Relevant bibliographies by topics / MYC, breast cancer, epigenetic reprogramming

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Academic literature on the topic 'MYC, breast cancer, epigenetic reprogramming'

Author: Grafiati
Published: 9 March 2023
Last updated: 10 March 2023

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Journal articles on the topic "MYC, breast cancer, epigenetic reprogramming"

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Laurent, Audrey, Thierry Madigou, Maud Bizot, Marion Turpin, Gaëlle Palierne, Elise Mahé, Sarah Guimard, et al. "TET2-mediated epigenetic reprogramming of breast cancer cells impairs lysosome biogenesis." Life Science Alliance 5, no. 7 (March 29, 2022): e202101283. http://dx.doi.org/10.26508/lsa.202101283.

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Methylation and demethylation of cytosines in DNA are believed to act as keystones of cell-specific gene expression by controlling the chromatin structure and accessibility to transcription factors. Cancer cells have their own transcriptional programs, and we sought to alter such a cancer-specific program by enforcing expression of the catalytic domain (CD) of the methylcytosine dioxygenase TET2 in breast cancer cells. The TET2 CD decreased the tumorigenic potential of cancer cells through both activation and repression of a repertoire of genes that, interestingly, differed in part from the one observed upon treatment with the hypomethylating agent decitabine. In addition to promoting the establishment of an antiviral state, TET2 activated 5mC turnover at thousands of MYC-binding motifs and down-regulated a panel of known MYC-repressed genes involved in lysosome biogenesis and function. Thus, an extensive cross-talk between TET2 and the oncogenic transcription factor MYC establishes a lysosomal storage disease–like state that contributes to an exacerbated sensitivity to autophagy inducers.
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Białopiotrowicz, Emilia, Monika Noyszewska-Kania, Neli Kachamakova-Trojanowska, Agnieszka Łoboda, Magdalena Cybulska, Aleksandra Grochowska, Michał Kopczyński, et al. "Serine Biosynthesis Pathway Supports MYC–miR-494–EZH2 Feed-Forward Circuit Necessary to Maintain Metabolic and Epigenetic Reprogramming of Burkitt Lymphoma Cells." Cancers 12, no. 3 (March 3, 2020): 580. http://dx.doi.org/10.3390/cancers12030580.

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Burkitt lymphoma (BL) is a rapidly growing tumor, characterized by high anabolic requirements. The MYC oncogene plays a central role in the pathogenesis of this malignancy, controlling genes involved in apoptosis, proliferation, and cellular metabolism. Serine biosynthesis pathway (SBP) couples glycolysis to folate and methionine cycles, supporting biosynthesis of certain amino acids, nucleotides, glutathione, and a methyl group donor, S-adenosylmethionine (SAM). We report that BLs overexpress SBP enzymes, phosphoglycerate dehydrogenase (PHGDH) and phosphoserine aminotransferase 1 (PSAT1). Both genes are controlled by the MYC-dependent ATF4 transcription factor. Genetic ablation of PHGDH/PSAT1 or chemical PHGDH inhibition with NCT-503 decreased BL cell lines proliferation and clonogenicity. NCT-503 reduced glutathione level, increased reactive oxygen species abundance, and induced apoptosis. Consistent with the role of SAM as a methyl donor, NCT-503 decreased DNA and histone methylation, and led to the re-expression of ID4, KLF4, CDKN2B and TXNIP tumor suppressors. High H3K27me3 level is known to repress the MYC negative regulator miR-494. NCT-503 decreased H3K27me3 abundance, increased the miR-494 level, and reduced the expression of MYC and MYC-dependent histone methyltransferase, EZH2. Surprisingly, chemical/genetic disruption of SBP did not delay BL and breast cancer xenografts growth, suggesting the existence of mechanisms compensating the PHGDH/PSAT1 absence in vivo.
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Chavdoula, Evangelia, Vollter Anastas, Alessandro La Ferlita, Julian Aldana, Anuvrat Sircar, Michael A. Freitas, Lalit Sehgal, and Philip N. Tsichlis. "Abstract 3019: The epigenetic factor KDM2B alters the serine-glycine synthesis pathway and the one-carbon metabolism (SGOC) in triple-negative breast cancer." Cancer Research 82, no. 12_Supplement (June 15, 2022): 3019. http://dx.doi.org/10.1158/1538-7445.am2022-3019.

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Abstract Epigenetic and metabolic alterations in cancer cells are intertwined. The concentration of metabolites can influence the activity of chromatin modifiers, which in turn can act as metabolic sensors that translate changes in cellular metabolism to transcriptional reprogramming. In the present study, we investigated the role of histone demethylase KDM2B in the metabolic reprogramming of the triple-negative breast cancer (TNBC), in which KDM2B is selectively expressed at high levels. Knockdown of KDM2B in TNBC cell lines reduced their proliferation rate and tumor growth in vivo. Transcriptomic, proteomic, and metabolomic profiling demonstrated that the Serine-Glycine pathway and One Carbon metabolism (SGOC) and other amino acid biosynthetic and catabolic processes are downregulated by the knockdown of KDM2B. Additionally, we see reduction of metabolites produced via these pathways (purines, pyrimidines, formate, glutathione and NADPH). Importantly, the expression of the enzymes involved in the SGOC metabolic pathway (e.g. PHGDH, PSAT1, PSPH, SHMT2, MTHFD1L, MTHFD2 and DHFR) depends on c-MYC, NRF2, and ATF4 which our data show that they are under the positive regulatory control of KDM2B. The epistatic relationship between these factors, with the expression of the enzymes of the SGOC pathway and the effects of the KDM2B knockdown on chromatin occupancy and accessibility of the promoters of these factors is in progress and will be presented. Analysis of TCGA data showed positive and statistically significant correlations between KDM2B and the SGOC gene signature in TNBC patients. In addition, the metabolic pathway signature that distinguishes control and shKDM2B-transduced cells corresponds to the metabolic signature of a subset of TNBCs, which have been reported to carry poor prognosis. The present study highlights the role of the epigenetic factor KDM2B as an upstream regulator of the metabolic reprogramming of TNBC. Citation Format: Evangelia Chavdoula, Vollter Anastas, Alessandro La Ferlita, Julian Aldana, Anuvrat Sircar, Michael A. Freitas, Lalit Sehgal, Philip N. Tsichlis. The epigenetic factor KDM2B alters the serine-glycine synthesis pathway and the one-carbon metabolism (SGOC) in triple-negative breast 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 3019.
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Ferreira, Alexandra G., Olga Zimmermannova, Ervin Ascic, Ilia Kurochkin, Diego Soto-Cabrera, Ariane Eceiza, Hreinn Benonisson, et al. "Abstract A40: Restoring tumor immunogenicity with dendritic cell reprogramming." Cancer Immunology Research 10, no. 12_Supplement (December 1, 2022): A40. http://dx.doi.org/10.1158/2326-6074.tumimm22-a40.

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Abstract Immunotherapy is revolutionizing cancer treatment, but success is limited to a fraction of patients. Tumor immunosurveillance and immunotherapy relies on presentation of tumor-associated antigens by conventional dendritic cells type 1 (cDC1). However, tumors develop mechanisms to avoid immune recognition such as downregulation of antigen presentation and exclusion of cDC1. We have previously demonstrated that enforced expression of the transcription factors PU.1, IRF8 and BATF3 (PIB) imposes the lineage conversion of fibroblasts to cDC1 by direct cell reprogramming. Here, we hypothesize that PIB reprograms cancer cells directly into functional tumor-antigen presenting cells (tumor-APCs) with enhanced immunogenicity. First, we show that enforced expression of PIB in a wide range of murine and human cancer cells from different origins is sufficient to induce surface expression of hematopoietic and DC-lineage specific markers (CD45 and Clec9a). Moreover, reprogramming restored the expression of antigen presentation complexes (MHC-I and MHC-II) and activated the expression of the co-stimulatory molecules CD40, CD80 and CD86, required for productive T cell activation. Transcriptomic analysis using mRNA-sequencing showed that PIB imposes a global cDC1 gene signature and an antigen presentation program in tumor cells as early as day 3 of reprogramming, overriding the original cancer cell program. Furthermore, Assay for Transposase-Accessible Chromatin (ATAC) sequencing analysis revealed that PIB-mediated cDC1 reprogramming elicited rapid epigenetic remodeling followed by gradual rewiring of transcriptional program and stabilization of cDC1 identity. Functionally, tumor-APCs present endogenous antigens on MHC-I, prime naïve CD8+ T and become prone to CD8+ T cell mediated killing. Tumor-APCs secrete pro-inflammatory cytokines (IL-12) and chemoattractants (CXCL10), uptake and process exogenous antigens, phagocyte dead cells, and cross-present exogenous antigens to activate naïve T-cells. In addition, reprogrammed tumor cells harboring TP53, KRAS and PTEN mutations downregulated proliferation and showed impaired tumorigenicity in vitro and in vivo. Importantly, we show that intra-tumoral injection of reprogrammed tumor-APCs elicited tumour growth control in vivo alongside increasing infiltration of CD8+ T and NK cells in B16-OVA tumors. Finally, we showed that our approach can be employed to convert primary cancer cells derived from melanoma, lung, breast, pancreatic, urothelial, and head and neck carcinomas as well as cancer associated fibroblasts. In summary, we provide evidence for the direct reprogramming of tumor cells into immunogenic cDC1-like cells, with restored antigen presentation capacity and the ability to reinstate anti-tumor immunity. Our approach elicits the immune system against cancer and counteract major tumor evasion mechanisms including tumor heterogeneity and impaired antigen presentation, laying the foundation for developing immunotherapeutic strategies based on the cellular reprogramming of human cancer cells. Citation Format: Alexandra G. Ferreira, Olga Zimmermannova, Ervin Ascic, Ilia Kurochkin, Diego Soto-Cabrera, Ariane Eceiza, Hreinn Benonisson, Inês Caiado, Rita Silvério-Alves, Fábio F. Rosa, Cristiana F. Pires, David Gomez-Jimenez, Carina Bernardo, Monika Bauden, Roland Anderson, Mattias Höglund, Kenichi Miharada, Yukio Nakamura, Lennart Greiff, Malin Lindstedt, Carlos-Filipe Pereira. Restoring tumor immunogenicity with dendritic cell reprogramming [abstract]. In: Proceedings of the AACR Special Conference: Tumor Immunology and Immunotherapy; 2022 Oct 21-24; Boston, MA. Philadelphia (PA): AACR; Cancer Immunol Res 2022;10(12 Suppl):Abstract nr A40.
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Lacouture, Aurélie, Cynthia Jobin, Alisson Clemenceau, Cindy Weidmann, Line Berthiaume, Dominic Bastien, Isabelle Laverdière, et al. "Abstract P5-02-01: A FACS-free purification method to study estrogen signaling, organoid formation, and metabolic reprogramming in mammary epithelial cells." Cancer Research 82, no. 4_Supplement (February 15, 2022): P5–02–01—P5–02–01. http://dx.doi.org/10.1158/1538-7445.sabcs21-p5-02-01.

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Abstract Mammary epithelial cells (MECs) are known to have their metabolism reprogrammed following pregnancy to allow the increased energy requirements for lactation. The estrogen receptor α (ERα) is mainly associated with the regulation of biological pathways linked to mammary gland development but its influence on MECs metabolism is still unknown. Our hypothesis is that ERα reprograms cell metabolism in normal MECs, a phenomenon that would be reprogrammed during breast carcinogenesis. Few in vitro models are used to study MECs, and most of them do not express ERα. Primary MECs can be used to overcome this issue, but methods to purify these cells generally require flow cytometry and fluorescence-activated cell sorting (FACS), which require specialized instruments and expertise. Herein, we present in detail a FACS-free protocol for purification and primary culture of mouse MECs to study ERα metabolic functions using mass spectrometry (MS). Purified MECs from nulliparous mice remain differentiated for up to six days with >85% luminal epithelial cells in two-dimensional culture. When seeded in Matrigel, they form organoids that recapitulate the mammary gland morphology in vivo by developing lumens, contractile cells, and lobular structures. MECs express a functional ERα signaling pathway in both two- and three-dimensional cell culture, as shown at the mRNA and protein levels and by the phenotypic characterization. Extracellular metabolic flux analysis showed that estrogens induce a metabolic switch favouring aerobic glycolysis over mitochondrial respiration in MECs grown in two-dimensions, a phenomenon known as the Warburg effect. We also performed (MS)-based metabolomics in organoids. Estrogens altered the levels of metabolites from various pathways, including aerobic glycolysis, citric acid cycle, urea cycle, and amino acid metabolism, demonstrating that ERα reprograms cell metabolism in mammary organoids. To further understand this reprogramming, stable isotope tracer analysis in primary culture organoids are currently performed. In addition, pregnancy and breast-feeding are known to be protective against breast carcinogenesis. Consequently, we also performed MEC purification and organoid culture using mammary glands from multiparous mice. Intriguingly, organoid phenotypic characterization indicated a difference in organoid structures between MECs from nulliparous and multiparous mice. Furthermore, we observe significant differences in estrogenic response between both conditions, suggesting that pregnancy and/or lactation promotes the establishment of specific epigenetic marks that are preserved even ex vivo. Chromatin immunoprecipitation of specific histone marks and MS-based metabolic studies are ongoing to better understand the different responses of mammary organoids to estrogens between nulliparous and multiparous mice. Overall, we have optimized mouse MEC isolation and purification for two- and three-dimensional cultures and for MS-based metabolomics. We demonstrated that these organoids retain a functional ERα pathway over time and that ERα significantly reprograms multiple metabolic pathways. This model represents a valuable tool to study how estrogens modulate mammary gland biology, and particularly how these hormones reprogram metabolism during lactation and breast carcinogenesis. Citation Format: Aurélie Lacouture, Cynthia Jobin, Alisson Clemenceau, Cindy Weidmann, Line Berthiaume, Dominic Bastien, Isabelle Laverdière, Martin Pelletier, Caroline Diorio, Francine Durocher, Étienne Audet-Walsh. A FACS-free purification method to study estrogen signaling, organoid formation, and metabolic reprogramming in mammary epithelial cells [abstract]. In: Proceedings of the 2021 San Antonio Breast Cancer Symposium; 2021 Dec 7-10; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2022;82(4 Suppl):Abstract nr P5-02-01.
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LaFlamme, Brooke. "Epigenetic reprogramming in treatment-resistant breast cancer." Nature Genetics 46, no. 5 (April 28, 2014): 423. http://dx.doi.org/10.1038/ng.2977.

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Berger, Adeline, Nicholas J. Brady, Rohan Bareja, Brian Robinson, Vincenza Conteduca, Michael A. Augello, Loredana Puca, et al. "N-Myc–mediated epigenetic reprogramming drives lineage plasticity in advanced prostate cancer." Journal of Clinical Investigation 129, no. 9 (August 19, 2019): 3924–40. http://dx.doi.org/10.1172/jci127961.

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Suriyamurthy, Sudha, David Baker, Peter ten Dijke, and Prasanna Vasudevan Iyengar. "Epigenetic Reprogramming of TGF-β Signaling in Breast Cancer." Cancers 11, no. 5 (May 24, 2019): 726. http://dx.doi.org/10.3390/cancers11050726.

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The Transforming Growth Factor-β (TGF-β) signaling pathway has a well-documented, context-dependent role in breast cancer development. In normal and premalignant cells, it acts as a tumor suppressor. By contrast, during the malignant phases of breast cancer progression, the TGF-β signaling pathway elicits tumor promoting effects particularly by driving the epithelial to mesenchymal transition (EMT), which enhances tumor cell migration, invasion and ultimately metastasis to distant organs. The molecular and cellular mechanisms that govern this dual capacity are being uncovered at multiple molecular levels. This review will focus on recent advances relating to how epigenetic changes such as acetylation and methylation control the outcome of TGF-β signaling and alter the fate of breast cancer cells. In addition, we will highlight how this knowledge can be further exploited to curb tumorigenesis by selective targeting of the TGF-β signaling pathway.
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Pathiraja, T. N., S. R. Nayak, Y. Xi, S. Jiang, J. P. Garee, D. P. Edwards, A. V. Lee, et al. "Epigenetic Reprogramming of HOXC10 in Endocrine-Resistant Breast Cancer." Science Translational Medicine 6, no. 229 (March 26, 2014): 229ra41. http://dx.doi.org/10.1126/scitranslmed.3008326.

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Sharma, D., B. B. Knight, R. Yacoub, T. Liu, L. Taliaferro-Smith, A. Nagalingam, and R. M. O'Regan. "Using epigenetic reprogramming to target triple-negative breast cancer." Journal of Clinical Oncology 27, no. 15_suppl (May 20, 2009): e14565-e14565. http://dx.doi.org/10.1200/jco.2009.27.15_suppl.e14565.

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e14565 Background: The outcome for patients with breast cancer has been significantly improved by the use of targeted agents. The prognosis of triple negative (TN) breast cancers, which do not express hormone receptors (ER, PR) or Her2, is poor, because of an aggressive clinical course and lack of targeted therapeutic agents. Epigenetic silencing of specific genes has been observed in breast cancer and some of these genes are more important due to available targeted therapies such as ER. Since all endocrine therapies are designed to block ER function in some way, the identification of new therapies or strategies that could sensitize TN breast cancers to existing endocrine therapy could provide a revolutionary means of treating this aggressive subtype of cancer Methods: We examined the efficacy of combined treatment of HDAC inhibitor LBH589 and DNMT inhibitor decitabine to regenerate ER and PR in TN breast cancer cells using RT-PCR and immunoblotting. Changes in growth and proliferation of TN breast cancer cells in response to LBH589 and decitabine treatment were determined by XTT, BrdU incorporation and colony formation assay. Changes in apoptotic proteins were determined by western blotting. Athymic nude mice were used to establish pre-clinical models for TN breast cancer cells and effectiveness of combined treatment of LBH589 and decitabine was determined. Tumors biopsies were analyzed for ER and PR re-expression by western blot analysis and immunohistochemistry at the end of the treatment. Results: Combined treatment of LBH589 and decitabine resulted in re-expression of ER and PR in TN breast cancers in vitro and in vivo. Although re-expression of ER and PR were noted following LBH589 treatment alone, re-expression was more robust with the combination. TN breast cancer cells showing re-expressed ER can be targeted with tamoxifen. Tamoxifen inhibits growth of TN breast cancer cells re- expressing ER by triggering apoptosis. Conclusions: The importance of epigenetic events such as DNA methylation and HDAC inhibition in tumor progression is becoming increasingly evident. A trial evaluating the ability of LBH589 and decitabine to re- express ER, which can then be targeted by tamoxifen, is planned in patients with metastatic TN breast cancer. No significant financial relationships to disclose.
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Dissertations / Theses on the topic "MYC, breast cancer, epigenetic reprogramming"

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POLI, VITTORIA. "MYC agisce da fattore di riprogrammazione tumorale tramite induzione di uno stato di staminalità cellulare in cellule epiteliali umane della ghiandola mammaria." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2016. http://hdl.handle.net/10281/117389.

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Cancer is both a genetic and an epigenetic disease whose outcome is influenced by tumor microenvironment. These three determinants represent the major driving forces of tumorigenesis and cause the functional heterogeneity observed in most of the cancer types. Both normal and neoplastic cell populations are known to harbor subpopulations of Stem Cells (SCs) that can both self-renew and spawn more differentiated progeny that, in the case of cancer, forms the tumor bulk. For what concerns Cancer Stem Cells (CSCs), they are proposed to held most of the tumor initiating potential and a higher proportion of CSCs within a tumor often correlates with poorer prognosis. Accumulating evidences indicate that SCs transcriptional program of both normal and neoplastic tissues rely on common molecular regulators including important developmental signals, such as the WNT pathway, whose de-regulation is causative of tumor initiation. Given their importance in the maintenance and propagation of cancer, identifying the cell of origin of CSCs would represent a great opportunity for understanding the molecular mechanisms underlying the onset of tumorigenesis, thereby offering new therapeutic strategies. A likely scenario of how multistep tumorigenesis may proceeds is that pools of transit amplifying progenitor cells, that are mitotically more active and more numerous than SCs, may serve as targets of somatic and epigenetic alterations that would cause their de-differentiation, pushing them back to the SCs compartment. This emerging model is based upon recent findings that hierarchically organized cell populations are, at least in epithelial tissues such as the mammary gland, more plastic than previously imagined. In this view, cell transformation can be described as a cell reprogramming process toward a SC-like state, in which a committed cell has to over-come a number of epigenetic barriers, that normally stabilize it, in order to alter its identity. Although promising, the mechanisms that should drive to the epigenetic reprogramming of committed cells are largely undefined and the putative role of developmental signals in this process has not been elucidated so far. We hypothesize that the proto-oncogene c-MYC could represent a bona fide tumor reprogramming factor. c-MYC over-expression in cancer cells can result from constitutive activation of a number of developmental pathways that lay up-stream c-MYC expression, such as the WNT/β-Catenin pathway constitutive activation is a rate-limiting step in tumorigenesis. On the basis of the findings obtained in our laboratory, MYC is able to sustain embryonic stem cells self-renewal by activating the WNT/β-Catenin pathway, through direct recruitment of Polycomb Repressive Complex 2 (PRC2) on the promoter of the two major inhibitors DKK1 and SFRP1. We hypothesize that a similar mechanism could explain what happens in the early events of tumorigenesis. More specifically, MYC over-expression in committed cells could induce their reprogramming to a SC-like state, through induction of autocrine WNT pathway hyper-activation, therefore favoring the acquisition of further genetic and epigenetic insults, that would induce the uprising of a CSC phenotype. Our results indicate that MYC over-expression in human Immortalized Mammary Epithelial Cells (IMECs) induces a cellular reprogramming towards a luminal progenitor cell-like state and that such condition is associated to hyper-activation of the WNT/β-Catenin pathway. Unlikely wild type cells, MYC-enriched pool of progenitor cells is prone to originate CSCs, since an additional genetic insult, such as over-expression of PIK3CAH1047R, is sufficient to endow IMEC MYC with tumorigenic capacity, while has no effect on wild type cells.
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Leong, Yeh Chwan. "Reprogramming to cancer induced pluripotent stem cells elucidates the contribution of genetic and epigenetic alterations to breast carcinogenesis." Thesis, University of Nottingham, 2018. http://eprints.nottingham.ac.uk/53330/.

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The induced pluripotent stem cells (iPSCs) technology has revolutionized disease modelling by enabling the generation of patient-specific pluripotent stem cells for the study of complex disorders such as cancer. Somatic cell reprogramming through iPSCs induces global epigenetic reconfiguration of the chromatin which converts cancer cells to an embryonic stem cell-like state with potential reversion of tumorigenicity. Therefore, reprogramming can be used to answer the question as to whether epigenetic alterations alone can be sufficient to induce carcinogenesis, independent of genetic defects. In addition, it can used to dissect the relative contribution of genetics and epigenetics and epigenetics to tumorigenicity. In this study, the triple negative breast cancer (TNBC) cell line BT-549 and oestrogen receptor positive (ER+) cell line MCF7 were successfully reprogrammed by using the non-integrative episomal vectors expressing OCT4, SOX2, L-MYC, KLF4, LIN28, EBNA1, shRNA against TP53, and microRNA-302/367 cluster together with treatment of sodium butyrate. Pluripotency of cancer-derived iPSCs was confirmed by RT-PCR, RT-qPCR and immunofluorescence staining for expression of pluripotency markers. Differentiation potential of iPSCs was also assessed by using in vitro differentiation either spontaneous or directed to the mammary lineage. Functional assays indicated potential loss of tumorigenicity in re-differentiated cells derived from cancer iPSCs. The same approach was applied to study an immortalised, non-malignant mammary epithelial cell line MCF10A and two of its derived isogenic lines harbouring the two most frequent mutations in breast cancer, PIK3CAH1047R (+/-) and TP53(-/-), created by using CRISPR-Cas9 gene editing. Reprogramming induced a tumorigenic phenotype in iPSCs (PIK3CAH1047R (+/-) isogenic line only) and re-differentiated progenies (in both wild type MCF10A and PIK3CAH1047R (+/-) cell lines), suggesting the contribution of PIK3CA mutation in enhancing malignant transformation. Results in this study suggested that epigenetics alone and/or its interaction with genetic defects (e.g. PIK3CA mutation) has significant impact on breast cancer carcinogenesis. The dissection of the molecular mechanisms underlying the loss and gain of tumorigenicity using the iPSC models generated in this study could provide general understandings on breast carcinogenesis, which in turn could have important clinical implications.
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Payne, Kyle K. "Immunotherapy of Cancer: Reprogramming Tumor/Immune Cellular Crosstalk to Improve Anti-Tumor Efficacy." VCU Scholars Compass, 2015. http://scholarscompass.vcu.edu/etd/3939.

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Immunotherapy of cancer has been shown to be promising in prolonging patient survival. However, complete elimination of cancer and life-long relapse-free survival remain to be major challenge for anti-cancer therapeutics. We have previously reported that ex vivo reprogramming of tumor-sensitized immune cells by bryostatin 1/ionomycin (B/I) and the gamma-chain (γ-c) cytokines IL-2, IL-7, and IL-15 resulted in the generation of memory T cells as well as CD25+ NKT cells and CD25+ NK cells. Adoptive cellular therapy (ACT) utilizing these reprogrammed immune cells protected FVBN202 mice from tumor challenge, and overcame the suppressive functions of myeloid-derived suppressor cells (MDSCs). We then demonstrated that the presence of CD25+ NKT cells was required for anti-tumor efficacy of T cells as well as their resistance to MDSCs. Similar results were obtained by reprogramming of peripheral blood mononuclear cells (PBMC) from patients with early stage breast cancer, demonstrating that an increased frequency of CD25+ NKT cells in reprogrammed immune cells was associated with modulation of MDSCs to CD11b-HLA-DR+ immune stimulatory cells. Here, we tested the efficacy of immunotherapy in a therapeutic setting against established primary breast cancer (Chapter One), experimental metastatic breast cancer (Chapter Three) as well as against minimal residual disease (MRD) in patients with multiple myeloma (Chapter Two). We evaluated the ability of reprogrammed immune cells, including CD25+ NKT cells, to convert MDSCs to myeloid immune stimulatory cells, in vivo; this resulted in the identification and characterization of a novel antigen presenting cell (APC). These novel immune stimulatory cells differed from conventional APCs, including dendritic cells (DCs) and macrophages. We have also demonstrated that enhancing immunogenicity of mammary tumors by treatment with Decitabine (Dec) along with overcoming MDSCs by utilizing reprogrammed T cells and NKT cells in ACT prolongs survival of animals, but fails to eliminate the tumor. However, targeting cancer during a setting of MDR, when tumor cells are dormant, results in objective responses as evidenced in our multiple myeloma studies. This suggests that targeting breast cancer with immunotherapy following conventional therapies, in a setting of residual disease when tumor cells are dormant, may be effective in eliminating such residual cells or maintaining dormancy and extending time-to-relapse for breast cancer patients.
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Conference papers on the topic "MYC, breast cancer, epigenetic reprogramming"

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Berger, Adeline, Nicholas Brady, Rohan Bareja, Brian Robinson, Vincenza Conteduca, Michael Augello, Loredana Puca, et al. "Abstract 2099: N-Myc-mediated epigenetic reprogramming drives lineage plasticity in advanced prostate cancer." 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.sabcs18-2099.

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Berger, Adeline, Nicholas Brady, Rohan Bareja, Brian Robinson, Vincenza Conteduca, Michael Augello, Loredana Puca, et al. "Abstract 2099: N-Myc-mediated epigenetic reprogramming drives lineage plasticity in advanced prostate cancer." 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.am2019-2099.

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Christova, Rossitza, Kevin Petrie, Nidhi Bansal, Boris Leibovitch, Louise Howell, Veronica Gil, Ming-Ming Zhou, et al. "Abstract 411: Targeted PF1, JARID1B inhibition induces epigenetic reprogramming in triple negative breast cancer." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-411.

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Zou, June X., Junjian Wang, Zhijian Duan, Hongwu Chen, Hsing-Jien Kung, Xinbin Chen, Leigh C. Murphy, and Alexander Borowsky. "Abstract 2433: Metabolic reprogramming by an epigenetic mechanism in endocrine therapy resistance of breast cancer." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-2433.

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Jokela, Tiina A., Dustin Schones, and Mark A. LaBarge. "Abstract P6-03-04: Microenvironment-induced epigenetic reprogramming imposes drug-tolerant states in breast cancer cells." In Abstracts: 2019 San Antonio Breast Cancer Symposium; December 10-14, 2019; San Antonio, Texas. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.sabcs19-p6-03-04.

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Wang, Zhiyu, Neng Wang, Shengqi Wang, and Yifeng Zheng. "Abstract 1924: Caveolin-1 inhibits mammary carcinogenesisviasuppressing c-myc-induced metabolism reprogramming in breast cancer stem 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.am2017-1924.

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Poli, V., L. Fagnocchi, A. Fasciani, A. Turdo, M. Giaggianesi, V. Vaira, S. Bicciato, M. Todaro, and A. Zippo. "PO-298 MYC favours the onset of tumour initiating cells by inducing epigenetic reprogramming of mammary epithelial cells towards a stem cell-like state." In Abstracts of the 25th Biennial Congress of the European Association for Cancer Research, Amsterdam, The Netherlands, 30 June – 3 July 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/esmoopen-2018-eacr25.329.

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Sengupta, Surojeet, Shuait Nair, Lu Jin, Catherine M. Sevigny, Brandon Jones, and Robert Clarke. "Abstract PS17-50: Nuclear expression of acetyl-CoA producing enzymes and their roles in epigenetic reprogramming in breast cancer cells." In Abstracts: 2020 San Antonio Breast Cancer Virtual Symposium; December 8-11, 2020; San Antonio, Texas. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.sabcs20-ps17-50.

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Waxman, Samuel, Eduardo Farias, Kevin Petrie, Boris Leibovitch, Edgardo Ariztia, Janice Murtagh, Manuel Boix Chornet, Tino Schenk, and Arthur Zelent. "Abstract 572: Interference with Sin3 PAH-2 domain function induces epigenetic reprogramming, differentiation and growth inhibition in breast cancer cells." 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.am10-572.

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Su, Yanrong, Nathan R. Hopfinger, Thomas J. Pogash, Theresa D. Nguyen, Julia Santucci-Pereira, and Jose Russo. "Abstract 423: Epigenetic reprogramming of epithelial-mesenchymal transition in triple-negative breast cancer cells with DNA methyltransferase and histone deacetylase inhibitors." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-423.

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You might also be interested in the extended bibliographies on the topic 'MYC, breast cancer, epigenetic reprogramming' for particular source types:
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