-wide DNA binding regions of FOXM1, identifying a shortlist of putative FOXM1 target genes. We then identified those genes with evidence of transcriptional regulation by FOXM1 in primary oesophageal tissue specimens and in OE33 OAC cells subjected to FOXM1-directed RNA interference, using the Nanostring mRNA quantification technique. True direct FOXM1 target genes were defined as those genes that are bound by FOXM1 at their regulatory regions in OE33 cells, significantly downregulated in FOXM1-depleted OE33 cells and significantly overexpressed in primary oesophageal tissues expressing high FOXM1 mRNA levels. We identified the following genes as direct FOXM1 transcriptional targets: CDKN3, CCNB1, CCNF, KIF14, KPNA2, UBE2C, MKI67, GTSE1, TPX2, KIF23, FAM64A, UHRF1, MAD2L1, ANLN, DBF4, ETV4 and ZNF367. All of these genes have functions in cell cycle-related processes, apart from ETV4 and ZNF367 which function as transcriptional activators. The expression levels of ETV4 and UHRF1 were significantly associated with locally advanced disease (advanced T stage) and metastatic disease respectively. Identification of these new FOXM1 transcriptional targets in oesophageal tissues provides further insights into the molecular pathobiology of OAC, by identifying new gene pathways that are upregulated as a result of FOXM1 overexpression in OAC.
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Gherardi, Samuele <1981&gt. "Myc-mediated control of gene transcription in cancer cells." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2010. http://amsdottorato.unibo.it/2809/1/Gherardi_Samuele_Tesi.pdf.

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The Myc oncoproteins belong to a family of transcription factors composed by Myc, N-Myc and L-Myc. The most studied components of this family are Myc and N-Myc because their expressions are frequently deregulated in a wide range of cancers. These oncoproteins can act both as activators or repressors of gene transcription. As activators, they heterodimerize with Max (Myc associated X-factor) and the heterodimer recognizes and binds a specific sequence elements (E-Box) onto gene promoters recruiting histone acetylase and inducing transcriptional activation. Myc-mediated transcriptional repression is a quite debated issue. One of the first mechanisms defined for the Myc-mediated transcriptional repression consisted in the interaction of Myc-Max complex Sp1 and/or Miz1 transcription factors already bound to gene promoters. This interaction may interfere with their activation functions by recruiting co-repressors such as Dnmt3 or HDACs. Moreover, in the absence of , Myc may interfere with the Sp1 activation function by direct interaction and subsequent recruitment of HDACs. More recently the Myc/Max complex was also shown to mediate transcriptional repression by direct binding to peculiar E-box. In this study we analyzed the role of Myc overexpression in Osteosarcoma and Neuroblastoma oncogenesis and the mechanisms underling to Myc function. Myc overexpression is known to correlate with chemoresistance in Osteosarcoma cells. We extended this study by demonstrating that c-Myc induces transcription of a panel of ABC drug transporter genes. ABCs are a large family trans-membrane transporter deeply involved in multi drug resistance. Furthermore expression levels of Myc, ABCC1, ABCC4 and ABCF1 were proved to be important prognostic tool to predict conventional therapy failure. N-Myc amplification/overexpression is the most important prognostic factor for Neuroblastoma. Cyclin G2 and Clusterin are two genes often down regulated in neuroblastoma cells. Cyclin G2 is an atypical member of Cyclin family and its expression is associated with terminal differentiation and apoptosis. Moreover it blocks cell cycle progression and induces cell growth arrest. Instead, CLU is a multifunctional protein involved in many physiological and pathological processes. Several lines of evidences support the view that CLU may act as a tumour suppressor in Neuroblastoma. In this thesis I showed that N-Myc represses CCNG2 and CLU transcription by different mechanisms. • N-Myc represses CCNG2 transcription by directly interacting with Sp1 bound in CCNG2 promoter and recruiting HDAC2. Importantly, reactivation of CCNG2 expression through epigenetic drugs partially reduces N-Myc and HDAC2 mediated cell proliferation. • N-Myc/Max complex represses CLU expression by direct binding to a peculiar E-box element on CLU promoter and by recruitment of HDACs and Polycomb Complexes, to the CLU promoter. Overall our findings strongly support the model in which Myc overexpression/amplification may contribute to some aspects of oncogenesis by a dual action: i) transcription activation of genes that confer a multidrug resistant phenotype to cancer cells; ii), transcription repression of genes involved in cell cycle inhibition and cellular differentiation.
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Gherardi, Samuele <1981&gt. "Myc-mediated control of gene transcription in cancer cells." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2010. http://amsdottorato.unibo.it/2809/.

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The Myc oncoproteins belong to a family of transcription factors composed by Myc, N-Myc and L-Myc. The most studied components of this family are Myc and N-Myc because their expressions are frequently deregulated in a wide range of cancers. These oncoproteins can act both as activators or repressors of gene transcription. As activators, they heterodimerize with Max (Myc associated X-factor) and the heterodimer recognizes and binds a specific sequence elements (E-Box) onto gene promoters recruiting histone acetylase and inducing transcriptional activation. Myc-mediated transcriptional repression is a quite debated issue. One of the first mechanisms defined for the Myc-mediated transcriptional repression consisted in the interaction of Myc-Max complex Sp1 and/or Miz1 transcription factors already bound to gene promoters. This interaction may interfere with their activation functions by recruiting co-repressors such as Dnmt3 or HDACs. Moreover, in the absence of , Myc may interfere with the Sp1 activation function by direct interaction and subsequent recruitment of HDACs. More recently the Myc/Max complex was also shown to mediate transcriptional repression by direct binding to peculiar E-box. In this study we analyzed the role of Myc overexpression in Osteosarcoma and Neuroblastoma oncogenesis and the mechanisms underling to Myc function. Myc overexpression is known to correlate with chemoresistance in Osteosarcoma cells. We extended this study by demonstrating that c-Myc induces transcription of a panel of ABC drug transporter genes. ABCs are a large family trans-membrane transporter deeply involved in multi drug resistance. Furthermore expression levels of Myc, ABCC1, ABCC4 and ABCF1 were proved to be important prognostic tool to predict conventional therapy failure. N-Myc amplification/overexpression is the most important prognostic factor for Neuroblastoma. Cyclin G2 and Clusterin are two genes often down regulated in neuroblastoma cells. Cyclin G2 is an atypical member of Cyclin family and its expression is associated with terminal differentiation and apoptosis. Moreover it blocks cell cycle progression and induces cell growth arrest. Instead, CLU is a multifunctional protein involved in many physiological and pathological processes. Several lines of evidences support the view that CLU may act as a tumour suppressor in Neuroblastoma. In this thesis I showed that N-Myc represses CCNG2 and CLU transcription by different mechanisms. • N-Myc represses CCNG2 transcription by directly interacting with Sp1 bound in CCNG2 promoter and recruiting HDAC2. Importantly, reactivation of CCNG2 expression through epigenetic drugs partially reduces N-Myc and HDAC2 mediated cell proliferation. • N-Myc/Max complex represses CLU expression by direct binding to a peculiar E-box element on CLU promoter and by recruitment of HDACs and Polycomb Complexes, to the CLU promoter. Overall our findings strongly support the model in which Myc overexpression/amplification may contribute to some aspects of oncogenesis by a dual action: i) transcription activation of genes that confer a multidrug resistant phenotype to cancer cells; ii), transcription repression of genes involved in cell cycle inhibition and cellular differentiation.
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Books on the topic "Cancer transcription"

1

Kumar, Rakesh, ed. Nuclear Signaling Pathways and Targeting Transcription in Cancer. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-8039-6.

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Rakesh, Kumar. Nuclear signaling pathways and targeting transcription in cancer. New York: Humana Press, 2014.

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B, La Thangue Nicholas, and Bandara Lasantha R, eds. Targets for cancer chemotherapy: Transcription factors and other nuclear proteins. Totowa, N.J: Humana Press, 2002.

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B, La Thangue Nicholas, and Bandara Lasantha R, eds. Targets for cancer chemotherapy: Transcription factors and other nuclear proteins. Totowa, N.J: Humana Press, 2002.

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1939-, Wilson Samuel H., and Hoagland Mahlon B, eds. Cancer biology and biosynthesis. Boca Raton, Fla: CRC Press, 1991.

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Sanno, Naoko. Cytochemical and molecular biological aspects of the pituitary and pituitary adenomas: Cell differentiation and transcription factors. Jena, Germany: Urban & Fischer, 2001.

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Pappas, Kyrie Jean. Transcriptional control of tumor suppressor genes in cancer. [New York, N.Y.?]: [publisher not identified], 2017.

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Eric, Verdin, ed. Histone deacetylases: Transcriptional regulation and other cellular functions. Totowa, N.J: Humana Press, 2006.

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Kumar, Rakesh. Nuclear Signaling Pathways and Targeting Transcription in Cancer. Humana, 2015.

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Thurston, David E., and Khondaker Miraz Rahman. Small-Molecule Transcription Factor Inhibitors in Oncology. Royal Society of Chemistry, The, 2018.

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Book chapters on the topic "Cancer transcription"

1

Sheen, J. H., and R. B. Dickson. "c-Myc in Cellular Transformation and Cancer." In Transcription Factors, 309–23. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-642-18932-6_10.

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Dittmer, Jürgen. "Ets Transcription Factors." In Encyclopedia of Cancer, 1–4. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27841-9_2034-2.

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Senyuk, Vitalyi. "AME Transcription Factor." In Encyclopedia of Cancer, 1–4. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27841-9_217-2.

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Cano, Amparo, and M. Angela Nieto. "Snail Transcription Factors." In Encyclopedia of Cancer, 1–6. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-27841-9_5389-3.

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Dittmer, Jürgen. "Ets Transcription Factors." In Encyclopedia of Cancer, 1649–53. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-662-46875-3_2034.

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Senyuk, Vitalyi. "AME Transcription Factor." In Encyclopedia of Cancer, 197–200. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-662-46875-3_217.

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Cano, Amparo, and M. Angela Nieto. "Snail Transcription Factors." In Encyclopedia of Cancer, 4274–79. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-662-46875-3_5389.

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Dittmer, Jürgen. "Ets Transcription Factors." In Encyclopedia of Cancer, 1339–43. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_2034.

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Senyuk, Vitalyi. "AME Transcription Factor." In Encyclopedia of Cancer, 150–53. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_217.

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Cano, Amparo, and M. Angela Neto. "Snail Transcription Factors." In Encyclopedia of Cancer, 3456–59. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_5389.

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Conference papers on the topic "Cancer transcription"

1

Ahmad, Salma, Hanan Nazar, Nouralhuda Alatieh, Maryam Al-Mansoob, Zainab Farooq, Muna Yusuf, and Allal Ouhtit. "Validation of Novel Transcriptional Targets that Underpin CD44-promoted breast cancer cell invasion." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2021. http://dx.doi.org/10.29117/quarfe.2021.0153.

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Introduction: Breast cancer (BC) is the most common cancer worldwide, and metastasis is its worst aspect and the first cause of death. Metastasis is a multistep process, where an invasion is a recurring event. The process of BC cell invasion involves three major factors, including cell adhesion molecules (CAM), proteinases and Growth factors.CD44, a family of CAM proteins and the hyaluronic acid (HA) cell surface receptor, acts as cell differentiation, cell migration/invasion and apoptosis regulator. Rationale: We have previously established a tetracycline (Tet)-OFF-regulated expression system, both in vitro and in vivo (Hill et al, 2006). As a complementary approach, the highly metastatic MDA-MB-231 BC cells expressing high levels of endogenous CD44s (the standard form of CD44), was cultured in the presence and absence of 50 µg/ml of HA. RNA samples were isolated from both cell experimental models, and microarray analysis (12K CHIP from Affymetrix) was applied. More than 200 CD44s transcriptional target genes were identified and were sub-divided into groups of genes based on their function: cell motility, cytoskeletal organization, ability to degrade ECM, and cell survival. Hypothesis: Among these 200 identified genes, we selected seven genes (ICAP-1, KYNU, AHR, SIRT1, SRSF8, PRAD1, and SOD2) and hypothesized that based on evidence from literature, these genes are potential novel targets of CD44-downstream signaling mediating BC cell invasion. Specific Aims: Pursuant to this goal, we proposed the following objectives: 1- Structural validation of ICAP-1, KYNU, AHR, SIRT1, SRSF8, PRAD1 and SOD2 as novel transcriptional targets of CD44/HA-downstream signaling at both RNA and Protein level using reverse transcription polymerase chain reaction (RT-PCR) and Western Blot respectively. 2-Functional validation of ICAP-1, KYNU, AHR, SIRT1, SRSF8, PRAD1and SOD2 as novel transcriptional targets that underpin CD44-promoted BC cell migration using wound healing assay after the transfection with siRNA. Innovation/Consclusion: This study validated seven transcriptional targets of CD44/HA-downstream signaling promoting BC cell invasion. Ongoing experiments aim to dissect the signaling pathways that link CD44 activation by HA to the transcription of these seven genes.
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Henikoff, Steven, Christopher M. Weber, Sheila S. Teves, and Srinivas Ramachandran. "Abstract IA09: Nucleosome barriers to transcription." In Abstracts: AACR Special Conference: Chromatin and Epigenetics in Cancer; September 24-27, 2015; Atlanta, GA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.chromepi15-ia09.

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Yue, Er, Guangchao Yang, Yuanfei Yao, Guangyu Wang, Yanqiao Zhang, and Edward W. Wang. "Abstract 1153: Targeting CA125 transcription for ovarian cancer treatment." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-1153.

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Carroll, Jason S. "Abstract IA05: Understanding estrogen receptor transcription in breast cancer." In Abstracts: AACR Special Conference on Advances in Breast Cancer Research: Genetics, Biology, and Clinical Applications - October 3-6, 2013; San Diego, CA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1557-3125.advbc-ia05.

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Liu, Yu, Yang Liu, Zhengtao Xiao, and Xuerui Yang. "Abstract A2-54: DNA methylation-dependent transcription regulatory networks elucidate dynamics of transcription regulatory circuitry in cancers." In Abstracts: AACR Special Conference: Translation of the Cancer Genome; February 7-9, 2015; San Francisco, CA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.transcagen-a2-54.

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Verdine, Gregory L. "Abstract IA1-2: Drugging oncogenic transcription factors." In Abstracts: AACR International Conference on Translational Cancer Medicine-- Jul 11-14, 2010; San Francisco, CA. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1078-0432.tcmusa10-ia1-2.

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Liu, Yu, Yang Liu, Zhengtao Xiao, and Xuerui Yang. "Abstract B2-25: DNA methylation-dependent transcription regulatory networks elucidate dynamics of transcription regulatory circuitry in cancers." In Abstracts: AACR Special Conference: Computational and Systems Biology of Cancer; February 8-11, 2015; San Francisco, CA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.compsysbio-b2-25.

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Morales-Peñaloza, A., C. D. Meza-López, and J. J. Godina-Nava. "Mathematical modeling of DNA's transcription process for the cancer study." In MEDICAL PHYSICS: Twelfth Mexican Symposium on Medical Physics. AIP, 2012. http://dx.doi.org/10.1063/1.4764631.

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Bushweller, John. "Abstract SY15-03: Drugging “undruggable” transcription factor drivers in cancer." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-sy15-03.

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Stegmaier, Kimberly, Brian Crompton, Jonathan Jessneck, Kenneth Ross, Supriya Gupta, Lynn Ver Plank, Wendy Winckler, and Nicola Tolliday. "Abstract LB-240: Modulating transcription factor abnormalities in pediatric cancer." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-lb-240.

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Reports on the topic "Cancer transcription"

1

Mellon, Isabel. Transcription-Coupled Repair and Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, June 2001. http://dx.doi.org/10.21236/ada400021.

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Mellon, Isabel. Transcription-Coupled Repair and Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, June 2002. http://dx.doi.org/10.21236/ada417977.

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Mellon, Isabel. Transcription-Coupled Repair and Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, June 1999. http://dx.doi.org/10.21236/ada391167.

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Merine, Kendra M., and Jeffrey R. Marks. Rapamycin Inhibits Estrogen-Mediated Transcription in Breast Cancer Cell Lines. Fort Belvoir, VA: Defense Technical Information Center, July 2000. http://dx.doi.org/10.21236/ada406142.

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Libermann, Towia A. A Novel Prostate Epithelium-Specific Transcription Factor in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, June 2004. http://dx.doi.org/10.21236/ada428537.

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Hesterman, Eli, Myles A. Brown, and Yongfeng Shang. Dynamics of Estrogen Receptor Transcription Complex Assembly in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 2002. http://dx.doi.org/10.21236/ada412699.

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Anose, Bynthia M., and Michel M. Sanders. Role of AREB6/ZEB Transcription Factor in Invasive Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, May 2003. http://dx.doi.org/10.21236/ada416730.

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Liberman, Towie A. A Novel Prostate Epithelium-Specific Transcription Factor in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, June 2003. http://dx.doi.org/10.21236/ada417956.

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Schaber, John D. Expression and Activation of STAT Transcription Factors in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, April 1998. http://dx.doi.org/10.21236/ad1012061.

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Liu, Jingwen. Negative Regulation of Tumor Suppressor p53 Transcription in Breast Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, July 2001. http://dx.doi.org/10.21236/ada396148.

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