Relevant bibliographies by topics / Cancer cells Breast Genes

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Cancer cells Breast Genes'

Author: Grafiati
Published: 4 June 2021
Last updated: 7 February 2022

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Journal articles on the topic "Cancer cells Breast Genes"

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Dai, Xiaofeng, Rong Ma, Xijiang Zhao, and Fengfeng Zhou. "Epigenetic profiles capturing breast cancer stemness for triple negative breast cancer control." Epigenomics 11, no. 16 (2019): 1811–25. http://dx.doi.org/10.2217/epi-2019-0266.

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Aim: Triple-negative breast cancers (TNBCs) contain a higher percentage of breast cancer stem cells (BCSCs) than the other subtypes and lack effective yet safe-targeted therapies. We would like to unveil genes relevant to the therapeutic control of breast cancer stemness at the epigenetic level. Methods: We sequenced the transcriptome of BCSCs isolated from TNBCs, identified genes differentially expressed in these cells and subjected to DNA methylation and established the Bayesian network as well as interactions out of them. Results & conclusion: We presented a core epigenetic BCSC gene pa
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Liu, Li, Yudong Wu, Cheng Zhang, et al. "Cancer-associated adipocyte-derived G-CSF promotes breast cancer malignancy via Stat3 signaling." Journal of Molecular Cell Biology 12, no. 9 (2020): 723–37. http://dx.doi.org/10.1093/jmcb/mjaa016.

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Abstract Adipocyte is the most predominant cell type in the tumor microenvironment of breast cancer and plays a pivotal role in cancer progression, yet the underlying mechanisms and functional mediators remain elusive. We isolated primary preadipocytes from mammary fat pads of human breast cancer patients and generated mature adipocytes and cancer-associated adipocytes (CAAs) in vitro. The CAAs exhibited significantly different gene expression profiles as assessed by transcriptome sequencing. One of the highly expressed genes in CAAs is granulocyte colony-stimulating factor (G-CSF). Treatment
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Hwang-Verslues, Wendy W., King-Jen Chang, Eva Y. H. P. Lee, and Wen-Hwa Lee. "Breast Cancer Stem Cells and Tumor Suppressor Genes." Journal of the Formosan Medical Association 107, no. 10 (2008): 751–66. http://dx.doi.org/10.1016/s0929-6646(08)60188-6.

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Kim, Young-Ho, Hyun-Kyoung Kim, Hee Yeon Kim, et al. "FAK-Copy-Gain Is a Predictive Marker for Sensitivity to FAK Inhibition in Breast Cancer." Cancers 11, no. 9 (2019): 1288. http://dx.doi.org/10.3390/cancers11091288.

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Background: Cancers with copy-gain drug-target genes are excellent candidates for targeted therapy. In order to search for new predictive marker genes, we investigated the correlation between sensitivity to targeted drugs and the copy gain of candidate target genes in NCI-60 cells. Methods: For eight candidate genes showing copy gains in NCI-60 cells identified in our previous study, sensitivity to corresponding target drugs was tested on cells showing copy gains of the candidate genes. Results: Breast cancer cells with Focal Adhesion Kinase (FAK)-copy-gain showed a significantly higher sensit
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Bogacz, Anna, Marlena Wolek, Bogna Juskowiak, et al. "Expression of genes modulated by epigallocatechin-3-gallate in breast cancer cells." Herba Polonica 64, no. 3 (2018): 31–37. http://dx.doi.org/10.2478/hepo-2018-0016.

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Summary Introduction: Breast cancer is the most common malignant cancer among women. Both drug resistance and metastasis are major problems in the treatment of breast cancer. Therefore, adjuvant therapy may improve patients’ survival and affect their quality of life. It is suggested that epigallocatechin gallate (EGCG) which is well known for its chemopreventive activity and acts on numerous molecular targets may inhibit the growth and metastasis of some cancers. Hence, discovering the metastatic molecular mechanisms for breast cancer may be useful for therapy. Objective: The aim of the study
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Zhang, Suping, Han Zhang, Emanuela M. Ghia, et al. "Inhibition of chemotherapy resistant breast cancer stem cells by a ROR1 specific antibody." Proceedings of the National Academy of Sciences 116, no. 4 (2019): 1370–77. http://dx.doi.org/10.1073/pnas.1816262116.

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Breast cancers enduring treatment with chemotherapy may be enriched for cancer stem cells or tumor-initiating cells, which have an enhanced capacity for self-renewal, tumor initiation, and/or metastasis. Breast cancer cells that express the type I tyrosine kinaselike orphan receptor ROR1 also may have such features. Here we find that the expression of ROR1 increased in breast cancer cells following treatment with chemotherapy, which also enhanced expression of genes induced by the activation of Rho-GTPases, Hippo-YAP/TAZ, or B lymphoma Mo-MLV insertion region 1 homolog (BMI1). Expression of RO
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Neiger, Hannah E., Emily L. Siegler, and Yihui Shi. "Breast Cancer Predisposition Genes and Synthetic Lethality." International Journal of Molecular Sciences 22, no. 11 (2021): 5614. http://dx.doi.org/10.3390/ijms22115614.

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BRCA1 and BRCA2 are tumor suppressor genes with pivotal roles in the development of breast and ovarian cancers. These genes are essential for DNA double-strand break repair via homologous recombination (HR), which is a virtually error-free DNA repair mechanism. Following BRCA1 or BRCA2 mutations, HR is compromised, forcing cells to adopt alternative error-prone repair pathways that often result in tumorigenesis. Synthetic lethality refers to cell death caused by simultaneous perturbations of two genes while change of any one of them alone is nonlethal. Therefore, synthetic lethality can be ins
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R., Abhirup H., Priyanka Kenchetty, and Aishwarya K. Chidananda. "Breast ovarian cancer syndrome." International Surgery Journal 8, no. 8 (2021): 2454. http://dx.doi.org/10.18203/2349-2902.isj20213144.

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BRCA1 and BRCA2, known as breast and ovarian cancer predisposition genes, were discovered in the 1990s. As part of a normal genetic structure, these genes are intrinsic to all human beings, but they are mutated in some individuals increasing the risk for breast and ovarian cancers development. BRCA1 is not only expressed in endocrine tissues but is also detected in other cells such as the neuroepithelial cells in the early stage of cell development. Like BRCA1, BRCA2 is also expressed in a wide variety of tissues and is observed with higher rates in the breast and thymus and with lower rates i
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Rossi, Fabiana Alejandra, Ezequiel Hernán Calvo Roitberg, Juliana Haydeé Enriqué Steinberg, Molishree Umesh Joshi, Joaquín Maximiliano Espinosa, and Mario Rossi. "HERC1 Regulates Breast Cancer Cells Migration and Invasion." Cancers 13, no. 6 (2021): 1309. http://dx.doi.org/10.3390/cancers13061309.

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Tumor cell migration and invasion into adjacent tissues is one of the hallmarks of cancer and the first step towards secondary tumors formation, which represents the leading cause of cancer-related deaths. This process is considered an unmet clinical need in the treatment of this disease, particularly in breast cancers characterized by high aggressiveness and metastatic potential. To identify and characterize genes with novel functions as regulators of tumor cell migration and invasion, we performed a genetic loss-of-function screen using a shRNA library directed against the Ubiquitin Proteaso
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Wijshake, Tobias, Zhongju Zou, Beibei Chen, et al. "Tumor-suppressor function of Beclin 1 in breast cancer cells requires E-cadherin." Proceedings of the National Academy of Sciences 118, no. 5 (2021): e2020478118. http://dx.doi.org/10.1073/pnas.2020478118.

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Beclin 1, an autophagy and haploinsufficient tumor-suppressor protein, is frequently monoallelically deleted in breast and ovarian cancers. However, the precise mechanisms by which Beclin 1 inhibits tumor growth remain largely unknown. To address this question, we performed a genome-wide CRISPR/Cas9 screen in MCF7 breast cancer cells to identify genes whose loss of function reverse Beclin 1-dependent inhibition of cellular proliferation. Small guide RNAs targeting CDH1 and CTNNA1, tumor-suppressor genes that encode cadherin/catenin complex members E-cadherin and alpha-catenin, respectively, we
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Dissertations / Theses on the topic "Cancer cells Breast Genes"

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Wright, Paul Kingsley. "Identification of oestrogen-regulated genes in breast cancer cells." Thesis, University of Newcastle Upon Tyne, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.493073.

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Oestrogens are critical agents in the aetiopathogenesis of breast cancer. Oestradiol (E2) acts via the oestrogen receptor (ER) to control the expression of specific genes, the full repertoire of which has not been established.
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Kao, Ruey-Ho. "Application of differential display technique to breast cancer tissue." Thesis, King's College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.342256.

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Melkoumian, Zaroui K. "Pharmacological regulation of c-myc gene expression in human breast cancer cells." Morgantown, W. Va. : [West Virginia University Libraries], 2001. http://etd.wvu.edu/templates/showETD.cfm?recnum=2218.

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Thesis (Ph. D.)--West Virginia University, 2001.<br>Title from document title page. Document formatted into pages; contains x, 152 p. : ill. (some col.). Vita. Includes abstract. Includes bibliographical references (p. 119-149).
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Chen, Chien-Cheng. "Mechanisms of transcriptional activation of estrogen responsive genes in breast cancer cells." Thesis, [College Station, Tex. : Texas A&M University, 2006. http://hdl.handle.net/1969.1/ETD-TAMU-1869.

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Lafta, Inam Jasim. "STAG3 gene expression in breast cancer cells." Thesis, University of Sheffield, 2016. http://etheses.whiterose.ac.uk/12329/.

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The expression of cohesin genes has been found to be disregulated in a number of cancers including prostate, breast and squamous cell carcinoma; and mutations in genes that encode cohesin components have been noticed in colorectal cancer and myeloid malignancies (reviewed by Rhodes et al., 2011). It has been suggested that members of the cohesin complex might be considered as a subgroup of cancer biomarkers (Xu et al., 2011a). Therefore, this study focused on studying the expression of STAG genes in breast cancer cell lines and primary breast tumours. More attention was paid for STAG3, because
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Eyre, Rachel. "Determining the genes responsible for drug resistance in ovarian and breast cancer stem cells." Thesis, University of Newcastle Upon Tyne, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.576535.

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The majority of deaths in ovarian and breast cancer are caused by recurrent metastatic disease which is usually multidrug resistant. This progression has been hypothesised to be due in part to the presence of cancer stem cells, a subset of cells which are capable of self renewal and are able to survive chemotherapy and migrate to distant sites. Side population (SP) cells, identified by the efflux of the DNA binding dye Hoechst 33342 through ABC transporters, are a known adult stem cell group and have been suggested as a cancer stem cell in various cancers. The aims of this study were (i) to de
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Crook, Simon. "Identification and verification of genes regulated in breast cancer cells by the antiprogestin, Onapristone." Thesis, University of Nottingham, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.250455.

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Akhavantabasi, Shiva. "Functional Characterization Of Two Potential Breast Cancer Related Genes." Phd thesis, METU, 2012. http://etd.lib.metu.edu.tr/upload/12614275/index.pdf.

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Cancer may arise as a result of deregulation of oncogenes and/or tumor suppressors. Although much progress has been made for the identification of such cancer related genes, our understanding of the complex tumorigenesis pathways is still not complete. Therefore, to improve our understanding of how certain basic mechanisms work in normal and in cancer cells, we aimed to characterize two different breast cancer related genes. First part of the study focused on subcellular localization USP32 (Ubiquitin Specific Protease 32) to help understand the function of this uncharacterized gene. USP32 is a
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Davis, Jessica. "Identification of novel anti-hormone-induced pro-survival genes in oestrogen receptor-positive breast cancer cells." Thesis, Cardiff University, 2016. http://orca.cf.ac.uk/98607/.

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The growth inhibitory actions of antihormones in the treatment of oestrogen receptor-positive (ER+) breast cancer are compromised by the development of resistance. There is emerging evidence that antihormones can rapidly induce expression of genes that enable cells to survive the initial impact of these agents and ultimately aid the acquisition of resistance. The aims of this thesis were to identify novel antihormone-induced pro-survival genes in a panel of ER+ breast cancer cell lines and to determine whether such genes contribute to the limited efficacy of antihormones during response and su
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Wiese, Meike. "Characterisation of HP1γ in mammalian cells". Thesis, University of Cambridge, 2018. https://www.repository.cam.ac.uk/handle/1810/273362.

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The degree of chromatin compaction plays a fundamental role in controlling the accessibility of DNA to the transcription machinery as well as other DNA-dependent biological pathways. The mammalian HP1 (Heterochromatin protein 1) protein family consists of three members: HP1α, β and γ. Each paralogue regulates formation and maintenance of heterochromatin by binding to the repressive chromatin marks H3K9me2/3 with their chromodomains (CDs). Despite high sequence conservation, each HP1 paralogue possesses specific functions, which are likely to be cell type specific. The aim of my thesis was to f
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Books on the topic "Cancer cells Breast Genes"

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O'Connell, Fiona Claire. Morphology and gene expression in the postnatal mouse mammary gland. University College Dublin, 1997.

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Vonderhaar, Barbara K., and Gilbert H. Smith. Stem cells and breast cancer. IOS Press, 2008.

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Tumor suppressor genes in breast cancer. Nova Publishers, 2008.

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Risky genes: Genetics, breast cancer, and Jewish identity. Routledge, 2013.

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To, Minh Dong. Identification of transcriptionally deregulated genes in breast cancer. National Library of Canada, 1998.

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Sethi, Seema. miRNAs and Target Genes in Breast Cancer Metastasis. Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-08162-5.

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Gibbon, Sahra. Breast Cancer Genes and the Gendering of Knowledge. Palgrave Macmillan UK, 2007. http://dx.doi.org/10.1057/9780230626553.

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Pham, Phuc Van. Breast Cancer Stem Cells & Therapy Resistance. Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-22020-8.

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Piñeiro, Roberto, ed. Circulating Tumor Cells in Breast Cancer Metastatic Disease. Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-35805-1.

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Moelleken, Brent Roderick Wilfred. Tamoxifen - 5-fluorouracil synergy in human breast cancer cell lines: Correlating in vitro synergy with the current estrogen receptor model. s.n.], 1985.

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Book chapters on the topic "Cancer cells Breast Genes"

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Jiang, Jinxia, Min Feng, Annemarie Jacob, Lin Z. Li, and He N. Xu. "Optical Redox Imaging Differentiates Triple-Negative Breast Cancer Subtypes." In Advances in Experimental Medicine and Biology. Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-48238-1_40.

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AbstractTriple-negative breast cancer (TNBC) is a highly diverse group of cancers with limited treatment options, responsible for about 15% of all breast cancers. TNBC cells differ from each other in many ways such as gene expression, metabolic activity, tumorigenicity, and invasiveness. Recently, many research and clinical efforts have focused on metabolically targeted therapy for TNBC. Metabolic characterization of TNBC cell lines can facilitate the assessment of therapeutic effects and assist in metabolic drug development. Herein, we used optical redox imaging (ORI) techniques to characterize TNBC subtypes metabolically. We found that various TNBC cell lines had differing redox statuses (levels of reduced nicotinamide adenine dinucleotide (NADH), oxidized flavin adenine dinucleotide (FAD), and the redox ratio (FAD/(NADH+FAD)). We then metabolically perturbed the cells with mitochondrial inhibitors and an uncoupler and performed ORI accordingly. As expected, we observed that these TNBC cell lines had similar response patterns to the metabolic perturbations. However, they exhibited differing redox plasticity. These results suggest that subtypes of TNBC cells are different metabolically and that ORI can serve as a sensitive technique for the metabolic profiling of TNBC cells.
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Musgrove, Elizabeth A., Michael F. Buckley, Anna deFazio, Colin K. W. Watts, and Robert L. Sutherland. "Expression and Regulation of Cyclin Genes in Breast Cancer Cells." In The Cell Cycle. Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2421-2_38.

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Streuli, Charles H., and Mina J. Bissell. "Mammary epithelial cells, extracellular matrix, and gene expression." In Regulatory Mechanisms in Breast Cancer. Springer US, 1991. http://dx.doi.org/10.1007/978-1-4615-3940-7_17.

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Cassanelli, Sylvie, Agnès Mialhe, Josette Louis, and Daniel Seigneurin. "Videomicrofluorometry of Progesterone Receptors and Their Genes in Breast Cancer Cells." In Analytical Use of Fluorescent Probes in Oncology. Springer US, 1996. http://dx.doi.org/10.1007/978-1-4615-5845-3_18.

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Roberti, Annalisa, Marcella Macaluso, and Antonio Giordano. "Alterations in Cell Cycle Regulatory Genes in Breast Cancer." In Breast Cancer in the Post-Genomic Era. Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-945-1_4.

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Zou, Zhiqiang, Anthony Anisowicz, Kristina Rafidi, and Ruth Sager. "Down Regulation of Candidate Tumor Suppressor Genes in Breast Cancer." In The Cell Cycle. Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2421-2_37.

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Aldaz, C. Marcelo, Andrzej Bednarek, April Charpentier, Michael MacLeod, Kathleen Hawkins, and Kendra Laflin. "Serial Analysis of Gene Expression in Breast Cancer Cells." In Hormonal Carcinogenesis III. Springer New York, 2001. http://dx.doi.org/10.1007/978-1-4612-2092-3_10.

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Hu, Juan, Hongpeng He, Hao Zhou, et al. "SNP Affects the Mobility of Breast Cancer Cells and the Expression of Metastasis-Related Genes." In Lecture Notes in Electrical Engineering. Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-662-46318-5_20.

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Basu, Subhash, Rui Ma, Joseph R. Moskal, Manju Basu, and Sipra Banerjee. "Apoptosis of Breast Cancer Cells: Modulation of Genes for Glycoconjugate Biosynthesis and Targeted Drug Delivery." In Advances in Experimental Medicine and Biology. Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-3381-1_16.

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Ma, Rui, Elizabeth A. Hopp, N. Matthew Decker, et al. "Regulation of Glycosyltransferase Genes in Apoptotic Breast Cancer Cells Induced by l-PPMP and Cisplatin." In Advances in Experimental Medicine and Biology. Springer US, 2011. http://dx.doi.org/10.1007/978-1-4419-7877-6_33.

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Conference papers on the topic "Cancer cells Breast Genes"

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Anderson, Deborah, Shari Smith, Farah Goubran, and Paul Mellor. "Abstract 4852: Targeting cancer progression genes upregulated in CREB3L1-deficient breast cancer cells." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-4852.

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"Impact of Heparan Sulphate Binding Domain of Chemokine CCL21 to Migration of Breast Cancer Cells." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0132.

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Lymph node metastasis constitutes a key event in breast cancer progression. Chemokines are small proteins, which can promote metastatic spread by inducing cancer cell migration and invasion. Chemokine function is dependant upon their binding to both cell surface heparan sulphate (HS) molecules and to their specific receptor. Our group has demonstrated a significant increase in chemokine receptor CCR7 expression in cancerous breast epithelia compared to healthy controls. This study is designed to test the hypothesis that a non-HS binding forms of chemokine CCL21 can disrupt the normal response
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Alamoudi, Aliaa A., Hanan A. Bashmail, Ghada M. Ajabnoor, et al. "Abstract 3876: Thymoquinone induces the expression of clock genes in breast cancer cells." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-3876.

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Alamoudi, Aliaa A., Hanan A. Bashmail, Ghada M. Ajabnoor, et al. "Abstract 3876: Thymoquinone induces the expression of clock genes in breast cancer cells." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-3876.

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Andres, SA, DA Kerr II, DF Englert, DJ Wilson, and JL Wittliff. "Expression of small sets of genes in carcinoma and stromal cells predict clinical behavior of human breast cancer." In CTRC-AACR San Antonio Breast Cancer Symposium: 2008 Abstracts. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-6146.

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"PAMAM Dendrimers as anti-HER2 Positive Breast Cancer Treatment." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0176.

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Background: Poly (amidoamine) dendrimers (PAMAMs) are widely used in drug delivery systems and gene transfection as drug carriers. They also exert several biological effects like modulating gene expression, particularly EGFR (ErbB1) signaling pathway, which raises the question of whether these polymers can also inhibit the phosphorylation of HER2 (ErbB2) in breast cancer. However, this area hasn’t been investigated before. Methods: In this study, we evaluated the anticancer effects of different generations and surface chemistries of PAMAMs on HER2 positive breast cancer cells (SkBr3 and ZR-75
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Wikman, Harriet, Volkmar Müller, Dirk Kemming, et al. "Abstract 3393: Identification of genes mediating early dissemination of tumor cells in breast cancer." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-3393.

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Barua, David, Afrin Sultana, Md Nahidul Islam, Ananya Gupta та Sanjeev Gupta. "Abstract 5843: XBP1 regulates the expression of cell cycle associated genes in ERα positive breast cancer cells". У Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-5843.

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Souchelnytskyi, Serhiy. "Systemic properties of Carcinogenesis: Lessons from studies on the Earth and in the Space." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0118.

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proteins and genes act in coordinated ways, and their relations are visualized as networks. Networks are more accurate descriptions of cancer regulatory mechanisms, in comparison to lists of oncogenes and tumor suppressors. To extract essential regulators (nodes) and connections (edges), interrogations of these networks are performed, e.g. cancer cells are subjected to different treatments. Interrogations force cancer cells to engage nodes and edges essential for maintaining cancer properties, i.e. drivers, and nonessential followers. The challenge is to discriminate which of the mechanisms dr
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Chen, Kok Hao, and Jong Hyun Choi. "Nanoparticle-Aptamer: An Effective Growth Inhibitor for Human Cancer Cells." In ASME 2009 International Mechanical Engineering Congress and Exposition. ASMEDC, 2009. http://dx.doi.org/10.1115/imece2009-11966.

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Semiconductor nanocrystals have unique optical properties due to quantum confinement effects, and a variety of promising approaches have been devised to interface the nanomaterials with biomolecules for bioimaging and therapeutic applications. Such bio-interface can be facilitated via a DNA template for nanoparticles as oligonucleotides can mediate the aqueous-phase nucleation and capping of semiconductor nanocrystals.[1,2] Here, we report a novel scheme of synthesizing fluorescent nanocrystal quantum dots (NQDs) using DNA aptamers and the use of this biotic/abiotic nanoparticle system for gro
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Reports on the topic "Cancer cells Breast Genes"

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Davie, James R. Isolation of Estrogen-Responsive Genes in Human Breast Cancer Cells. Defense Technical Information Center, 2001. http://dx.doi.org/10.21236/ada399358.

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Davis, James R. Isolation of Estrogen-Responsive Genes in Human Breast Cancer Cells. Defense Technical Information Center, 2003. http://dx.doi.org/10.21236/ada420776.

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Hannon, Gregory J. Synthetic Lethality in Breast Cancer Cells: Genes Required for Tumor Survival. Defense Technical Information Center, 2001. http://dx.doi.org/10.21236/ada395967.

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Hannon, Gregory J. Synthetic Lethality in Breast Cancer Cells: Genes Required for Tumor Survival. Defense Technical Information Center, 2001. http://dx.doi.org/10.21236/ada396005.

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Hannon, Gregory J. Synthetic Lethality in Breast Cancer Cells: Genes Required for Tumor Survival. Defense Technical Information Center, 2002. http://dx.doi.org/10.21236/ada407287.

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Hannon, Gregory J. Synthetic Lethality in Breast Cancer Cells: Genes Required for Tumor Survival. Defense Technical Information Center, 2004. http://dx.doi.org/10.21236/ada434066.

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Hannon, Gregory J. Synthetic Lethality in Breast Cancer Cells: Genes Required for Tumor Survival. Defense Technical Information Center, 2004. http://dx.doi.org/10.21236/ada434625.

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Hannon, Gregory J. Synthetic Lethality in Breast Cancer Cells: Genes Required for Tumor Survival. Defense Technical Information Center, 2003. http://dx.doi.org/10.21236/ada422976.

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Reddy, Deepthi E. Identification and Localization of Genes Which Restore Senescence in Breast Cancer Cells. Defense Technical Information Center, 1999. http://dx.doi.org/10.21236/ada374347.

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Shu, Hong-Bing. Cloning and Characterization of Genes that Inhibit TRAIL-Induced Apoptosis of Breast Cancer Cells. Defense Technical Information Center, 2003. http://dx.doi.org/10.21236/ada421784.

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