Relevant bibliographies by topics / Cancer cells Breast Genes

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  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 (December 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 panel consisting of eight genes that can be used for BCSCs and TNBCs identification, and revealed the dominant roles of FOXA1 and GATA3 in orchestrating breast cancer heterogeneity and stemness.
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Liu, Li, Yudong Wu, Cheng Zhang, Chong Zhou, Yining Li, Yi Zeng, Chunbo Zhang, et al. "Cancer-associated adipocyte-derived G-CSF promotes breast cancer malignancy via Stat3 signaling." Journal of Molecular Cell Biology 12, no. 9 (April 2, 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 with recombinant human G-CSF protein or stable expression of human G-CSF in triple-negative breast cancer (TNBC) cell lines enhanced epithelial–mesenchymal transition, migration, and invasion of cancer cells, by activating Stat3. Accordantly, targeting G-CSF/Stat3 signaling with G-CSF-neutralizing antibody, a chemical inhibitor, or siRNAs for Stat3 could all abrogate CAA- or G-CSF-induced migration and invasion of breast cancer cells. The pro-invasive genes MMP2 and MMP9 were identified as target genes of G-CSF in TNBC cells. Furthermore, in human breast cancer tissues, elevated G-CSF expression in adipocytes is well correlated with activated Stat3 signal in cancer cells. Together, our results suggest a novel strategy to intervene with invasive breast cancers by targeting CAA-derived G-CSF.
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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 (October 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, HyeRan Gawk, Seung-Hyun Bae, Hye Won Sim, Eun-Kyung Kang, Ju-Young Seoh, Hyonchol Jang, and Kyeong-Man Hong. "FAK-Copy-Gain Is a Predictive Marker for Sensitivity to FAK Inhibition in Breast Cancer." Cancers 11, no. 9 (September 2, 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 sensitivity to the target inhibitor, FAK inhibitor 14 (F14). In addition, treatment of F14 or FAK-knockdown showed a specific apoptotic effect only in breast cancer cells showing FAK-copy-gain. Expression-profiling analyses on inducible FAK shRNA-transfected cells showed that FAK/AKT signaling might be important to the apoptotic effect by target inhibition. An animal experiment employing a mouse xenograft model also showed a significant growth-inhibitory effect of F14 on breast cancer cells showing FAK-copy-gain, but not on those without FAK-copy-gain. Conclusion: FAK-copy-gain may be a predictive marker for FAK inhibition therapy in breast cancer.
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Bogacz, Anna, Marlena Wolek, Bogna Juskowiak, Monika Karasiewicz, Adam Kamiński, Izabela Uzar, Anna Polaszewska, Zofia Kostrzewa, and Bogusław Czerny. "Expression of genes modulated by epigallocatechin-3-gallate in breast cancer cells." Herba Polonica 64, no. 3 (September 1, 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 was to determine the effect of EGGC on the mRNA expression level of genes such as ZEB1, ABCB1, MDM2, TWIST1 and PTEN in MCF-7 breast cancer cells. Methods: MCF7/DOX were cultured in the presence of 0.2 μM DOX and EGCG (20-50 μM). The mRNA expression level was determined by real-time quantitative PCR using RealTime ready Custom Panel 96 kit. Results: Our results showed an important increase (about 2-fold for 20 μM EGCG + 0.2 μM DOX and 2.5-fold for 50 μM EGCG + 0.2 μM DOX, p<0.05) in ZEB1 expression levels. In case of ABCB1 gene lack of influence on the mRNA level was observed (p>0.05). We also observed significant decrease of ZEB1 expression in MCF7 cells with 20 μM and 50 μM EGCG (p<0.05). In addition, EGCG (20 μM) caused an increase of MDM2 and PTEN mRNA levels in almost 100% (p<0.05) and 40% (p>0.05), respectively. Lack of the influence of EGCG was noted for the TWIST1 gene expression. In case of MCF7/DOX we showed an increase of mRNA level of PTEN gene about 50% (p<0.05). Conclusions: These results suggest that EGCG may be potentially used in adjuvant therapy in the breast cancer treatment.
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Zhang, Suping, Han Zhang, Emanuela M. Ghia, Jiajia Huang, Liufeng Wu, Jianchao Zhang, Sharon Lam, 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 (January 8, 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 ROR1 also enhanced the capacity of breast cancer cells to invade Matrigel, form spheroids, engraft in Rag2−/−γc−/− mice, or survive treatment with paclitaxel. Treatment of mice bearing breast cancer patient-derived xenografts (PDXs) with the humanized anti-ROR1 monoclonal antibody cirmtuzumab repressed expression of genes associated with breast cancer stemness, reduced activation of Rho-GTPases, Hippo-YAP/TAZ, or BMI1, and impaired the capacity of breast cancer PDXs to metastasize or reengraft Rag2−/−γc−/− mice. Finally, treatment of PDX-bearing mice with cirmtuzumab and paclitaxel was more effective than treatment with either alone in eradicating breast cancer PDXs. These results indicate that targeting ROR1 may improve the response to chemotherapy of patients with breast cancer.
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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 (May 25, 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 instrumental in identifying new therapeutic targets for BRCA1/2 mutations. PARP is an established synthetic lethal partner of the BRCA genes. Its role is imperative in the single-strand break DNA repair system. Recently, Olaparib (a PARP inhibitor) was approved for treatment of BRCA1/2 breast and ovarian cancer as the first successful synthetic lethality-based therapy, showing considerable success in the development of effective targeted cancer therapeutics. Nevertheless, the possibility of drug resistance to targeted cancer therapy based on synthetic lethality necessitates the development of additional therapeutic options. This literature review addresses cancer predisposition genes, including BRCA1, BRCA2, and PALB2, synthetic lethality in the context of DNA repair machinery, as well as available treatment options.
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R., Abhirup H., Priyanka Kenchetty, and Aishwarya K. Chidananda. "Breast ovarian cancer syndrome." International Surgery Journal 8, no. 8 (July 28, 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 in the lung, ovary and spleen. We presented to you a case of 40 year old female admitted in surgical ward with lump in the left breast since 2 months with ipsilateral discrete axillary lymphadenopathy. Bilateral sono-mammography showed BIRADS V lesion in left breasts with satellite nodules. Ultrasonography of abdomen and pelvis showed large left adnexal solid mass lesion and right sided ovarian cyst with retrocaval, preaortic lymphadenopathy. Patient underwent a diagnostic laparoscopy which was converted to a laparotomy. Total abdominal hysterectomy with bilateral salphingo-oophorectomy was done. For the breast lump, patient underwent left sided modified radical mastectomy. Gene testing for revealed BRCA1 positivity. Chemotherapy was given to cover both breast and ovarian carcinoma. Patient came back with abdominal distension after 9 months and was offered palliative care. Patient succumbed for disease after 1 year after diagnosis. We reviewed the literature for the same.
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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 (March 15, 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 Proteasome System (UPS) in a highly invasive breast cancer derived cell line. Among the candidates, we validated HERC1 as a gene regulating cell migration and invasion. Furthermore, using animal models, our results indicate that HERC1 silencing affects primary tumor growth and lung colonization. Finally, we conducted an in silico analysis using publicly available protein expression data and observed an inverse correlation between HERC1 expression levels and breast cancer patients’ overall survival. Altogether, our findings demonstrate that HERC1 might represent a novel therapeutic target for the development or improvement of breast cancer treatment.
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Wijshake, Tobias, Zhongju Zou, Beibei Chen, Lin Zhong, Guanghua Xiao, Yang Xie, John G. Doench, Lynda Bennett, and Beth Levine. "Tumor-suppressor function of Beclin 1 in breast cancer cells requires E-cadherin." Proceedings of the National Academy of Sciences 118, no. 5 (January 25, 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, were highly enriched in the screen. CRISPR/Cas9-mediated knockout of CDH1 or CTNNA1 reversed Beclin 1-dependent suppression of breast cancer cell proliferation and anchorage-independent growth. Moreover, deletion of CDH1 or CTNNA1 inhibited the tumor-suppressor effects of Beclin 1 in breast cancer xenografts. Enforced Beclin 1 expression in MCF7 cells and tumor xenografts increased cell surface localization of E-cadherin and decreased expression of mesenchymal markers and beta-catenin/Wnt target genes. Furthermore, CRISPR/Cas9-mediated knockout of BECN1 and the autophagy class III phosphatidylinositol kinase complex 2 (PI3KC3-C2) gene, UVRAG, but not PI3KC3-C1–specific ATG14 or other autophagy genes ATG13, ATG5, or ATG7, resulted in decreased E-cadherin plasma membrane and increased cytoplasmic E-cadherin localization. Taken together, these data reveal previously unrecognized cooperation between Beclin 1 and E-cadherin–mediated tumor suppression in breast cancer cells.
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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.
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 in addition of being the meiotic component of cohesin is also a member of Cancer Testis (CT) antigens. CT antigens have been used successfully as cancer biomarkers as well as therapeutic targets for various malignancies. Our findings show that the STAG1, STAG2 and STAG3 genes are highly expressed at the mRNA level in the breast cancer cell lines including: MCF-7, T-47D, MDA-MB-231 and MDA-MB-468 and primary breast tumours as well compared to normal breast tissue or normal breast cell line, MCF-10A, using qRT-PCR. Interestingly, a tendency for increasing STAG3 mRNA expression was recorded from stage I through stage IV of breast tumour implying that there might be increased expression as the tumour develops. Therefore, STAG3 expression was confirmed at the protein level by immunoblotting, where STAG3 protein bands were produced by all of the studied cancer cells when compared with the normal breast. Jurkat cells were used as a positive control as STAG3 expression in these had been previously established. Further confirmation of STAG3 protein signal was achieved in primary breast tumour tissue sections compared with the normal tissue using immunohistochemistry. Overall, these data suggest that STAG3 may be a suitable novel biomarker for breast cancer detection. Because STAG3 is a potential therapeutic target for breast cancer, RNA interference was successfully used to deplete STAG3 in MCF-7 cells. Analysis of the cell cycle profile by FACS revealed an accumulation of cells in G1 phase, and simultaneous reduction in the number of cells in both S and G2/M phases of the cell cycle. However, when depleting STAG3 using other si-RNAs specific for STAG3, more breast cancer dead cells were reported in MTT toxicity assay compared to MCF-10A. Finally, we studied STAG3 regulation by the transcription factors, E2F4/E2F6, no correlation was found between STAG3 expression and either of E2Fs as depleting any of them did not affect STAG3 expression. Interestingly, we found that RNAi-mediated E2F6 silencing, but not E2F4, in cancer cells caused cell death. On the other hand, MCF-10A cells depleted of E2F6 showed higher survival fraction in MTT. This finding suggests E2F6 as another potential therapeutic target for breast cancer.
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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 determine the presence and prevalence of SP cells in ovarian and breast cancer cell lines and clinical samples, and (ii) to ascertain their role both as cancer stem cells and in cancer drug resistance through ABC transporter identification and specific transporter knockdown. SP cells were identified in both ovarian and breast cancer cell lines and clinical samples. These SP cells expressed known stem cell genes and exhibited stem cell characteristics. SP cells in both ovarian and breast cancer cell lines were more drug resistant than non- SP (NSP, bulk tumour cells), and furthermore this drug resistance was shown to be due to expression of different ABC transporters in different tissue specific cancers. ABCG2 was found to be the predominate transporter expressed in breast cancer cell line derived SP populations, however silencing ABCG2 in MCF-7 breast cancer cell SP did not either completely inhibit SP presence or increase cell sensitivity to chemotherapy. In contrast ABCB1 was the predominant transporter expressed in ovarian cancer cell line (IGROV1 and HeyA8MDR) derived SP cells and silencing this transporter both fully inhibited SP cells and significantly increased SP cell death following treatment with paclitaxel. In clinical samples, the presence of SP cells in fine needle aspirates from breast cancer patients correlated to oestrogen receptor negative disease and the triple negative phenotype (ER-,PR-,HER2-), a marker of poor patient prognosis. This study has provided evidence of a role for SP cells in both breast and ovarian cancer. SP cells have a possible prognostic role in breast cancer, and ABCB1 should be considered as a therapeutic target in ovarian cancer.
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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 member of deubiquitinating enzymes (DUBs) and the gene maps to a gene rich region on 17q23. Genes on 17q23 are known to undergo amplification and overexpression in a subset of breast cancer cells and tumors. DUBs are known to be implicated in a variety of cellular functions including protein degradation, receptor endocytosis and vesicle trafficking. Therefore to elucidate the function of USP32, we localized the full length USP32 protein fused to GFP, in HeLa cells, using Fluorescence Protease Protection (FPP) assay and confocal microscopy. Results suggested a Golgi localization for USP32 as confirmed by co-localization study via BODIPY-TR, a Golgi specific marker. Additional investigations to find the role of USP32 in Golgi will further clarify the function of this candidate oncogene. Second part of the study focused on a potential tumor suppressor. For this purpose, we functionally characterized miR-125b, a microRNA gene as a potential tumor suppressor in breast cancer. microRNAs are regulators of gene expression and their deregulation is detected in cancer cells. miR-125b is reported as a down regulated microRNA in breast cancers. In this study, we investigated the expression, function and possible targets of miR-125b in breast cancer cell lines (BCCLs). Our results revealed a dramatic down regulation of miR-125b in a panel of BCCLs. Restoring the expression of miR-125b in low miR-125b expressing cells decreased the cell proliferation and migration as well as cytoplasmic protrusions, detected by staining of actin filaments. While connection of miR-125b and cell motility based on ERBB2 targeting has been reported earlier, here we present data on ERBB2 independent effects of miR-125b on cell migration in non-ERBB2 overexpressing breast cancer cells. Our results showed involvement of a miR-125b target, ARID3B, in cell motility and migration. Our findings showed miR-125b to be an important regulator of cell proliferation and migration in ERBB2 negative breast cancer cells, possibly through regulating multiple targets.
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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 subsequently contribute to the emergence of resistant cell growth. Microarray analysis, together with a stringent filtering process, identified 14 pro-survival genes significantly induced by at least one antihormone treatment (10 day tamoxifen, fulvestrant or oestrogen deprivation) in ER+ MCF-7 breast cancer cells, with increased expression maintained into cell models of antihormone-resistance. Of these 15 genes, 5 (GABBR2, CLU, CTNND2, BCL3 and TSC22D3) were significantly induced by all antihormone treatments. PCR and/or Western blotting demonstrated antihormone-induced expression of these 5 genes in T47D (ER+/HER2-), BT474 and MDA-MB-361 (ER+/HER2+) cell lines. The role of BCL3 and CLU during antihormone response and resistance were next investigated. siRNA-mediated BCL3 knockdown had no effect on cell survival but reduced proliferation of tamoxifen-resistant (TAMR) and oestrogen deprivationresistant (XR) cells. Immunoprecipitation and immunofluorescence studies revealed nuclear localisation and direct association of BCL3 and p50 in TAMR and XR cells. However, during response, BCL3 was located in the nucleus and p50 in the cytoplasm. In contrast, siRNA-mediated CLU knockdown reduced proliferation of fulvestrant-treated MCF-7 cells but was without effect on the growth of resistant cells. To conclude,this thesis has identified one antihormone-induced gene (CLU), which appears to limit response, and a second (BCL3), which appears to promote the growth of antihormone-resistant cells, potentially via activation of NFκB-mediated gene transcription.
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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 find novel functions for HP1γ in mouse embryonic stem cells (mESCs) and breast cancer cells. Mass spectrometry analysis identified citrullination of residues R38 and R39 within the CD of HP1γ. I show that these residues are citrullinated by peptidyl arginine deiminase 4 (PADI4) in vitro and in vivo. Mutations in HP1γ (R38/9A), designed to mimic the loss of charge accompanied with citrullination, affect HP1γ’s binding to H3K9me3 peptides and reduce its residence time on chromatin in differentiated mESCs, indicating a role for citrullination in regulating HP1γ binding to chromatin during differentiation. Furthermore, I studied the phenotype of HP1γ depletion in two human breast cancer models and found that HP1γ is essential for cell proliferation and viability of cancer, but not of normal epithelial cells. I performed whole transcriptome analysis in breast cancer cells depleted of HP1γ and cross-referenced it with its genomic localisation, which identified increased expression of interferon/antiviral defense genes and activation of pro-apoptotic pathways. Whilst genes involved in these pathways were not directly bound by HP1γ, this analysis also identified HP1γ as a novel regulator of zinc finger (ZNF) genes. In summary, I identified novel post-translational modifications in HP1γ and characterised them in mESCs. I further demonstrated a role for HP1γ regulating breast cancer cell viability and identified HP1γ as a novel regulator of ZNF genes. My findings highlight HP1γ as a potential target for breast cancer therapy.
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Books on the topic "Cancer cells Breast Genes"

1

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

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

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Tumor suppressor genes in breast cancer. Hauppauge (NY), USA: Nova Publishers, 2008.

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

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

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Sethi, Seema. miRNAs and Target Genes in Breast Cancer Metastasis. Cham: 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. London: Palgrave Macmillan UK, 2007. http://dx.doi.org/10.1057/9780230626553.

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Pham, Phuc Van. Breast Cancer Stem Cells & Therapy Resistance. Cham: 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. Cham: 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. [New Haven: 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, 253–58. Cham: 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, 323–29. Boston, MA: 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, 365–81. Boston, MA: 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, 181–88. Boston, MA: 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, 55–77. Totowa, NJ: 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, 319–22. Boston, MA: 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, 113–23. New York, NY: 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, Dandan Wang, Yijie Wang, Xuena Liu, Yongwei Lai, and Tongcun Zhang. "SNP Affects the Mobility of Breast Cancer Cells and the Expression of Metastasis-Related Genes." In Lecture Notes in Electrical Engineering, 181–88. Berlin, Heidelberg: 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, 233–55. New York, NY: 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, Audrey Loucks, James R. Johnson, Joseph Moskal, Manju Basu, Sipra Banerjee, and Subhash Basu. "Regulation of Glycosyltransferase Genes in Apoptotic Breast Cancer Cells Induced by l-PPMP and Cisplatin." In Advances in Experimental Medicine and Biology, 621–42. Boston, MA: 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 to CCL21, therefore reducing the metastasis of CCR7-expressing cancer cells. Truncated CCL21 chemokine (Δ98- 134 c-terminal basic extension), was synthesised to investigate a possible linkage between chemokine binding capacity and cell activation. Wild type (WT) and mutant-CCL21 were tested for their ability to stimulate a dose-dependent increase in intracellular-free calcium in peripheral blood mononuclear cell (PBMC) and breast cancer epithelial cells MDA-MB-231. Mutant-CCL21 at concentrations 5 and 10nM showed potential to mobilise Ca2+ at levels similar to that produced by WT-CCl21. A series of experiments was performed to determine how deletion of the HS-binding site altered the ability of CCL21 to stimulate chemotaxis within a concentration gradient generated by free solute diffusion. PBMC stimulated to migrate by wild-type CCL21 was not significantly different from that stimulated by mutant (P> 0.05). Similar results were observed in assays using MDA-MB-231 cells. A further series of experiments was performed to compare the potential of WT and mutant-CCL21 to stimulate the migration of cells across endothelium. In contrast to results for trans-filter migration, it was found that the non HSbinding mutant stimulated no increased in transendothelial cell migration above the background at each of the tested concentrations, 10, 30 and 50 nM respectively (P>0.05). However, WT-CCL21 stimulated significant increased PBMC migration at each of the tested concentration (all P <0.001). Furthermore, the effect of heparin on chemotactic properties of WT and mutant- CCL21 was examined. Interestingly, heparin (250 µg/ml) completely inhibit the chemotaxis mediated by WT-CCL21 (5nM) (P < 0.001), whereas it did not inhibit the chemotaxis at concentrations 100, 250 & 500 µg/ml in response to mutant CCL21 (5nM) (P > 0.05). Similar assay will be performed using MDA-MB-231 cells. Work is ongoing to characterise the biophysical properties of mutant-CCL21 and determine its potential role for a therapeutic blockade of the migration of breast cancer cells in-vivo. Our primarily data showed that mutant CCL21 in xenograft brain tumor models showed substantial inhibition of tumour growth. Our results indicate that truncated CCL21 chemokine might be a potential preventive biofactor for human breast cancer metastasis by targeting chemokine receptor genes.
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Alamoudi, Aliaa A., Hanan A. Bashmail, Ghada M. Ajabnoor, Hani Choudhry, Mohammed A. Hassan, Alia M. Aldahlawi, and Ahmed A. Al-abd. "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, Hani Choudhry, Mohammed A. Hassan, Alia M. Aldahlawi, and Ahmed A. Al-abd. "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 cell lines). Cell viability and morphological changes were evaluated upon treatment with PAMAMs. In addition, their effect on colony formation in soft agar was assessed. Additionally, western blot was performed to understand the underlying mechanisms of action. Results: PAMAMs anticancer effects were found to follow a specific trend, as they were more significant in cationic polymers and in higher generations. Cationic PAMAMs reduced cell viability of HER2 positive breast cancer cells up to 5.1% in SkBr3 and to 28% in ZR75 (p<0.001), in a dose and time-dependent manner. Cationic polymers also resulted in changing the morphology in the examined cell lines, as well as inhibiting colony formation in soft agar compared to controls (p<0.001). The mechanism of action was found to be mediated by inhibiting the phosphorylation of erbB2 and JNK1/2/3. Conclusion: These anticancer effects of PAMAM dendrimers make them promising molecules, which can add benefit to current anti-HER2 treatments and be employed successfully in different biomedical applications.
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Wikman, Harriet, Volkmar Müller, Dirk Kemming, Sabine Riethdorf, Kathrin Eylmann, Jolanthe Kropidlowski, Roland Eils, 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, and Sanjeev Gupta. "Abstract 5843: XBP1 regulates the expression of cell cycle associated genes in ERα positive breast cancer cells." In 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 drive tumorigenesis, and which are followers. Interrogation of cancer cells under variable g-forces is the treatment to which cancer cells are not normally exposed. Therefore, low (weightlessness) and high (acceleration) g-forces may trigger responses, which may differ in part of followers from responses on the Earth, but still engage carcinogenesis-essential drivers nodes and edges. Methodology: Experimental interrogation of human cancer cells to generate carcinogenesis-related regulatory networks was performed by using proteomics, cell biology, biochemistry, immunohistochemistry and bioinformatics tools. We used also reported datasets deposited in various databases. These networks were analyzed with algorithms to extract drivers of carcinogenesis. Results: Systemic analysis of human breast carcinogenesis has shown mechanisms of engagement of all known cancer hallmarks. Moreover, novel hallmarks have emerged, e.g. involvement of mechanisms of virus-cell interaction and RNA/miR processing. The breast cancer networks are rich, with >6,000 involved proteins and genes. The richness of the networks may explain many clinical observations, e.g. personalized response to treatments. Systemic analysis highlighted novel opportunities for treatment of cancer, by identifying key nodes of known and novel hallmark mechanisms. Systemic properties of the cancer network provides an opportunity to study compensatory mechanisms. These compensatory mechanisms frequently contribute to development of resistance to treatment. These mechanisms will be discussed. Cancer cells are not “wired” to function in weightlessness. The cells would have to adapt. This adaptation will include preserving mechanisms driving carcinogenesis, in addition to the space-only-related adaptation. Key carcinogenesis regulators in the space would be the same as on the Earth, while “passenger”-mechanisms would differ. Systems biology allows integration of a space- and the Earth-data, and would extract key regulators, and, subsequently lead to better diagnostic. Conclusion: Systemic analysis of carcinogenesis studies with different ways of interrogation delivered better diagnostic and novel modalities of treatment.
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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 growth inhibition of MCF-7 human breast cancer cells for the first time. Particularly, we used two DNA sequences for this purpose, which have been developed as anti-cancer agents: 5-GGT GGT GGT GGT TGT GGT GGT GGT GG-3 (also called, AGRO) and 5-(GT)15-3.[3–5] This study may ultimately form the basis of unique nanoparticle-based therapeutics with the additional ability to optically report molecular recognition. Figure 1a shows the photoluminescence (PL) spectra of GT- and AGRO-passivated PbS QD that fluoresce in the near IR, centered at approximately 980 nm. A typical synthesis procedure involves rapid addition of sodium sulfide in the mixture solution of DNA and Pb acetate at a molar ratio of 2:4:1. The resulting nanocrystals are washed to remove unreacted DNA and ions by adding mixture solution of NaCl and isopropanol, followed by centrifugation. The precipitated nanocrystals are collected and re-suspended in aqueous solution by mild sonication. Optical absorption measurements reveal that approximately 90 and 77% of GT and AGRO DNA is removed after the washing process. The particle size distribution in Figure 1b suggests that the GT sequence-capped PbS particles are primarily in 3–5 nm diameter range. These nanocrystals can be easily incorporated with mammalian cells and remain highly fluorescent in sub-cellular environments. Figure 1c serially presents an optical image of a MCF-7 cell and a PL image of the AGRO-capped QD incorporated with the cell. Figure 1. (a) Normalized fluorescence spectra of PbS QD synthesized with GT and AGRO sequences, which were previously developed as anti-cancer agents. The DNA-capped QD fluoresce in the near IR centered at ∼980 nm. (b) TEM image of GT-templated nanocrystals ranging 3–5 nm in diameter. (c) Optical image of an MCF-7 human breast cancer cell after a 12-hour exposure to aptamer-capped QD. (d) PL image of AGRO-QD incorporated with the cell, indicating that these nanocrystals remain highly fluorescent in sub-cellular environments. One immediate concern for interfacing inorganic nanocrystals with cells and tissue for labeling or therapeutics is their cytotoxicity. The nanoparticle cytotoxicity is primarily determined by material composition and surface chemistry, and QD are potentially toxic by generating reactive oxygen species or by leaching heavy metal ions when decomposed.[6] We examined the toxicity of aptamer-passivated nanocrystals with NIH-3T3 mouse fibroblast cells. The cells were exposed to PbS nanocrystals for 2 days before a standard MTT assay as shown in Figure 2, where there is no apparent cytotoxicity at these doses. In contrast, Pb acetate exerts statistically significant toxicity. This observation suggests a stable surface passivation by the DNA aptamers and the absence of appreciable Pb2+ leaching. Figure 2. Viability of 3T3 mouse fibroblast cells after a 2-day exposure to DNA aptamer-capped nanocrystals. There is no apparent dose-dependent toxicity, whereas a statistically significant reduction in cell viability is observed with Pb ions. Note that Pb acetate at 133 μM is equivalent to the Pb2+ amount that was used for PbS nanocrystal synthesis at maximum concentration. Error bars are standard deviations of independent experiments. *Statistically different from control (p&lt;0.005). Finally, we examined if these cyto-compatible nanoparticle-aptamers remained therapeutically active for cancer cell growth inhibition. The MTT assay results in Figure 3a show significantly decreased growth of breast cancer cells incorporated with AGRO, GT, and the corresponding templated nanocrystals, as anticipated. In contrast, 5-(GC)15-3 and the QDs synthesized with the same sequence, which were used as negative controls along with zero-dose control cells, did not alter cell viability significantly. Here, we define the growth inhibition efficacy as (100 − cell viability) per DNA of a sample, because the DNA concentration is significantly decreased during the particle washing. The nanoparticle-aptamers demonstrate 3–4 times greater therapeutic activities compared to the corresponding aptamer drugs (Figure 3b). We speculate that when a nanoparticle-aptamer is internalized by the cancer cells, it forms an intracellular complex with nucleolin and nuclear factor-κB (NF-κB) essential modulator, thereby inhibiting NF-κB activation that would cause transcription of proliferation and anti-apoptotic genes.[7] The nanoparticle-aptamers may more effectively block the pathways for creating anti-apoptotic genes or facilitate the cellular delivery of aptamers via nanoparticle uptake. Our additional investigation indicates that the same DNA capping chemistry can be utilized to produce aptamer-mediated Fe3O4 nanocrystals, which may be potentially useful in MRI and therapeutics, considering their magnetic properties and biocompatibility. In summary, the nanoparticle-based therapeutic schemes developed here should be valuable in developing a multifunctional drug delivery and imaging agent for biological systems. Figure 3. Anti-proliferation of MCF-7 human breast cancer cells with aptamer-passivated nanocrystals. (a) Viability of MCF-7 cells exposed to AGRO and GT sequences, and AGRO-/GT-capped QD for 7 days. The DNA concentration was 10 uM, while the particles were incubated with cells at 75 nM. (b) Growth inhibition efficacy is defined as (100 − cell viability) per DNA to correct the DNA concentration after particle washing.
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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. Fort Belvoir, VA: Defense Technical Information Center, October 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. Fort Belvoir, VA: Defense Technical Information Center, October 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. Fort Belvoir, VA: Defense Technical Information Center, June 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. Fort Belvoir, VA: Defense Technical Information Center, July 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. Fort Belvoir, VA: Defense Technical Information Center, July 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. Fort Belvoir, VA: Defense Technical Information Center, July 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. Fort Belvoir, VA: Defense Technical Information Center, July 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. Fort Belvoir, VA: Defense Technical Information Center, July 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. Fort Belvoir, VA: Defense Technical Information Center, August 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. Fort Belvoir, VA: Defense Technical Information Center, April 2003. http://dx.doi.org/10.21236/ada421784.

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